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Affinity Biosciences anti p pi3k
Anti P Pi3k, supplied by Affinity Biosciences, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p+pi3k/anti+pi3k/pmc13251493-131-18-21
Average 86 stars, based on 1 article reviews

anti p pi3k - by Bioz Stars, 2026-09

86/100 stars

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Pyrolysis Gas Chromatography:

Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity
Article Snippet: Cyclin B (#4138), Vimentin (#5741), N-cadherin (#13116), p38 (#9212), and p-p38 (#4511S) antibodies were purchased from Cell Signaling Technology (USA). .. Cytochrome c (CYT-C) (#AF0146), cleaved-PARP (#AF7023), Bcl-2 (#AF6139), cleaved-caspase 9 (#AF5240), cleaved-caspase 3 (#AF7022), matrix metalloproteinase 2 (MMP2) (#AF5330), MMP7 (#AF0218), peroxisome proliferator-activated receptor-γ-coactivator 1α (PGC-1α) (#AF5395), nuclear respiratory factor 1 (NRF1) (#AF5298), NRF2 (#AF0639), mitochondrial transcription factor A (TFAM) (#AF0531), PI3K (#AF6241), p-PI3K (#AF3242), AKT (#AF6261), p-AKT (#AF0016), extracellular signal-related kinase (ERK) (#AF0155), Jun N-terminal kinase (JNK) (#AF6318), p-ERK (#AF1015), p-JNK (#AF3318), and Snail (#AF6032) antibodies were purchased from Affinity Biosciences (USA). ..

Aqueous Normal-phase Chromatography:

Article Title: Chronic intermittent hypoxia exacerbates isoproterenol-induced cardiac hypertrophy and apoptosis
Article Snippet: .. The following antibodies were used: ANP (1:1,000, Abcam, ab189921), BNP (1:1,000, Thermo Fisher Scientific, PA5-102596), caspase-3 (1:500, Thermo Fisher Scientific, 43-7800), cleaved caspase-3 (1:1,000, Cell Signaling Technology, 9664), Bax (1:2,000, Abmart, T40051 ), Bcl-2 (1:500, Abmart, T40056 ), PI3K (1:1,000, Affinity Biosciences, AF6241), p-PI3K (1:1,000, Affinity Biosciences, AF3241), Akt (1:1,000, Cell Signaling Technology, 4,691), p-Akt (1:1,000, Cell Signaling Technology, 9271), mTOR (1:1,000, Cell Signaling Technology, 2983), p-mTOR (1:1,000, Cell Signaling Technology, 5536), and GAPDH (1:10,000, Abcam, ab181602). .. After incubation with secondary antibodies, goat anti-rabbit IgG (1:20,000, ZSGB-Bio, ZB-5301) or goat anti-mouse IgG (1:20,000, ZSGB-Bio, ZB-5305) for 1 h, protein blots were imaged using the Quantity One software (Bio-Rad, USA).

Blocking Assay:

Article Title: Taraxasterol alleviates osteoporosis by targeting PI3K/AKT/PPARγ signaling axis to suppress necroptosis and reverse osteogenic-adipogenic differentiation imbalance in BMSCs.
Article Snippet: .. Following permeabilization and blocking, samples were exposed to primary antibodies against RIPK1 (#3493, CST, USA), RIPK3 (#95,702, CST, USA), p-RIPK3 (#91,702, CST, USA), p-MLKL (#37,333, CST, USA), PPARγ (#81,490–5-RR, Proteintech, USA), and p-PI3K (#AF6241, Affinity Biosciences, USA) at 4 ◦C overnight. .. The following day, samples were incubated for 1 h with appropriate species-specific secondary antibodies (1:500, #4408, CST, USA; #4413, CST, USA) protected from light.

Article Title: Macrophage membrane-biomimetic bimetallic manganese-platinum nanozymes ameliorate intrapulmonary oxidative stress and inflammation in experimental COPD
Article Snippet: Equal amounts of protein were separated by 10% SDS-polyacrylamide gel electrophoresis and subsequently transferred onto polyvinylidene fluoride (PVDF) membranes (Millipore, Germany). .. After blocking with 5% non-fat milk, the membranes were incubated overnight at 4 °C with specific primary antibodies against the following targets: CD11b (1:1000; Abclonal, Wuhan, China), CD18 (1:1000; Abclonal, Wuhan, China), p-PI3K (1:1000; Affinity Biosciences, Jiangsu, China), PI3K (1:5000; Proteintech, Wuhan, China), p-AKT (1:1000; Proteintech, Wuhan, China), AKT (1:5000; Proteintech, Wuhan, China), and GAPDH (1:5000; Proteintech, Wuhan, China). .. Following three washes with TBST, the membranes were incubated with appropriate horseradish peroxidase (HRP)-conjugated secondary antibodies (1:5000; Proteintech, Wuhan, China) for 1 h at room temperature.

Article Title: Resveratrol triggers autophagy-dependent apoptosis via suppressing the PI3K/AKT/mTOR pathway in Chlamydia psittaci-infected cells.
Article Snippet: 24 Chlamydia psittaci, a zoonotic pathogen, promotes its intracellular survival by 25 dysregulating host cell death pathways.. This study demonstrates that resveratrol (Res), 26 a natural polyphenol, counteracts this pathogenic strategy in infected human bronchial 27 epithelial (HBE) cells by inducing autophagy-dependent apoptosis.. Res exhibited 28 excellent biocompatibility, maintaining cell viability above 85% at concentrations ≤ 29 100 μmol/L after 24 h treatment.

Incubation:

Article Title: Hyperoside prevents osteoporosis by activating the PI3K/AKT signaling pathway to inhibit oxidative stress and promote osteogenesis
Article Snippet: The sections were then treated with 3% H 2 O 2 to block endogenous peroxidase activity, followed by blocking with 5% normal goat serum (cat. no. C0265; Beyotime Biotechnology) for 30 min at room temperature. .. The sections were incubated overnight at 4°C with the following primary antibodies: p-PI3K (cat. no. AF3242; 1:200) and p-AKT (cat. no. AF0016; 1:200) (all from Affinity Biosciences). ..

Control:

Image Search Results

The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.

Journal: Poultry Science

Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

doi: 10.1016/j.psj.2026.106922

Figure Lengend Snippet: The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.

Article Snippet: p-PI3K Rabbit Ab , Abmart , P76365R4 , 1: 1500.

Techniques: Expressing

The protein activity changes of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2, and Caspase 3 in E.tenella host cells.

Journal: Poultry Science

Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

doi: 10.1016/j.psj.2026.106922

Figure Lengend Snippet: The protein activity changes of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2, and Caspase 3 in E.tenella host cells.

Article Snippet: p-PI3K Rabbit Ab , Abmart , P76365R4 , 1: 1500.

Techniques: Activity Assay

Tryptophanol treatment alleviated POF symptoms by inhibiting PI3K/AKT and MAPK pathways. A Experimental scheme. B Estrus status of mice ( n = 8). C Body weights of mice ( n = 8). D Ovary weights of mice ( n = 8). E Representative Ovary from the Control, the POF and the NCG groups mice with H&E and IHC staining. H&E scale bar = 200 μm; IHC scale bar = 100 μm. F Quantification of primordial, primary, secondary, antral follicles, corpora lutea and corpora atretica per ovary. n = 3 ovaries per each condition. Levels of FSH ( G ), LH ( H ), E 2 ( I ) in mouse serum ( n = 6). Levels of ROS ( J ), MDA ( K ), SOD ( L ), GSH-Px ( M ) in mouse ovaries ( n = 3–4). N Western blotting ( a ) and quantitative ( b ) analysis of proteins ( n = 3). O Litter sizes of mice ( n = 3). Data presented as the mean ± SD, statistical significance was determined using one-way or two-way ANOVA. * p < 0.05, ** p < 0.01. *** p < 0.001. Different lowercase letters indicate significant differences ( p < 0.05)

Journal: Journal of Ovarian Research

Article Title: Gut microbiota-derived Tryptophanol driven by N-Carbamylglutamate alleviates premature ovarian failure through inhibiting oxidative stress

doi: 10.1186/s13048-026-02152-4

Figure Lengend Snippet: Tryptophanol treatment alleviated POF symptoms by inhibiting PI3K/AKT and MAPK pathways. A Experimental scheme. B Estrus status of mice ( n = 8). C Body weights of mice ( n = 8). D Ovary weights of mice ( n = 8). E Representative Ovary from the Control, the POF and the NCG groups mice with H&E and IHC staining. H&E scale bar = 200 μm; IHC scale bar = 100 μm. F Quantification of primordial, primary, secondary, antral follicles, corpora lutea and corpora atretica per ovary. n = 3 ovaries per each condition. Levels of FSH ( G ), LH ( H ), E 2 ( I ) in mouse serum ( n = 6). Levels of ROS ( J ), MDA ( K ), SOD ( L ), GSH-Px ( M ) in mouse ovaries ( n = 3–4). N Western blotting ( a ) and quantitative ( b ) analysis of proteins ( n = 3). O Litter sizes of mice ( n = 3). Data presented as the mean ± SD, statistical significance was determined using one-way or two-way ANOVA. * p < 0.05, ** p < 0.01. *** p < 0.001. Different lowercase letters indicate significant differences ( p < 0.05)

Article Snippet: The membrane was blocked with 5% bovine serum albumin (BSA; Sigma) for 1 h at room temperature, followed by overnight incubation at 4 °C with the primary antibodies: rabbit Cleaved caspase 3 (MCE, HY- P80623 , 1:800), rabbit BAX (Bioworld, BS61098, 1:800), rabbit BCL2 (Bioworld, BS1511, 1:800), rabbit ERK1/2 (Bioworld, BS90472, 1:1,000), rabbit p-ERK1/2 (Bioworld, BS4621P, 1:1,000), rabbit p38 (Bioworld, BS4635, 1:1,000), rabbit p-p38 (Bioworld, BS4766, 1:1,000), rabbit PI3K (MCE, HY- P80867 , 1:1,000); rabbit p-PI3K (MCE, HY- P80846 , 1:1,000), rabbit AKT (Bioworld, MB3288 1:1,000); rabbit p-AKT (Bioworld, BS4007 1:1,000); rabbit IL-6 (Abclonal, A0286, 1:800), rabbit IL-1β (MCE, HY- P80720 , 1:1,000), rabbit Occludin (Abclonal, A2601, 1:1,000); rabbit ZO-1 (Bioworld, BS71522, 1:1,000); rabbit GPX4 (MCE, HY- P80450 , 1:1,000); mouse GAPDH (Bioworld, MB001, 1:1,000); rabbit SOD2 (Bioworld, BS6734, 1:1,000).

Techniques: Control, Immunohistochemistry, Western Blot

Tryptophanol treatment alleviated POF by inhibiting PI3K/AKT and MAPK pathways in vitro . A Experimental scheme. B Different concentrations of Cy on GCs viability was assessed by CCK8 assay. C and E Different concentrations of Trp on GCs viability was assessed by CCK8 assay. D The effect of Trp on GCs cell viability following Cy treatment. The control and treatment groups were stained with DCFH-DA, the cells were washed and examined by fluorescence microscopy. Scale bar = 50 μm. F The fluorescence intensity of ROS in mouse GCs. G The level of MDA in mouse GCs. H Flow cytometry apoptosis analysis graph and cell death rate in different groups. The level of SOD ( I ), GSH-Px ( J ), and E 2 ( K ) in mouse GCs. ( L ) Western blotting ( a ) and quantitative ( b ) analysis of proteins ( n = 3). All values are presented as the mean ± SD ( n = 3). Different lowercase letters indicate significant differences compared to the control group ( p < 0.05)

Journal: Journal of Ovarian Research

Article Title: Gut microbiota-derived Tryptophanol driven by N-Carbamylglutamate alleviates premature ovarian failure through inhibiting oxidative stress

doi: 10.1186/s13048-026-02152-4

Figure Lengend Snippet: Tryptophanol treatment alleviated POF by inhibiting PI3K/AKT and MAPK pathways in vitro . A Experimental scheme. B Different concentrations of Cy on GCs viability was assessed by CCK8 assay. C and E Different concentrations of Trp on GCs viability was assessed by CCK8 assay. D The effect of Trp on GCs cell viability following Cy treatment. The control and treatment groups were stained with DCFH-DA, the cells were washed and examined by fluorescence microscopy. Scale bar = 50 μm. F The fluorescence intensity of ROS in mouse GCs. G The level of MDA in mouse GCs. H Flow cytometry apoptosis analysis graph and cell death rate in different groups. The level of SOD ( I ), GSH-Px ( J ), and E 2 ( K ) in mouse GCs. ( L ) Western blotting ( a ) and quantitative ( b ) analysis of proteins ( n = 3). All values are presented as the mean ± SD ( n = 3). Different lowercase letters indicate significant differences compared to the control group ( p < 0.05)

Techniques: In Vitro, CCK-8 Assay, Control, Staining, Fluorescence, Microscopy, Flow Cytometry, Western Blot

TNKS1 can activate the PI3K/AKT pathway by inhibiting the expression of PTEN in glioma cells.Western blotting was used to detect the expression of PTEN in U87 and U251 cell lines (A); the CCK-8 assay was used to measure the viability of U87 and U251 glioma cells treated with different concentrations of LY294002 and 740 Y-P (B); Western blotting was also used to detect the expression of PI3K, p-AKT/AKT in U87 and U251 cell lines (C).*P < 0.05 vs si-NC，@P < 0.05 vs si-NC+Agonist，#P < 0.05 vs si-TNKS1，&P < 0.05 vs OE-TNKS1.

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can activate the PI3K/AKT pathway by inhibiting the expression of PTEN in glioma cells.Western blotting was used to detect the expression of PTEN in U87 and U251 cell lines (A); the CCK-8 assay was used to measure the viability of U87 and U251 glioma cells treated with different concentrations of LY294002 and 740 Y-P (B); Western blotting was also used to detect the expression of PI3K, p-AKT/AKT in U87 and U251 cell lines (C).*P < 0.05 vs si-NC，@P < 0.05 vs si-NC+Agonist，#P < 0.05 vs si-TNKS1，&P < 0.05 vs OE-TNKS1.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques: Expressing, Western Blot, CCK-8 Assay

TNKS1 can regulate the proliferation and glycolysis of glioma cells by mediating the PTEN-PI3K/AKT pathway.Cell viability of various groups in U87 and U251 cell lines (A); detection of glucose (GLU) and lactate (LA) levels in the culture supernatant of various groups in U87 and U251 cell lines using biochemical assay kits (B); qPCR was used to detect the mRNA levels of GLUT1 and HK2 in various groups of U87 and U251 cell lines (C). Statistical significance *p < 0.05, **p < 0.01, ***p < 0.001, **** p < 0.0001,

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can regulate the proliferation and glycolysis of glioma cells by mediating the PTEN-PI3K/AKT pathway.Cell viability of various groups in U87 and U251 cell lines (A); detection of glucose (GLU) and lactate (LA) levels in the culture supernatant of various groups in U87 and U251 cell lines using biochemical assay kits (B); qPCR was used to detect the mRNA levels of GLUT1 and HK2 in various groups of U87 and U251 cell lines (C). Statistical significance *p < 0.05, **p < 0.01, ***p < 0.001, **** p < 0.0001,"ns" P ≥ 0.05.

Techniques:

TNKS1 can regulate the PTEN-PI3K/AKT pathway in glioma xenografts.Western blotting was used to detect the protein expression levels of PTEN, PI3K, p-AKT, and AKT in cells from each group.* P < 0.05 vs TNKS1-siRNA NC, @ P < 0.05 vs TNKS1-siRNA，# P < 0.05 vs Inhibitor.

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can regulate the PTEN-PI3K/AKT pathway in glioma xenografts.Western blotting was used to detect the protein expression levels of PTEN, PI3K, p-AKT, and AKT in cells from each group.* P < 0.05 vs TNKS1-siRNA NC, @ P < 0.05 vs TNKS1-siRNA，# P < 0.05 vs Inhibitor.

Techniques: Western Blot, Expressing

Mechanisms of NSC Differentiation into Neurons Promoted by Composite In Vitro. A) Schematic of the interactive system with NSCs and the composites. B) Representative confocal images of NSCs treated with distinct groups for 72 h. NSCs were stained with Tuj-1 (red), GFAP (green), and DAPI (blue). Scale bar: 50 μm. C-D) Quantitative analysis of Tuj-1 (C) and GFAP (D) fluorescence intensity in each group (n = 4). E) Western blot bands of Tuj-1 and GFAP protein expression in NSCs treated with separate groups. F-G) Quantitative analysis of Tuj-1/GAPDH (F) and GFAP/GAPDH (G) ratios in each group (n = 3). H) Volcano plots of DEGs in the hUCMSC-Exo + PM vs. control. DEGs are defined as |log2FC| ≥ 1 with q < 0.05. I-J) GO and KEGG pathway enrichment analysis of DEGs in NSCs after intervention with hUCMSC-Exo + PM. K) Heatmap showing the expression levels of significantly altered genes in the hUCMSC-Exo + PM and Control. L) GSEA showing pathways significantly positively correlated with DEGs in the hUCMSC-Exo + PM group. Enrichment scores (ES), P values, and false discovery rates (FDR) values are indicated for each pathway. M) Western blot bands of p-CaMK II, CaMK II, p-CREB, CREB, p-PI3K, PI3K, p-AKT, and AKT protein expression in NSCs treated with distinct groups. N) Quantitative analysis of p-CaMK II/CaMK II, p-CREB/CREB, p-PI3K/PI3K, and p-AKT/AKT ratios (n = 3). All data are presented as the mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Journal: Bioactive Materials

Article Title: Integrated cryopreservation-thawing-transplantation platform for neural stem cell-based spinal cord injury repair

doi: 10.1016/j.bioactmat.2026.01.024

Figure Lengend Snippet: Mechanisms of NSC Differentiation into Neurons Promoted by Composite In Vitro. A) Schematic of the interactive system with NSCs and the composites. B) Representative confocal images of NSCs treated with distinct groups for 72 h. NSCs were stained with Tuj-1 (red), GFAP (green), and DAPI (blue). Scale bar: 50 μm. C-D) Quantitative analysis of Tuj-1 (C) and GFAP (D) fluorescence intensity in each group (n = 4). E) Western blot bands of Tuj-1 and GFAP protein expression in NSCs treated with separate groups. F-G) Quantitative analysis of Tuj-1/GAPDH (F) and GFAP/GAPDH (G) ratios in each group (n = 3). H) Volcano plots of DEGs in the hUCMSC-Exo + PM vs. control. DEGs are defined as |log2FC| ≥ 1 with q < 0.05. I-J) GO and KEGG pathway enrichment analysis of DEGs in NSCs after intervention with hUCMSC-Exo + PM. K) Heatmap showing the expression levels of significantly altered genes in the hUCMSC-Exo + PM and Control. L) GSEA showing pathways significantly positively correlated with DEGs in the hUCMSC-Exo + PM group. Enrichment scores (ES), P values, and false discovery rates (FDR) values are indicated for each pathway. M) Western blot bands of p-CaMK II, CaMK II, p-CREB, CREB, p-PI3K, PI3K, p-AKT, and AKT protein expression in NSCs treated with distinct groups. N) Quantitative analysis of p-CaMK II/CaMK II, p-CREB/CREB, p-PI3K/PI3K, and p-AKT/AKT ratios (n = 3). All data are presented as the mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: The primary antibodies used in this research are listed below: CD68 (Abcam, Cambridge, UK), CD206 (Abcam, Cambridge, UK), GFAP (Bioss, Beijing, China), iNOS (Abcam, Cambridge, UK), Tuj-1 (Abcam, Cambridge, UK), NF-200 (Invitrogen, CA, USA), MBP (Abcam, Cambridge, UK), HIF-1α (Abcam, Cambridge, UK), VEGFA (Abcam, Cambridge, UK), P-CaMKII (Abcam, Cambridge, UK), CaMKII (Abcam, Cambridge, UK), P-CREB (Cell Signaling Technology, USA), CREB (Cell Signaling Technology, USA), P-PI3K (Cell Signaling Technology, USA), PI3K (Cell Signaling Technology, USA), P-AKT (Cell Signaling Technology, USA), AKT (Cell Signaling Technology, USA), Cleaved-Caspase3 (Cell Signaling Technology, USA), Bcl-2 (Cell Signaling Technology, USA), Bax (Cell Signaling Technology, USA), GAPDH (Proteintech, IL, USA).

Techniques: In Vitro, Staining, Fluorescence, Western Blot, Expressing, Control

FFBXP ameliorated psoriasis mice through multi-target and multi signaling pathways. A The mRNA expression of IL-17A in the skin tissues of each group of mice ( n = 3). B The expression of IL-17A protein in the skin tissues of each group of mice ( n = 3). C The expression of p-PI3K, PI3K, AKT1, and p-AKT1 proteins in the skin tissues of each group of mice ( n = 3). D The expression of p-JAK2, JAK2, STAT3, and p-STAT3 proteins in the skin tissues of each group of mice ( n = 3). ### p < 0.001 vs. Control; * p < 0.05; ** p < 0.01; *** p < 0.001 vs. Model

Journal: Chinese Medicine

Article Title: Integrating network pharmacology, transcriptomics, and experimental validation: Compound Baixianpi Formula targets IL-17A to inhibit dual PI3K-AKT/JAK2-STAT3 pathways for psoriasis improvement

doi: 10.1186/s13020-026-01386-0

Figure Lengend Snippet: FFBXP ameliorated psoriasis mice through multi-target and multi signaling pathways. A The mRNA expression of IL-17A in the skin tissues of each group of mice ( n = 3). B The expression of IL-17A protein in the skin tissues of each group of mice ( n = 3). C The expression of p-PI3K, PI3K, AKT1, and p-AKT1 proteins in the skin tissues of each group of mice ( n = 3). D The expression of p-JAK2, JAK2, STAT3, and p-STAT3 proteins in the skin tissues of each group of mice ( n = 3). ### p < 0.001 vs. Control; * p < 0.05; ** p < 0.01; *** p < 0.001 vs. Model

Article Snippet: The antibodies (GAPDH, IL-17A, p-PI3K, PI3K, p-AKT, AKT1, p-JAK2, JAK2, p-STAT3, STAT3) used in the experiment were obtained from Affinity Biosciences.

Techniques: Protein-Protein interactions, Expressing, Control

FFBXP ameliorated TNF-a induced HaCaT cells through multi-target and multi signaling pathways. A The mRNA expression of IL-17A in each group of HaCaT cells ( n = 3). B The expression of IL-17A protein in each group of HaCaT cells ( n = 3). C The immunofluorescence expression of IL-17A in each group of HaCaT cells ( n = 3). D The expression of p-PI3K, PI3K, AKT1, and p-AKT1 proteins in each group of HaCaTcells ( n = 3). E The expression of p-JAK2, JAK2, STAT3, and p-STAT3 proteins in each group of HaCaT cells ( n = 3). # p < 0.05; ## p < 0.01; ### p < 0.001 vs. Control; * p < 0.05; ** p < 0.01; *** p < 0.001 vs. Model

Journal: Chinese Medicine

doi: 10.1186/s13020-026-01386-0

Figure Lengend Snippet: FFBXP ameliorated TNF-a induced HaCaT cells through multi-target and multi signaling pathways. A The mRNA expression of IL-17A in each group of HaCaT cells ( n = 3). B The expression of IL-17A protein in each group of HaCaT cells ( n = 3). C The immunofluorescence expression of IL-17A in each group of HaCaT cells ( n = 3). D The expression of p-PI3K, PI3K, AKT1, and p-AKT1 proteins in each group of HaCaTcells ( n = 3). E The expression of p-JAK2, JAK2, STAT3, and p-STAT3 proteins in each group of HaCaT cells ( n = 3). # p < 0.05; ## p < 0.01; ### p < 0.001 vs. Control; * p < 0.05; ** p < 0.01; *** p < 0.001 vs. Model

Article Snippet: The antibodies (GAPDH, IL-17A, p-PI3K, PI3K, p-AKT, AKT1, p-JAK2, JAK2, p-STAT3, STAT3) used in the experiment were obtained from Affinity Biosciences.

Techniques: Protein-Protein interactions, Expressing, Immunofluorescence, Control

WBFC regulates ovarian function and activates PI3K/AKT/FOXO3a signaling in POI mice. Immunofluorescence and quantification of (A) p-PI3K, (B) p-AKT, and (C) p-FOXO3a in ovaries. (D) Western blot analysis of protein expression levels and semi-quantitative results of p-PI3K/PI3K, p-AKT/AKT, and p-FOXO3a/FOXO3a in ovarian tissues of POI mice treated with WBFC ( n = 3). Compared with the model group, * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bar represents 50 μm.

Journal: Pharmaceutical Biology

Article Title: Wubie Fanchun Formula-inducible metabolites in primary ovarian insufficiency model mice that facilitate ovarian renovation

doi: 10.1080/13880209.2026.2668132

Figure Lengend Snippet: WBFC regulates ovarian function and activates PI3K/AKT/FOXO3a signaling in POI mice. Immunofluorescence and quantification of (A) p-PI3K, (B) p-AKT, and (C) p-FOXO3a in ovaries. (D) Western blot analysis of protein expression levels and semi-quantitative results of p-PI3K/PI3K, p-AKT/AKT, and p-FOXO3a/FOXO3a in ovarian tissues of POI mice treated with WBFC ( n = 3). Compared with the model group, * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bar represents 50 μm.

Article Snippet: Subsequently, they were incubated overnight at 4 °C with the following specific primary antibodies: PI3K (1:200, 20584-1-AP, proteintech), p-PI3K (1:200, T40116 , Abmart), AKT (1:200, 4691, Cell Signaling Technology), p-AKT (1:200, 4060, Cell Signaling Technology), and p-FOXO3a (1:200, 28755-1-AP, proteintech).

Techniques: Immunofluorescence, Western Blot, Expressing

PI and GLN improve ovarian tissue morphology and ovarian function in 4-VCD induced POI mice. (A) HE-stained histopathological sections of ovarian tissue (400×) with a scale bar of 50 μm. (B) Statistics on the number of primordial follicles, primary follicles, secondary follicles, and sinus follicles of mice in each group. Compared with the model group, * p < 0.05, ** p < 0.01, *** p < 0.001. (C) PAS staining results of mouse liver tissue in each group. (D) Immunofluorescence analysis of the effect of on protein expression in ovarian tissue of POI mice: P-PI3K, P-AKT. Mean values are presented with ± SEM, n = 3. Compared with the model group, * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Pharmaceutical Biology

Article Title: Wubie Fanchun Formula-inducible metabolites in primary ovarian insufficiency model mice that facilitate ovarian renovation

doi: 10.1080/13880209.2026.2668132

Figure Lengend Snippet: PI and GLN improve ovarian tissue morphology and ovarian function in 4-VCD induced POI mice. (A) HE-stained histopathological sections of ovarian tissue (400×) with a scale bar of 50 μm. (B) Statistics on the number of primordial follicles, primary follicles, secondary follicles, and sinus follicles of mice in each group. Compared with the model group, * p < 0.05, ** p < 0.01, *** p < 0.001. (C) PAS staining results of mouse liver tissue in each group. (D) Immunofluorescence analysis of the effect of on protein expression in ovarian tissue of POI mice: P-PI3K, P-AKT. Mean values are presented with ± SEM, n = 3. Compared with the model group, * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Staining, Immunofluorescence, Expressing

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anti p pi3k (Affinity Biosciences)

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