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(A) Mechanism of SDD alleviating neuronal injury in CIH-exposed HT22 cells by <t>IGF1/IGFR</t> signaling pathway. (B) Role of IGF1/IGFR signaling pathway in alleviating CIH induced cognitive impairment by SDD treatment. (C) Mixed drug standards. (D) SDD water extract. 1: Catalpol, 2: Morroniside, 3: Loganin, 4: Ginsenoside Rb1, 5: Paeonol. Created with BioRender. com.

(A) Mechanism of SDD alleviating neuronal injury in CIH-exposed HT22 cells by <t>IGF1/IGFR</t> signaling pathway. (B) Role of IGF1/IGFR signaling pathway in alleviating CIH induced cognitive impairment by SDD treatment. (C) Mixed drug standards. (D) SDD water extract. 1: Catalpol, 2: Morroniside, 3: Loganin, 4: Ginsenoside Rb1, 5: Paeonol. Created with BioRender. com.

Igf1, supplied by Bioss, used in various techniques. Bioz Stars score: 93/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 27 article reviews

igf1 - by Bioz Stars, 2026-03

93/100 stars

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1) Product Images from "Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment"

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

Journal: Journal of Traditional and Complementary Medicine

doi: 10.1016/j.jtcme.2024.11.014

(A) Mechanism of SDD alleviating neuronal injury in CIH-exposed HT22 cells by IGF1/IGFR signaling pathway. (B) Role of IGF1/IGFR signaling pathway in alleviating CIH induced cognitive impairment by SDD treatment. (C) Mixed drug standards. (D) SDD water extract. 1: Catalpol, 2: Morroniside, 3: Loganin, 4: Ginsenoside Rb1, 5: Paeonol. Created with BioRender. com.

Figure Legend Snippet: (A) Mechanism of SDD alleviating neuronal injury in CIH-exposed HT22 cells by IGF1/IGFR signaling pathway. (B) Role of IGF1/IGFR signaling pathway in alleviating CIH induced cognitive impairment by SDD treatment. (C) Mixed drug standards. (D) SDD water extract. 1: Catalpol, 2: Morroniside, 3: Loganin, 4: Ginsenoside Rb1, 5: Paeonol. Created with BioRender. com.

Techniques Used:

Effects of CIH exposure on cell activity and IGF1/IGFR expression in HT22 cells. (A) Effects of CIH exposure on cell viability at different times. (B) IGF1 expression in HT22 cells at various CIH exposure times. (C) Secretion levels of IGF1 in cell cultures at different CIH exposure times. (D–E) HT22 cells expressing IGFR were detected by immunofluorescence at different CIH exposure times; arrows denote the positive cells (scale bar = 25 μm). (F) IGFR expression in HT22 cells after various CIH exposure times. The outcomes are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus 0 h CIH exposure.

Figure Legend Snippet: Effects of CIH exposure on cell activity and IGF1/IGFR expression in HT22 cells. (A) Effects of CIH exposure on cell viability at different times. (B) IGF1 expression in HT22 cells at various CIH exposure times. (C) Secretion levels of IGF1 in cell cultures at different CIH exposure times. (D–E) HT22 cells expressing IGFR were detected by immunofluorescence at different CIH exposure times; arrows denote the positive cells (scale bar = 25 μm). (F) IGFR expression in HT22 cells after various CIH exposure times. The outcomes are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus 0 h CIH exposure.

Techniques Used: Activity Assay, Expressing, Immunofluorescence, Standard Deviation

Effects of exogenous IGF1 on cell viability and mitochondrial dysfunction in CIH-exposed HT22 cells. (A) Effects of various IGF1 concentrations on cell viability. (B) TEM was used to detect mitochondria in HT22 cells that had been exposed to CIH (20000 × ). (C and E) Effects of exogenous IGF1 on the mitochondrial membrane potential of HT22 cells (scale bar = 50 μm). (D and F) Effects of exogenous IGF1 on ROS production in the mitochondria of CIH-exposed HT22 cells (scale bar = 25 μm). (G) Effects of exogenous IGF1 on mitochondrial ATP levels in CIH-exposed HT22 cells. (H) Effects of exogenous IGF1 on the level of mitochondrial respiratory chain complex Ι in HT22 cells exposed to CIH. (I) BDNF expression in CIH-exposed HT22 cells. (J) PSD-95 expression in CIH-exposed HT22 cells. (K) P-CREB/CREB expression in HT22 cells exposed to CIH. (L) P-ERK/ERK expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Figure Legend Snippet: Effects of exogenous IGF1 on cell viability and mitochondrial dysfunction in CIH-exposed HT22 cells. (A) Effects of various IGF1 concentrations on cell viability. (B) TEM was used to detect mitochondria in HT22 cells that had been exposed to CIH (20000 × ). (C and E) Effects of exogenous IGF1 on the mitochondrial membrane potential of HT22 cells (scale bar = 50 μm). (D and F) Effects of exogenous IGF1 on ROS production in the mitochondria of CIH-exposed HT22 cells (scale bar = 25 μm). (G) Effects of exogenous IGF1 on mitochondrial ATP levels in CIH-exposed HT22 cells. (H) Effects of exogenous IGF1 on the level of mitochondrial respiratory chain complex Ι in HT22 cells exposed to CIH. (I) BDNF expression in CIH-exposed HT22 cells. (J) PSD-95 expression in CIH-exposed HT22 cells. (K) P-CREB/CREB expression in HT22 cells exposed to CIH. (L) P-ERK/ERK expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Techniques Used: Membrane, Expressing, Standard Deviation

Effect of SDD on IGF1 and IGFR expression in HT22 cells under CIH conditions. (A) Western blotting of IGF1. (B) IGF1 expression in CIH-exposed HT22 cells. (C) Secretion levels of IGF1 in cell cultures exposed to CIH. (D–E) The number of IGFR-positive cells was detected by immunofluorescence in CIH-exposed HT22 cells; arrows denote the presence of positive cells (scale bar = 25 μm). (F) IGFR expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01 versus the CIH group.

Figure Legend Snippet: Effect of SDD on IGF1 and IGFR expression in HT22 cells under CIH conditions. (A) Western blotting of IGF1. (B) IGF1 expression in CIH-exposed HT22 cells. (C) Secretion levels of IGF1 in cell cultures exposed to CIH. (D–E) The number of IGFR-positive cells was detected by immunofluorescence in CIH-exposed HT22 cells; arrows denote the presence of positive cells (scale bar = 25 μm). (F) IGFR expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01 versus the CIH group.

Techniques Used: Expressing, Western Blot, Immunofluorescence, Standard Deviation

Effects of SDD on the IGF1/IGFR signaling pathway under CIH conditions. (A) Western blotting RAS, RAF, and MAPK. (B–D) RAS, RAF, and MAPK expression in CIH-exposed HT22 cells. (E) Western blotting of PI3K, P-AKT/AKT, and GSK3β in CIH-exposed HT22 cells. (F–H) PI3K, P-AKT/AKT, and GSK3β expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Figure Legend Snippet: Effects of SDD on the IGF1/IGFR signaling pathway under CIH conditions. (A) Western blotting RAS, RAF, and MAPK. (B–D) RAS, RAF, and MAPK expression in CIH-exposed HT22 cells. (E) Western blotting of PI3K, P-AKT/AKT, and GSK3β in CIH-exposed HT22 cells. (F–H) PI3K, P-AKT/AKT, and GSK3β expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Techniques Used: Western Blot, Expressing, Standard Deviation

Role of IGF1 siRNA and AG1024 in regulating the effects of SDD on the expression of IGF1/IGFR downstream signaling molecules in CIH-exposed HT22 cells. (A) Western blotting of RAS, RAF, and MAPK. (B–D) Expression of RAS, RAF, and MAPK in CIH-exposed HT22 cells. (E) Western blotting of PI3K, P-AKT/AKT, and GSK3β in CIH-exposed HT22 cells. (F–H) Expression of PI3K, P-AKT/AKT, and GSK3β in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Figure Legend Snippet: Role of IGF1 siRNA and AG1024 in regulating the effects of SDD on the expression of IGF1/IGFR downstream signaling molecules in CIH-exposed HT22 cells. (A) Western blotting of RAS, RAF, and MAPK. (B–D) Expression of RAS, RAF, and MAPK in CIH-exposed HT22 cells. (E) Western blotting of PI3K, P-AKT/AKT, and GSK3β in CIH-exposed HT22 cells. (F–H) Expression of PI3K, P-AKT/AKT, and GSK3β in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Techniques Used: Expressing, Western Blot, Standard Deviation

Role of IGF1 siRNA and AG1024 in improving the effects of SDD on neuronal injury in CIH-exposed HT22 cells. (A–B) PSD-95 and BDNF expression in CIH-exposed HT22 cells. (C–D) P-CREB/CREB and P-ERK/ERK expression in CIH-exposed HT22 cells. (E) TEM was used to detect mitochondria in CIH-exposed HT22 cells (20000 × ). (F and H) Mitochondrial membrane potential in CIH-exposed HT22 cells (scale bar = 50 μm). (G and I) Mitochondrial ROS in CIH-exposed HT22 cells (scale bar = 25 μm). (J) Mitochondrial ATP levels in CIH-exposed HT22 cells. (K) The level of mitochondrial respiratory chain complex Ι in CIH-exposed HT22 cells. (L) The viability of CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Figure Legend Snippet: Role of IGF1 siRNA and AG1024 in improving the effects of SDD on neuronal injury in CIH-exposed HT22 cells. (A–B) PSD-95 and BDNF expression in CIH-exposed HT22 cells. (C–D) P-CREB/CREB and P-ERK/ERK expression in CIH-exposed HT22 cells. (E) TEM was used to detect mitochondria in CIH-exposed HT22 cells (20000 × ). (F and H) Mitochondrial membrane potential in CIH-exposed HT22 cells (scale bar = 50 μm). (G and I) Mitochondrial ROS in CIH-exposed HT22 cells (scale bar = 25 μm). (J) Mitochondrial ATP levels in CIH-exposed HT22 cells. (K) The level of mitochondrial respiratory chain complex Ι in CIH-exposed HT22 cells. (L) The viability of CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Techniques Used: Expressing, Membrane, Standard Deviation

Role of IGF1 siRNA and AG1024 in the improvement effects of SDD by Morris water maze in CIH-exposed mice. (A) Escape latency (hidden platform). (B) Swimming speed (hidden platform). (C) Representative swimming tracks (probe test). (D) Platform-crossing number (probe test). (E–F) Distance traveled and time in the target quadrant (probe test). (G–H) Escape latency and swimming speed (visible platform). The results are presented as the mean ± standard deviation (SD). n = 6. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus. the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Figure Legend Snippet: Role of IGF1 siRNA and AG1024 in the improvement effects of SDD by Morris water maze in CIH-exposed mice. (A) Escape latency (hidden platform). (B) Swimming speed (hidden platform). (C) Representative swimming tracks (probe test). (D) Platform-crossing number (probe test). (E–F) Distance traveled and time in the target quadrant (probe test). (G–H) Escape latency and swimming speed (visible platform). The results are presented as the mean ± standard deviation (SD). n = 6. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus. the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Techniques Used: Standard Deviation

An illustration of the potential neuroprotective mechanism of SDD on CIH-exposed HT22 cells. SDD alleviates CIH-induced neuronal damage by improving mitochondrial dysfunction via activation of the IGF1/IGFR signaling pathway.

Figure Legend Snippet: An illustration of the potential neuroprotective mechanism of SDD on CIH-exposed HT22 cells. SDD alleviates CIH-induced neuronal damage by improving mitochondrial dysfunction via activation of the IGF1/IGFR signaling pathway.

Techniques Used: Activation Assay

Image Search Results

Relative mRNA expression levels of hydroxycarboxylic acid receptor 1 ( Hcar1 ), monocarboxylate transporter 2 ( Mct2, Slc16a7 ), Vascular endothelial growth factor ( Vegfa ), Brain-derived neurotrophic factor ( Bdnf ), and Insulin-like growth factor 1 ( Igf1 ) were quantified by RT-qPCR using the 2 ⁻ΔΔCt method in 5XFAD transgenic (Tg) and wild-type (WT) mice treated with lactate or vehicle. Tg lactate ( n = 10), Tg vehicle ( n = 11), WT lactate ( n = 7), and WT vehicle ( n = 8). Groups included both sexes and combined early- and late-treatment start cohorts. (a) Hcar1 expression showed a modest increase following lactate treatment in WT mice; however, no significant differences were observed in any of the groups. (b) Lactate administration significantly increased Mct2 expression in WT mice compared to vehicle-treated controls ( p = 0.021, d = 1.26). No significant changes were observed in Tg mice treated with lactate versus vehicle. (c) Bdnf expression was significantly higher in WT mice receiving lactate compared to vehicle-treated WT controls ( p < 0.001, d = 2.14). (d) Igf1 expression was significantly upregulated in WT mice receiving lactate compared to WT controls ( p = 0.033, d = 1.16). (e) Vegfa expression was significantly upregulated in lactate-treated WT mice compared to vehicle-treated WT controls ( p = 0.004, d = 1.60). Data are presented as individual data points, with statistical analyses performed using one-way ANOVA, followed by Fisher’s least significant test (LSD). Results are displayed as mean ± standard deviation (SD).

Journal: bioRxiv

Article Title: Lactate treatment improves brain biochemistry and cognitive function in transgenic Alzheimer’s and wild-type mice

doi: 10.64898/2026.01.28.702254

Figure Lengend Snippet: Relative mRNA expression levels of hydroxycarboxylic acid receptor 1 ( Hcar1 ), monocarboxylate transporter 2 ( Mct2, Slc16a7 ), Vascular endothelial growth factor ( Vegfa ), Brain-derived neurotrophic factor ( Bdnf ), and Insulin-like growth factor 1 ( Igf1 ) were quantified by RT-qPCR using the 2 ⁻ΔΔCt method in 5XFAD transgenic (Tg) and wild-type (WT) mice treated with lactate or vehicle. Tg lactate ( n = 10), Tg vehicle ( n = 11), WT lactate ( n = 7), and WT vehicle ( n = 8). Groups included both sexes and combined early- and late-treatment start cohorts. (a) Hcar1 expression showed a modest increase following lactate treatment in WT mice; however, no significant differences were observed in any of the groups. (b) Lactate administration significantly increased Mct2 expression in WT mice compared to vehicle-treated controls ( p = 0.021, d = 1.26). No significant changes were observed in Tg mice treated with lactate versus vehicle. (c) Bdnf expression was significantly higher in WT mice receiving lactate compared to vehicle-treated WT controls ( p < 0.001, d = 2.14). (d) Igf1 expression was significantly upregulated in WT mice receiving lactate compared to WT controls ( p = 0.033, d = 1.16). (e) Vegfa expression was significantly upregulated in lactate-treated WT mice compared to vehicle-treated WT controls ( p = 0.004, d = 1.60). Data are presented as individual data points, with statistical analyses performed using one-way ANOVA, followed by Fisher’s least significant test (LSD). Results are displayed as mean ± standard deviation (SD).

Article Snippet: Genes of interest, including Bdnf (Mm01334042_m1), Hcar1 (Mm00558586_s1), Igf1 (Mm00439560_m1), Il1b (Mm00434228_m1), Il4 (Mm00445259_m1), Il13 (Mm00434204_m1), Slc16a7 (Mct2) (Mm00441442_m1), Vegfa (Mm00437306_m1), were assessed.

Techniques: Expressing, Derivative Assay, Quantitative RT-PCR, Transgenic Assay, Standard Deviation

a Differentiation itinerary of the thymic epithelium showing DE (Definitive Endoderm), AFE (Anterior Foregut Endoderm), 3PPE (Third Pharyngeal Pouch Endoderm) and TEP (Thymic Epithelial Progenitor) stages (Created in BioRender. Guillonneau, C. (2025) https://BioRender.com/r5v7uln ). b Factors tested in DOE (abbreviations), their associated pathways and the timings corresponding to each tested stage transition (D5-D7: DE-to-AFE, D7-D11: AFE-to-3PPE and D11-D13: 3PPE-to-TEP). Plackett–Burman designs were used to estimate factor effects on differentiation at the three transitions, with two dose levels (−1/+1) per factor. c UMAP representations of early ( Left ) and late ( Right ) pharyngeal development scRNA-seq reference datasets, with clusters corresponding to stages of the thymic differentiation trajectory shown in color. Reference datasets: Han et al. (E8.5–E9.5) and Magaletta et al. (E9.5–E12.5). d Bulk RNA-seq results for each sample (vertical) treated with combinations of factors tested in DOE in four experiments (D5-D7, Han E8.5; D7-D11, Han and Magaletta E9.5; D11-D13, Magaletta E11.5/12.5) showing expression scores of marker genes for pharyngeal development clusters (horizontal). Cluster names corresponding to the thymic differentiation trajectory are highlighted in bold. The upper part of each heatmap shows the factor combinations applied, with high doses highlighted in orange. Statistical significance was assessed by ANOVA (Supplementary Fig. ). Significant factors are shown in red or blue, indicating those to be supplemented or excluded in the optimized protocol. Han et. al. dataset: D5 to D7: p = 0.02338 (Noggin); 4.246e-05 (IWR1); 0.05526 (LY3); 4.345.e-07 (RA)/D7 to D11: p = 5.233.e-05 (CHIR99); 0.0002875 (FLI06); 0.0015895 (IWR1). Magaletta et. al. dataset: D7 to D11: p = 1.877.e-05 (CHIR99); 1.877.e-05 (FLI06); 0.0003179 (IRW1)/D11 to D13: dots indicate suggestive p values, p = 0.089927 (BMP4); 0.079926 (IGF1); 0.086185 (RANKL). e Summary of pathway modulation: black, DOE-identified pathways to be activated (+) or inhibited (−); blue, pathways neutral in DOE but enhancing FOXN1 expression (BMP/FGF) or proliferation (FGF/EGF) at the TEP stage; green, the FGF pathway (not tested in DOE, post-DOE), activating FOXN1 at the TEP stage. DE Definitive Endoderm, AFE Anterior Foregut Endoderm, 3PPE Third Pharyngeal Pouch Endoderm, TEP Thymic Epithelial Progenitor. See corresponding factor names in ( b ) (Created in BioRender. Guillonneau, C. (2025) https://BioRender.com/ht4edy0 ). f Summary of the optimized protocol with full factor list, doses and exposure windows, DE Definitive Endoderm, AFE Anterior Foregut Endoderm, 3PPE Third Pharyngeal Pouch Endoderm, TEP Thymic Epithelial Progenitor.

Journal: Nature Communications

Article Title: Combinatory differentiation of human induced pluripotent stem cells generates functional thymic epithelium driving dendritic cell and CD4/CD8 T cell development

doi: 10.1038/s41467-026-68675-y

Figure Lengend Snippet: a Differentiation itinerary of the thymic epithelium showing DE (Definitive Endoderm), AFE (Anterior Foregut Endoderm), 3PPE (Third Pharyngeal Pouch Endoderm) and TEP (Thymic Epithelial Progenitor) stages (Created in BioRender. Guillonneau, C. (2025) https://BioRender.com/r5v7uln ). b Factors tested in DOE (abbreviations), their associated pathways and the timings corresponding to each tested stage transition (D5-D7: DE-to-AFE, D7-D11: AFE-to-3PPE and D11-D13: 3PPE-to-TEP). Plackett–Burman designs were used to estimate factor effects on differentiation at the three transitions, with two dose levels (−1/+1) per factor. c UMAP representations of early ( Left ) and late ( Right ) pharyngeal development scRNA-seq reference datasets, with clusters corresponding to stages of the thymic differentiation trajectory shown in color. Reference datasets: Han et al. (E8.5–E9.5) and Magaletta et al. (E9.5–E12.5). d Bulk RNA-seq results for each sample (vertical) treated with combinations of factors tested in DOE in four experiments (D5-D7, Han E8.5; D7-D11, Han and Magaletta E9.5; D11-D13, Magaletta E11.5/12.5) showing expression scores of marker genes for pharyngeal development clusters (horizontal). Cluster names corresponding to the thymic differentiation trajectory are highlighted in bold. The upper part of each heatmap shows the factor combinations applied, with high doses highlighted in orange. Statistical significance was assessed by ANOVA (Supplementary Fig. ). Significant factors are shown in red or blue, indicating those to be supplemented or excluded in the optimized protocol. Han et. al. dataset: D5 to D7: p = 0.02338 (Noggin); 4.246e-05 (IWR1); 0.05526 (LY3); 4.345.e-07 (RA)/D7 to D11: p = 5.233.e-05 (CHIR99); 0.0002875 (FLI06); 0.0015895 (IWR1). Magaletta et. al. dataset: D7 to D11: p = 1.877.e-05 (CHIR99); 1.877.e-05 (FLI06); 0.0003179 (IRW1)/D11 to D13: dots indicate suggestive p values, p = 0.089927 (BMP4); 0.079926 (IGF1); 0.086185 (RANKL). e Summary of pathway modulation: black, DOE-identified pathways to be activated (+) or inhibited (−); blue, pathways neutral in DOE but enhancing FOXN1 expression (BMP/FGF) or proliferation (FGF/EGF) at the TEP stage; green, the FGF pathway (not tested in DOE, post-DOE), activating FOXN1 at the TEP stage. DE Definitive Endoderm, AFE Anterior Foregut Endoderm, 3PPE Third Pharyngeal Pouch Endoderm, TEP Thymic Epithelial Progenitor. See corresponding factor names in ( b ) (Created in BioRender. Guillonneau, C. (2025) https://BioRender.com/ht4edy0 ). f Summary of the optimized protocol with full factor list, doses and exposure windows, DE Definitive Endoderm, AFE Anterior Foregut Endoderm, 3PPE Third Pharyngeal Pouch Endoderm, TEP Thymic Epithelial Progenitor.

Article Snippet: The supplementation included Activin A, CHIR99, BMP4 (Miltenyi, 130-111-167), retinoic acid (Sigma Aldrich, 302-79-4), FGF8 (BiotechneR&D, 423-F8), Noggin (Miltenyi 130-103-455), LY-364947 (Sigma Aldrich L6293-5MG), FGF10 (Miltenyi, 130-127-858), IGF1 (Miltenyi, 130-093-886), EGF (Miltenyi, 130-097-751), and RANK-L (BiotechneR&D: 6449-TEC).

Techniques: RNA Sequencing, Expressing, Marker

$a UMAP plots of 12 macrophage and DC subtypes from baseline and follow-up samples. IGF1 ⁺Macrophage cluster (cluster 3) highlighted. b Volcano plot of DEGs in IGF1 ⁺ macrophages between baseline and follow-up. Upregulated (red), downregulated (blue), stable (grey) genes shown. c Bar plots of top enriched Reactome pathways in IGF1 ⁺ macrophages from DEGs (two-sided Wilcoxon rank-sum test, adjusted P values). Pathway enrichment of top 20 upregulated genes via Enrichr (Reactome_Pathways_2024, hypergeometric test, unadjusted P values). d UMAP plots of key marker gene expression ( HP , IGF1 , RETN ) in macrophage subsets; color intensity reflects normalized UMI counts. e Violin plots of IGF1 , RETN , HP expression across disease phases (EGPA baseline, Cs-remission, Cs-relapse) in macrophages. f Immunofluorescent staining and quantification of IGF1⁺CD68⁺ macrophages in bronchial mucosae (biological replicates; EGPA n = 15, Cs-remission n = 3, Cs-relapse n = 5). Scale bars: 100 μm (upper), 20 μm (lower). g UMAP plots of 11 epithelial cell subsets from combined samples. h Heatmap of relative enrichment (observed/expected Ro/e) of epithelial subtypes across groups and sample types. i Dot plot of reciprocal epithelial ligand-receptor expression across subsets. Interaction pairs linked by color-coded lines; dot size reflects expression fraction, color intensity shows relative expression. j Violin plots of marker gene expression for goblet cell subsets (Goblet-1, Goblet−2) and ionocytes across groups. k Immunofluorescent staining and quantification of MUC5AC⁺ epithelial cells (biological replicates; EGPA n = 10, Cs-remission n = 3, Cs-relapse n = 5). Scale bar: 100 μm. Data presented as median with IQR. f , k Two-sided Kruskal–Wallis test with Dunn’s post-hoc and Bonferroni correction. * P < 0.05, ** P < 0.01, *** P < 0.001; NS, not significant. Exact P values in Supplementary Data . Cs-relapse corticosteroid relapse, Cs-remission corticosteroid remission, DC dendritic cell, DEGs differentially expressed genes, IGF1 insulin-like growth factor 1, MUC5AC mucin 5AC, Ro/e ratio of observed to expected.$

Journal: Nature Communications

Article Title: Airway immune profiles and therapeutic implications of IGF1 in eosinophilic granulomatosis with polyangiitis

doi: 10.1038/s41467-025-68104-6

Figure Lengend Snippet: a UMAP plots of 12 macrophage and DC subtypes from baseline and follow-up samples. IGF1 ⁺Macrophage cluster (cluster 3) highlighted. b Volcano plot of DEGs in IGF1 ⁺ macrophages between baseline and follow-up. Upregulated (red), downregulated (blue), stable (grey) genes shown. c Bar plots of top enriched Reactome pathways in IGF1 ⁺ macrophages from DEGs (two-sided Wilcoxon rank-sum test, adjusted P values). Pathway enrichment of top 20 upregulated genes via Enrichr (Reactome_Pathways_2024, hypergeometric test, unadjusted P values). d UMAP plots of key marker gene expression ( HP , IGF1 , RETN ) in macrophage subsets; color intensity reflects normalized UMI counts. e Violin plots of IGF1 , RETN , HP expression across disease phases (EGPA baseline, Cs-remission, Cs-relapse) in macrophages. f Immunofluorescent staining and quantification of IGF1⁺CD68⁺ macrophages in bronchial mucosae (biological replicates; EGPA n = 15, Cs-remission n = 3, Cs-relapse n = 5). Scale bars: 100 μm (upper), 20 μm (lower). g UMAP plots of 11 epithelial cell subsets from combined samples. h Heatmap of relative enrichment (observed/expected Ro/e) of epithelial subtypes across groups and sample types. i Dot plot of reciprocal epithelial ligand-receptor expression across subsets. Interaction pairs linked by color-coded lines; dot size reflects expression fraction, color intensity shows relative expression. j Violin plots of marker gene expression for goblet cell subsets (Goblet-1, Goblet−2) and ionocytes across groups. k Immunofluorescent staining and quantification of MUC5AC⁺ epithelial cells (biological replicates; EGPA n = 10, Cs-remission n = 3, Cs-relapse n = 5). Scale bar: 100 μm. Data presented as median with IQR. f , k Two-sided Kruskal–Wallis test with Dunn’s post-hoc and Bonferroni correction. * P < 0.05, ** P < 0.01, *** P < 0.001; NS, not significant. Exact P values in Supplementary Data . Cs-relapse corticosteroid relapse, Cs-remission corticosteroid remission, DC dendritic cell, DEGs differentially expressed genes, IGF1 insulin-like growth factor 1, MUC5AC mucin 5AC, Ro/e ratio of observed to expected.

Article Snippet: For human sputum IGF1 concentration detection, 100uL sputum supernatant was used (Multi Sciences, Cat# EK1131-96).

Techniques: Marker, Gene Expression, Expressing, Staining

a Immunofluorescent staining and quantification of IGF1⁺ epithelial cells at bronchial mucosae from control ( n = 6), SEA ( n = 9), EGPA ( n = 10), Cs-remission ( n = 3), and Cs-relapse ( n = 5) groups (biological replicates). Scale bar: 100 μm. b Bar plots of IGF1 concentrations in sputum samples from Control ( n = 13), SEA ( n = 23), and EGPA ( n = 21) (biological replicates). c Schematic of EGPA airway epithelial cells in ALI culture stimulated with IL-13, IL-33, or medium (Control). Bar plots show relative expression of IGF1 , IGF1R , and IGFBP3 , and IGF1 concentrations under different conditions. Data from 3 independent experiments (biological replicates). d Schematic of ALI system with IGF1 stimulation versus control. Representative histological (HE, PAS) and immunofluorescent (MUC5AC with DAPI) staining demonstrate morphological changes and mucin production (goblet hyperplasia) in ALI cultures with medium (Control) or IGF1 stimulation. Scale bars: 50 μm (HE, PAS), 20 μm (MUC5AC). Bar plots of IL-25, IL-33, and TSLP concentrations in culture supernatant at time points (Day 9, 13, 17, 21). Data from 3 independent experiments (biological replicates). e Scatter plot showing positive correlation between eosinophil abundance and IGF1 concentration in sputum from EGPA patients ( n = 21). f Schematic of proposed mechanism where IGF1 promotes goblet hyperplasia and augments T2-mediated inflammation through IGF1-IL25 loop, contributing to disease exacerbation in asthma and EGPA. Data presented as mean ± SD. a – c Two-sided one-way ANOVA with Tukey’s post-hoc test. d Two-sided unpaired t -test. e Two-sided Pearson correlation test. * P < 0.05, ** P < 0.01, *** P < 0.001; NS, not significant. Exact P values in Supplementary Data . ALI air-liquid interface, HE hematoxylin and eosin, IGF1R insulin-like growth factor 1 receptor, IGFBP3 insulin-like growth factor binding protein 3, PAS periodic acid-Schiff, TSLP thymic stromal lymphopoietin.

Journal: Nature Communications

Article Title: Airway immune profiles and therapeutic implications of IGF1 in eosinophilic granulomatosis with polyangiitis

doi: 10.1038/s41467-025-68104-6

Figure Lengend Snippet: a Immunofluorescent staining and quantification of IGF1⁺ epithelial cells at bronchial mucosae from control ( n = 6), SEA ( n = 9), EGPA ( n = 10), Cs-remission ( n = 3), and Cs-relapse ( n = 5) groups (biological replicates). Scale bar: 100 μm. b Bar plots of IGF1 concentrations in sputum samples from Control ( n = 13), SEA ( n = 23), and EGPA ( n = 21) (biological replicates). c Schematic of EGPA airway epithelial cells in ALI culture stimulated with IL-13, IL-33, or medium (Control). Bar plots show relative expression of IGF1 , IGF1R , and IGFBP3 , and IGF1 concentrations under different conditions. Data from 3 independent experiments (biological replicates). d Schematic of ALI system with IGF1 stimulation versus control. Representative histological (HE, PAS) and immunofluorescent (MUC5AC with DAPI) staining demonstrate morphological changes and mucin production (goblet hyperplasia) in ALI cultures with medium (Control) or IGF1 stimulation. Scale bars: 50 μm (HE, PAS), 20 μm (MUC5AC). Bar plots of IL-25, IL-33, and TSLP concentrations in culture supernatant at time points (Day 9, 13, 17, 21). Data from 3 independent experiments (biological replicates). e Scatter plot showing positive correlation between eosinophil abundance and IGF1 concentration in sputum from EGPA patients ( n = 21). f Schematic of proposed mechanism where IGF1 promotes goblet hyperplasia and augments T2-mediated inflammation through IGF1-IL25 loop, contributing to disease exacerbation in asthma and EGPA. Data presented as mean ± SD. a – c Two-sided one-way ANOVA with Tukey’s post-hoc test. d Two-sided unpaired t -test. e Two-sided Pearson correlation test. * P < 0.05, ** P < 0.01, *** P < 0.001; NS, not significant. Exact P values in Supplementary Data . ALI air-liquid interface, HE hematoxylin and eosin, IGF1R insulin-like growth factor 1 receptor, IGFBP3 insulin-like growth factor binding protein 3, PAS periodic acid-Schiff, TSLP thymic stromal lymphopoietin.

Article Snippet: For human sputum IGF1 concentration detection, 100uL sputum supernatant was used (Multi Sciences, Cat# EK1131-96).

Techniques: Staining, Control, Expressing, Concentration Assay, Binding Assay

a – e Anti-IGF1 treatment reduces eosinophilic inflammation and airway remodeling in IL-5 transgenic mice challenged with HDM and IL-33. Mice were divided into Control (PBS-treated), Model (HDM+IL-33 challenged), and Anti-IGF1 (HDM+IL-33+anti-IGF1 antibody) groups. a Total cell counts in bronchoalveolar lavage fluid (BALF) from control, model, and anti-IGF1-treated groups. b Eosinophil percentage in BALF. c Absolute eosinophil counts in BALF. d IL−25 levels in BALF quantified by ELISA. e Representative histological images of lung sections stained with hematoxylin and eosin (H&E, upper panels) and periodic acid-Schiff (PAS, lower panels), with corresponding inflammation and PAS score quantifications. Scale bar, 100 μm. f – h IGF1R deficiency modulates eosinophilic inflammation and airway remodeling via IL−25 in HDM+IL-33 challenged mice. f Total cell counts in BALF from wild-type (WT, Scgb1a1 -IRES-+/+ Igf1r f/f ), conditional knockout ( Scgb1a1 -IRES-Cre/+ Igf1r f/f , CKO), and CKO mice treated with recombinant IL-25 (rIL-25). All groups were challenged with HDM+IL-33. g Flow cytometric analysis of eosinophils (CD45 + Siglec-F + CD11c - ) in BALF. Representative plots and quantification of eosinophil percentages are shown. h Representative H&E (upper panels) and PAS (lower panels) staining of lung sections from WT, CKO, and CKO+rIL-25 groups, with quantification of inflammation and PAS scores. Scale bar, 100 μm. Statistical analysis: Data are presented as mean ± SD ( n = 5 mice per group). Statistical significance was determined using a two-sided one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001; NS, not significant. Exact P values and complete test statistics for a – h are provided in Supplementary Data . CKO conditional knockout, HDM house dust mite, rIL-25 recombinant IL-25, WT wild-type.

Journal: Nature Communications

Article Title: Airway immune profiles and therapeutic implications of IGF1 in eosinophilic granulomatosis with polyangiitis

doi: 10.1038/s41467-025-68104-6

Figure Lengend Snippet: a – e Anti-IGF1 treatment reduces eosinophilic inflammation and airway remodeling in IL-5 transgenic mice challenged with HDM and IL-33. Mice were divided into Control (PBS-treated), Model (HDM+IL-33 challenged), and Anti-IGF1 (HDM+IL-33+anti-IGF1 antibody) groups. a Total cell counts in bronchoalveolar lavage fluid (BALF) from control, model, and anti-IGF1-treated groups. b Eosinophil percentage in BALF. c Absolute eosinophil counts in BALF. d IL−25 levels in BALF quantified by ELISA. e Representative histological images of lung sections stained with hematoxylin and eosin (H&E, upper panels) and periodic acid-Schiff (PAS, lower panels), with corresponding inflammation and PAS score quantifications. Scale bar, 100 μm. f – h IGF1R deficiency modulates eosinophilic inflammation and airway remodeling via IL−25 in HDM+IL-33 challenged mice. f Total cell counts in BALF from wild-type (WT, Scgb1a1 -IRES-+/+ Igf1r f/f ), conditional knockout ( Scgb1a1 -IRES-Cre/+ Igf1r f/f , CKO), and CKO mice treated with recombinant IL-25 (rIL-25). All groups were challenged with HDM+IL-33. g Flow cytometric analysis of eosinophils (CD45 + Siglec-F + CD11c - ) in BALF. Representative plots and quantification of eosinophil percentages are shown. h Representative H&E (upper panels) and PAS (lower panels) staining of lung sections from WT, CKO, and CKO+rIL-25 groups, with quantification of inflammation and PAS scores. Scale bar, 100 μm. Statistical analysis: Data are presented as mean ± SD ( n = 5 mice per group). Statistical significance was determined using a two-sided one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001; NS, not significant. Exact P values and complete test statistics for a – h are provided in Supplementary Data . CKO conditional knockout, HDM house dust mite, rIL-25 recombinant IL-25, WT wild-type.

Article Snippet: For human sputum IGF1 concentration detection, 100uL sputum supernatant was used (Multi Sciences, Cat# EK1131-96).

Techniques: Transgenic Assay, Control, Enzyme-linked Immunosorbent Assay, Staining, Knock-Out, Recombinant

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: (A) Mechanism of SDD alleviating neuronal injury in CIH-exposed HT22 cells by IGF1/IGFR signaling pathway. (B) Role of IGF1/IGFR signaling pathway in alleviating CIH induced cognitive impairment by SDD treatment. (C) Mixed drug standards. (D) SDD water extract. 1: Catalpol, 2: Morroniside, 3: Loganin, 4: Ginsenoside Rb1, 5: Paeonol. Created with BioRender. com.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques:

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Effects of CIH exposure on cell activity and IGF1/IGFR expression in HT22 cells. (A) Effects of CIH exposure on cell viability at different times. (B) IGF1 expression in HT22 cells at various CIH exposure times. (C) Secretion levels of IGF1 in cell cultures at different CIH exposure times. (D–E) HT22 cells expressing IGFR were detected by immunofluorescence at different CIH exposure times; arrows denote the positive cells (scale bar = 25 μm). (F) IGFR expression in HT22 cells after various CIH exposure times. The outcomes are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus 0 h CIH exposure.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Activity Assay, Expressing, Immunofluorescence, Standard Deviation

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Effects of exogenous IGF1 on cell viability and mitochondrial dysfunction in CIH-exposed HT22 cells. (A) Effects of various IGF1 concentrations on cell viability. (B) TEM was used to detect mitochondria in HT22 cells that had been exposed to CIH (20000 × ). (C and E) Effects of exogenous IGF1 on the mitochondrial membrane potential of HT22 cells (scale bar = 50 μm). (D and F) Effects of exogenous IGF1 on ROS production in the mitochondria of CIH-exposed HT22 cells (scale bar = 25 μm). (G) Effects of exogenous IGF1 on mitochondrial ATP levels in CIH-exposed HT22 cells. (H) Effects of exogenous IGF1 on the level of mitochondrial respiratory chain complex Ι in HT22 cells exposed to CIH. (I) BDNF expression in CIH-exposed HT22 cells. (J) PSD-95 expression in CIH-exposed HT22 cells. (K) P-CREB/CREB expression in HT22 cells exposed to CIH. (L) P-ERK/ERK expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Membrane, Expressing, Standard Deviation

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Effect of SDD on IGF1 and IGFR expression in HT22 cells under CIH conditions. (A) Western blotting of IGF1. (B) IGF1 expression in CIH-exposed HT22 cells. (C) Secretion levels of IGF1 in cell cultures exposed to CIH. (D–E) The number of IGFR-positive cells was detected by immunofluorescence in CIH-exposed HT22 cells; arrows denote the presence of positive cells (scale bar = 25 μm). (F) IGFR expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01 versus the CIH group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Expressing, Western Blot, Immunofluorescence, Standard Deviation

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Effects of SDD on the IGF1/IGFR signaling pathway under CIH conditions. (A) Western blotting RAS, RAF, and MAPK. (B–D) RAS, RAF, and MAPK expression in CIH-exposed HT22 cells. (E) Western blotting of PI3K, P-AKT/AKT, and GSK3β in CIH-exposed HT22 cells. (F–H) PI3K, P-AKT/AKT, and GSK3β expression in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Western Blot, Expressing, Standard Deviation

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Role of IGF1 siRNA and AG1024 in regulating the effects of SDD on the expression of IGF1/IGFR downstream signaling molecules in CIH-exposed HT22 cells. (A) Western blotting of RAS, RAF, and MAPK. (B–D) Expression of RAS, RAF, and MAPK in CIH-exposed HT22 cells. (E) Western blotting of PI3K, P-AKT/AKT, and GSK3β in CIH-exposed HT22 cells. (F–H) Expression of PI3K, P-AKT/AKT, and GSK3β in CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Expressing, Western Blot, Standard Deviation

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Role of IGF1 siRNA and AG1024 in improving the effects of SDD on neuronal injury in CIH-exposed HT22 cells. (A–B) PSD-95 and BDNF expression in CIH-exposed HT22 cells. (C–D) P-CREB/CREB and P-ERK/ERK expression in CIH-exposed HT22 cells. (E) TEM was used to detect mitochondria in CIH-exposed HT22 cells (20000 × ). (F and H) Mitochondrial membrane potential in CIH-exposed HT22 cells (scale bar = 50 μm). (G and I) Mitochondrial ROS in CIH-exposed HT22 cells (scale bar = 25 μm). (J) Mitochondrial ATP levels in CIH-exposed HT22 cells. (K) The level of mitochondrial respiratory chain complex Ι in CIH-exposed HT22 cells. (L) The viability of CIH-exposed HT22 cells. The results are presented as the mean ± standard deviation (SD). n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus the CON group, # P < 0.05, ## P < 0.01 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Expressing, Membrane, Standard Deviation

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: Role of IGF1 siRNA and AG1024 in the improvement effects of SDD by Morris water maze in CIH-exposed mice. (A) Escape latency (hidden platform). (B) Swimming speed (hidden platform). (C) Representative swimming tracks (probe test). (D) Platform-crossing number (probe test). (E–F) Distance traveled and time in the target quadrant (probe test). (G–H) Escape latency and swimming speed (visible platform). The results are presented as the mean ± standard deviation (SD). n = 6. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 versus. the CON group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus the CIH group, △ P < 0.05, △△ P < 0.01, △△△ P < 0.001 versus the SDD group.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Standard Deviation

Journal: Journal of Traditional and Complementary Medicine

Article Title: Role of IGF1/IGFR signaling pathway in neuroprotective effect of Shengmai Dihuang Decoction on CIH-induced cognitive impairment

doi: 10.1016/j.jtcme.2024.11.014

Figure Lengend Snippet: An illustration of the potential neuroprotective mechanism of SDD on CIH-exposed HT22 cells. SDD alleviates CIH-induced neuronal damage by improving mitochondrial dysfunction via activation of the IGF1/IGFR signaling pathway.

Article Snippet: IGF1 (bs-0014R), IGFR (bs-4985R), P-CREB (bs-5256R), CREB (bsm-33196R), P-ERK (bs-3016R), and ERK (bsm-52259R) were purchased from Bioss Antibodies (Woburn, MA, USA).

Techniques: Activation Assay

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