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mediators il 6 (Cusabio)

Name: mediators il 6
Brand: Cusabio
Rating: 95 (91 reviews)

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Cusabio mediators il 6
Mediators Il 6, supplied by Cusabio, used in various techniques. Bioz Stars score: 95/100, based on 91 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Evaluation of key factors in LPS-induced inflammation model using BEAS-2B cells. ( A ) Cell viability was assessed using the CCK-8 assay after treating BEAS-2B cells with varying concentrations of LPS for 12 h. ( B ) Levels of pro-inflammatory cytokines TNF-α, IL-6, and IL-8 were measured in the culture supernatant of BEAS-2B cells by ELISA following 5 µg/ml LPS treatment. ( C ) BEAS-2B cell apoptosis was analyzed using Annexin V/PI flow cytometry after 5 µg/ml LPS exposure. The red box in the dot plots indicates the apoptotic cells. ( D ) qRT-PCR analysis of ADRA2A, IL5RA, and AGR2 expression levels in BEAS-2B cells. N = 3 (biological replicates). * p < 0.05, ** p < 0.01, vs. Control

Journal: Journal of Inflammation (London, England)

Article Title: ADRA2A contributes to airway inflammation and apoptosis in asthma through the ERK signaling in vitro and in vivo

doi: 10.1186/s12950-025-00480-8

Figure Lengend Snippet: Evaluation of key factors in LPS-induced inflammation model using BEAS-2B cells. ( A ) Cell viability was assessed using the CCK-8 assay after treating BEAS-2B cells with varying concentrations of LPS for 12 h. ( B ) Levels of pro-inflammatory cytokines TNF-α, IL-6, and IL-8 were measured in the culture supernatant of BEAS-2B cells by ELISA following 5 µg/ml LPS treatment. ( C ) BEAS-2B cell apoptosis was analyzed using Annexin V/PI flow cytometry after 5 µg/ml LPS exposure. The red box in the dot plots indicates the apoptotic cells. ( D ) qRT-PCR analysis of ADRA2A, IL5RA, and AGR2 expression levels in BEAS-2B cells. N = 3 (biological replicates). * p < 0.05, ** p < 0.01, vs. Control

Article Snippet: The commercial ELISA kits (Cusabio, Wuhan, China; TNF-α: CSB-E04740h/ CSB-E04741m, IL-6: CSB-E04638h/CSB-E04639m, IL-8: CSB-E04641h, IL-4: CSB-E04634m, IL-13: CSB-E04602m) were employed following the manufacturer’s protocols to measure tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), IL-8, IL-4, and IL-13 concentrations within the bronchoalveolar lavage fluid (BALF) or cell culture supernatants.

Techniques: CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Quantitative RT-PCR, Expressing, Control

ADRA2A knockdown attenuates LPS-induced inflammation and apoptosis in BEAS-2B cells. ( A - B ) ADRA2A knockdown was achieved in BEAS-2B cells by transfecting small interfering RNA against ADRA2A (si-ADRA2A) and validated using qRT-PCR and Immunoblotting. Then, BEAS-2B cells were transfected with si-ADRA2A, exposed to 5 µg/ml LPS, and examined for cell viability using CCK-8 assay ( C ); concentrations of TNF-α, IL-6, and IL-8 in the culture supernatant using ELISA ( D ); cell apoptosis using Flow cytometry ( E ), the red box in the dot plots indicates the apoptotic cells; protein levels of caspase-3, cleaved caspase-3, Bax, and Bcl-2 using Immunoblotting ( F ). N = 3 (biological replicates). * p < 0.05, ** p < 0.01, vs. Control; # p < 0.05, ## p < 0.01, vs. LPS + si-NC

Journal: Journal of Inflammation (London, England)

Article Title: ADRA2A contributes to airway inflammation and apoptosis in asthma through the ERK signaling in vitro and in vivo

doi: 10.1186/s12950-025-00480-8

Figure Lengend Snippet: ADRA2A knockdown attenuates LPS-induced inflammation and apoptosis in BEAS-2B cells. ( A - B ) ADRA2A knockdown was achieved in BEAS-2B cells by transfecting small interfering RNA against ADRA2A (si-ADRA2A) and validated using qRT-PCR and Immunoblotting. Then, BEAS-2B cells were transfected with si-ADRA2A, exposed to 5 µg/ml LPS, and examined for cell viability using CCK-8 assay ( C ); concentrations of TNF-α, IL-6, and IL-8 in the culture supernatant using ELISA ( D ); cell apoptosis using Flow cytometry ( E ), the red box in the dot plots indicates the apoptotic cells; protein levels of caspase-3, cleaved caspase-3, Bax, and Bcl-2 using Immunoblotting ( F ). N = 3 (biological replicates). * p < 0.05, ** p < 0.01, vs. Control; # p < 0.05, ## p < 0.01, vs. LPS + si-NC

Techniques: Knockdown, Small Interfering RNA, Quantitative RT-PCR, Western Blot, Transfection, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Control

ADRA2A overexpression exacerbates LPS-induced inflammation and apoptosis in BEAS-2B cells. ( A - B ) ADRA2A overexpression was achieved in BEAS-2B cells by transfecting ADRA2A-overexpressing plasmid (OE-ADRA2A) and validated using qRT-PCR and Immunoblotting. Then, BEAS-2B cells were transfected with OE-ADRA2A, exposed to 5 µg/ml LPS, and examined for cell viability using CCK-8 assay ( C ); concentrations of TNF-α, IL-6, and IL-8 in the culture supernatant using ELISA ( D ); cell apoptosis using Flow cytometry ( E ), the red box in the dot plots indicates the apoptotic cells; protein levels of caspase-3, cleaved caspase-3, Bax, and Bcl-2 using Immunoblotting ( F ). N = 3 (biological replicates). * p < 0.05, ** p < 0.01, vs. Control; # p < 0.05, ## p < 0.01, vs. LPS + Vector

Journal: Journal of Inflammation (London, England)

Article Title: ADRA2A contributes to airway inflammation and apoptosis in asthma through the ERK signaling in vitro and in vivo

doi: 10.1186/s12950-025-00480-8

Figure Lengend Snippet: ADRA2A overexpression exacerbates LPS-induced inflammation and apoptosis in BEAS-2B cells. ( A - B ) ADRA2A overexpression was achieved in BEAS-2B cells by transfecting ADRA2A-overexpressing plasmid (OE-ADRA2A) and validated using qRT-PCR and Immunoblotting. Then, BEAS-2B cells were transfected with OE-ADRA2A, exposed to 5 µg/ml LPS, and examined for cell viability using CCK-8 assay ( C ); concentrations of TNF-α, IL-6, and IL-8 in the culture supernatant using ELISA ( D ); cell apoptosis using Flow cytometry ( E ), the red box in the dot plots indicates the apoptotic cells; protein levels of caspase-3, cleaved caspase-3, Bax, and Bcl-2 using Immunoblotting ( F ). N = 3 (biological replicates). * p < 0.05, ** p < 0.01, vs. Control; # p < 0.05, ## p < 0.01, vs. LPS + Vector

Techniques: Over Expression, Plasmid Preparation, Quantitative RT-PCR, Western Blot, Transfection, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Control

ADRA2A knockdown ameliorates OVA-induced asthma-like features in model mice. The OVA-induced asthma model was established in mice and ADRA2A knockdown was achieved by lentivirus infection as described. ( A ) Immunoblotting was performed to detect ADRA2A levels in lung tissues to confirm the knockdown efficiency. ( B ) Measurement of airway hyperresponsiveness (AHR) in response to methacholine challenge. ( C ) Lung wet-to-dry weight ratio as an indicator of pulmonary edema. ( D ) Histological examination of lung tissue sections stained with hematoxylin and eosin ( H & E ) staining (upper) to assess inflammatory cell infiltration and periodic acid-Schiff (PAS) staining (middle) to evaluate goblet cell hyperplasia and mucus production and IHC staining (down) to detect ADRA2A protein level. Scale bar = 50–25 μm. ( E - F ) The inflammatory infiltration scores (inflammation score) and goblet cell hyperplasia scores (PAS score) were quantified by H&E and PAS staining, respectively. ( G ) The ADRA2A protein level were quantified by IHC staining. ( H ) Wright-Giemsa staining of BALF to quantify total inflammatory cells, eosinophils, neutrophils, lymphocyte, and macrophage. ( I ) ELISA for OVA-specific IgE levels in serum. ( J ) qRT-PCR analysis of TNF-α and IL-6 mRNA expression levels in lung tissues. ( K ) ELISA for TNF-α, IL-6, IL-4, and IL-13 levels in BALF. ( L ) Immunoblotting detecting apoptotic markers, including caspase-3, cleaved caspase-3, Bax, and Bcl-2, in lung tissues. N = 6 for B-K, or N = 3 for A and L (biological replicates). * p < 0.05, ** p < 0.01, vs. Control; # p < 0.05, ## p < 0.01, vs. OVA + Lv-shNC

Journal: Journal of Inflammation (London, England)

Article Title: ADRA2A contributes to airway inflammation and apoptosis in asthma through the ERK signaling in vitro and in vivo

doi: 10.1186/s12950-025-00480-8

Figure Lengend Snippet: ADRA2A knockdown ameliorates OVA-induced asthma-like features in model mice. The OVA-induced asthma model was established in mice and ADRA2A knockdown was achieved by lentivirus infection as described. ( A ) Immunoblotting was performed to detect ADRA2A levels in lung tissues to confirm the knockdown efficiency. ( B ) Measurement of airway hyperresponsiveness (AHR) in response to methacholine challenge. ( C ) Lung wet-to-dry weight ratio as an indicator of pulmonary edema. ( D ) Histological examination of lung tissue sections stained with hematoxylin and eosin ( H & E ) staining (upper) to assess inflammatory cell infiltration and periodic acid-Schiff (PAS) staining (middle) to evaluate goblet cell hyperplasia and mucus production and IHC staining (down) to detect ADRA2A protein level. Scale bar = 50–25 μm. ( E - F ) The inflammatory infiltration scores (inflammation score) and goblet cell hyperplasia scores (PAS score) were quantified by H&E and PAS staining, respectively. ( G ) The ADRA2A protein level were quantified by IHC staining. ( H ) Wright-Giemsa staining of BALF to quantify total inflammatory cells, eosinophils, neutrophils, lymphocyte, and macrophage. ( I ) ELISA for OVA-specific IgE levels in serum. ( J ) qRT-PCR analysis of TNF-α and IL-6 mRNA expression levels in lung tissues. ( K ) ELISA for TNF-α, IL-6, IL-4, and IL-13 levels in BALF. ( L ) Immunoblotting detecting apoptotic markers, including caspase-3, cleaved caspase-3, Bax, and Bcl-2, in lung tissues. N = 6 for B-K, or N = 3 for A and L (biological replicates). * p < 0.05, ** p < 0.01, vs. Control; # p < 0.05, ## p < 0.01, vs. OVA + Lv-shNC

Techniques: Knockdown, Infection, Western Blot, Staining, Immunohistochemistry, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR, Expressing, Control

ERK1/2 inhibiton restrains LPS-induced inflammation and apoptosis in BEAS-2B cells. BEAS-2B cells were transfected with OE-ADRA2A, exposed to 5 µg/ml LPS, and then treated with 1 µM ERK1/2 inhibitor (U0126), and examined for the protein levels of p-ERK (Thr202/Tyr204) and ERK by Immunoblotting (A); cell viability using CCK-8 assay (B); concentrations of TNF-α, IL-6, and IL-8 in the culture supernatant using ELISA (C); cell apoptosis using Flow cytometry (D), the red box in the dot plots indicates the apoptotic cells; Bcl-2 protein level using Immunoblotting (E). N = 3 (biological replicates). ** p < 0.01, vs. LPS; # p < 0.05, ## p < 0.01, vs. LPS + OE-ADRA2A

Journal: Journal of Inflammation (London, England)

Article Title: ADRA2A contributes to airway inflammation and apoptosis in asthma through the ERK signaling in vitro and in vivo

doi: 10.1186/s12950-025-00480-8

Figure Lengend Snippet: ERK1/2 inhibiton restrains LPS-induced inflammation and apoptosis in BEAS-2B cells. BEAS-2B cells were transfected with OE-ADRA2A, exposed to 5 µg/ml LPS, and then treated with 1 µM ERK1/2 inhibitor (U0126), and examined for the protein levels of p-ERK (Thr202/Tyr204) and ERK by Immunoblotting (A); cell viability using CCK-8 assay (B); concentrations of TNF-α, IL-6, and IL-8 in the culture supernatant using ELISA (C); cell apoptosis using Flow cytometry (D), the red box in the dot plots indicates the apoptotic cells; Bcl-2 protein level using Immunoblotting (E). N = 3 (biological replicates). ** p < 0.01, vs. LPS; # p < 0.05, ## p < 0.01, vs. LPS + OE-ADRA2A

Techniques: Transfection, Western Blot, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry

ERK1/2 inhibition relieves OVA-induced asthma-like features in model mice. The OVA-induced asthma model was established in mice and ERK1/2 inhibitor (U0126) was treated as described, and examined for the protein levels of ADRA2A, p-ERK (Thr202/Tyr204) and ERK by Immunoblotting ( A ); airway hyperresponsiveness (AHR) ( B ); lung wet-to-dry weight ratio ( C ); inflammatory cell infiltration by H&E staining (upper) and goblet cell hyperplasia and mucus production by periodic acid-Schiff (PAS) staining (down) ( D ), Scale bar = 50 μm; the inflammatory infiltration score (inflammation score) and goblet cell hyperplasia scores (PAS score) were quantified by H&E and PAS staining, respectively ( E - F ); total inflammatory cells, eosinophils, neutrophils, lymphocyte, and macrophage by Wright-Giemsa staining of BALF ( G ); OVA-specific IgE levels in serum by ELISA ( H ); TNF-α and IL-6 mRNA expression levels in lung tissues by qRT-PCR ( I ); TNF-α, IL-6, IL-4, and IL-13 levels in BALF by ELISA ( J ). N = 3 for A, N = 6 for the rest panels (biological replicates). * p < 0.05, ** p < 0.01, vs. OVA

Journal: Journal of Inflammation (London, England)

Article Title: ADRA2A contributes to airway inflammation and apoptosis in asthma through the ERK signaling in vitro and in vivo

doi: 10.1186/s12950-025-00480-8

Figure Lengend Snippet: ERK1/2 inhibition relieves OVA-induced asthma-like features in model mice. The OVA-induced asthma model was established in mice and ERK1/2 inhibitor (U0126) was treated as described, and examined for the protein levels of ADRA2A, p-ERK (Thr202/Tyr204) and ERK by Immunoblotting ( A ); airway hyperresponsiveness (AHR) ( B ); lung wet-to-dry weight ratio ( C ); inflammatory cell infiltration by H&E staining (upper) and goblet cell hyperplasia and mucus production by periodic acid-Schiff (PAS) staining (down) ( D ), Scale bar = 50 μm; the inflammatory infiltration score (inflammation score) and goblet cell hyperplasia scores (PAS score) were quantified by H&E and PAS staining, respectively ( E - F ); total inflammatory cells, eosinophils, neutrophils, lymphocyte, and macrophage by Wright-Giemsa staining of BALF ( G ); OVA-specific IgE levels in serum by ELISA ( H ); TNF-α and IL-6 mRNA expression levels in lung tissues by qRT-PCR ( I ); TNF-α, IL-6, IL-4, and IL-13 levels in BALF by ELISA ( J ). N = 3 for A, N = 6 for the rest panels (biological replicates). * p < 0.05, ** p < 0.01, vs. OVA

Techniques: Inhibition, Western Blot, Staining, Enzyme-linked Immunosorbent Assay, Expressing, Quantitative RT-PCR

Effects of Ang1-7 on viability, the ACE2/Ang1-7/Mas axis and autophagy in HG-induced HRMECs. ( A ) HRMECs were subjected to 48-h incubation with 5.5, 5.5 mM NG + 24.5 mannitol and 30 mM glucose (NG, MA and HG groups), respectively, followed by 100 nmol/L Ang1-7 treatment (HG + Ang1-7 group). MTT assay was used to detect cell viability in the three groups. ( B and C ) Cell apoptosis was assessed with the flow cytometry experiment. ( D – F ) Western blot was performed to measure protein expressions of ACE2 and Mas in the three groups. ( G ) ELISA was utilized to detect Ang1-7 level in the three groups. ( H – J ) Western blot was applied to measure protein expressions of LC3II/LC3I and P62 in the three groups. ( K ) and ( L ) Microstructural detection of autophagosomes by transmission electron microscopy (scale bar = 200 µm) in the three groups, arrow: autophagosomes. Data are shown as mean ± standard deviation (SD) (n = 3 biological replicates). GAPDH was used as the loading control. *** P < 0.001, versus NG; +++ P < 0.001, versus HG. HRMECs, human retinal microvascular endothelial cells; NG, normal glucose; HG, high glucose; Ang1-7, angiotensin 1–7; ACE2, angiotensin-converting enzyme 2; MTT, methylthiazolyldiphenyl-tetrazolium bromide; ELISA, Enzyme-linked immunosorbent assay.

Journal: Scientific Reports

Article Title: Ginsenoside Rg1 alleviates HG-induced autophagy of retinal microvascular endothelial cells by activating ACE2/Ang1-7/Mas in vitro

doi: 10.1038/s41598-025-29344-0

Figure Lengend Snippet: Effects of Ang1-7 on viability, the ACE2/Ang1-7/Mas axis and autophagy in HG-induced HRMECs. ( A ) HRMECs were subjected to 48-h incubation with 5.5, 5.5 mM NG + 24.5 mannitol and 30 mM glucose (NG, MA and HG groups), respectively, followed by 100 nmol/L Ang1-7 treatment (HG + Ang1-7 group). MTT assay was used to detect cell viability in the three groups. ( B and C ) Cell apoptosis was assessed with the flow cytometry experiment. ( D – F ) Western blot was performed to measure protein expressions of ACE2 and Mas in the three groups. ( G ) ELISA was utilized to detect Ang1-7 level in the three groups. ( H – J ) Western blot was applied to measure protein expressions of LC3II/LC3I and P62 in the three groups. ( K ) and ( L ) Microstructural detection of autophagosomes by transmission electron microscopy (scale bar = 200 µm) in the three groups, arrow: autophagosomes. Data are shown as mean ± standard deviation (SD) (n = 3 biological replicates). GAPDH was used as the loading control. *** P < 0.001, versus NG; +++ P < 0.001, versus HG. HRMECs, human retinal microvascular endothelial cells; NG, normal glucose; HG, high glucose; Ang1-7, angiotensin 1–7; ACE2, angiotensin-converting enzyme 2; MTT, methylthiazolyldiphenyl-tetrazolium bromide; ELISA, Enzyme-linked immunosorbent assay.

Article Snippet: The human ELISA kits Ang1-7 (CSB-E14242h, CUSABIO, Wuhan, China), TNF-α (CSB-E04736h-IS, CUSABIO, Wuhan, China) and IL-6 (CSB-E04638h, CUSABIO, Wuhan, China) were employed to detect the levels of Ang1-7, TNF-α, and IL-6 in HRMECs undergoing indicated treatments.

Techniques: Incubation, MTT Assay, Flow Cytometry, Western Blot, Enzyme-linked Immunosorbent Assay, Transmission Assay, Electron Microscopy, Standard Deviation, Control

The protective role of Rg1 in HG-induced HRMECs through the ACE2/Ang1-7/Mas axis. ( A ) HRMECs were subjected to 48-h incubation with 5.5 and 30 mM glucose (NG and HG groups), respectively, followed by treatments with 1 μmol/L A779 (a Mas receptor antagonist) and/or 10 μM Rg1 (HG + A779, HG + Rg1 and HG + Rg1 + A779 groups). MTT assay was used to detect cell viability in the five groups. ( B ) and ( C ) Cell apoptosis was assessed with the flow cytometry experiment. ( D – F ) Western blot was performed to measure protein expressions of ACE2 and Mas in the five groups. ( G ) ELISA was utilized to detect Ang1-7 level in the five groups. ( H ) and ( I ) Western blot was conducted to measure protein expressions of p-eNOS and eNOS in the five groups. ( J ) and ( K ) ELISA was used to detect the levels of TNF-α, and IL-6. ( L – N ) Western blot was conducted to measure protein expressions of LC3II/LC3I and P62 in the five groups. ( O ) and ( P ) Microstructural detection of autophagosomes by transmission electron microscopy (scale bar = 200 µm) in the five groups, arrow: autophagosomes. Data are shown as mean ± standard deviation (n = 3 biological replicates). GAPDH was used as the loading control. *** P < 0.001, versus NG; + P < 0.05, ++ P < 0.01, +++ P < 0.001, versus HG; # P < 0.05, ### P < 0.001, versus HG + Rg1; ^^^ P < 0.001, versus HG + A779. Rg1, ginsenoside Rg1.

Journal: Scientific Reports

Article Title: Ginsenoside Rg1 alleviates HG-induced autophagy of retinal microvascular endothelial cells by activating ACE2/Ang1-7/Mas in vitro

doi: 10.1038/s41598-025-29344-0

Figure Lengend Snippet: The protective role of Rg1 in HG-induced HRMECs through the ACE2/Ang1-7/Mas axis. ( A ) HRMECs were subjected to 48-h incubation with 5.5 and 30 mM glucose (NG and HG groups), respectively, followed by treatments with 1 μmol/L A779 (a Mas receptor antagonist) and/or 10 μM Rg1 (HG + A779, HG + Rg1 and HG + Rg1 + A779 groups). MTT assay was used to detect cell viability in the five groups. ( B ) and ( C ) Cell apoptosis was assessed with the flow cytometry experiment. ( D – F ) Western blot was performed to measure protein expressions of ACE2 and Mas in the five groups. ( G ) ELISA was utilized to detect Ang1-7 level in the five groups. ( H ) and ( I ) Western blot was conducted to measure protein expressions of p-eNOS and eNOS in the five groups. ( J ) and ( K ) ELISA was used to detect the levels of TNF-α, and IL-6. ( L – N ) Western blot was conducted to measure protein expressions of LC3II/LC3I and P62 in the five groups. ( O ) and ( P ) Microstructural detection of autophagosomes by transmission electron microscopy (scale bar = 200 µm) in the five groups, arrow: autophagosomes. Data are shown as mean ± standard deviation (n = 3 biological replicates). GAPDH was used as the loading control. *** P < 0.001, versus NG; + P < 0.05, ++ P < 0.01, +++ P < 0.001, versus HG; # P < 0.05, ### P < 0.001, versus HG + Rg1; ^^^ P < 0.001, versus HG + A779. Rg1, ginsenoside Rg1.

Techniques: Incubation, MTT Assay, Flow Cytometry, Western Blot, Enzyme-linked Immunosorbent Assay, Transmission Assay, Electron Microscopy, Standard Deviation, Control

Involvement of PI3K/Akt pathway in the mitigating effect of Rg1 on HG-caused dysfunctional HRMECs. ( A ) HRMECs were subjected to 48-h incubation with 30 mM glucose (HG group), followed by treatments with 10 μM Rg1 and/or 50 μM LY294002 (HG + Rg1, HG + LY294002 and HG + Rg1 + LY294002 groups). MTT assay was used to detect cell viability in the four groups. ( B and C ) Cell apoptosis was assessed with the flow cytometry experiment. ( D – H ) Western blot was performed to measure protein expressions of p-Akt/Akt, ACE2 and Mas in the four groups. ( I ) ELISA was utilized to detect Ang1-7 level in the four groups. ( J – L ) Western blot was conducted to measure protein expressions of LC3II/LC3I and P62 in the four groups. ( M ) and ( N ) Microstructural detection of autophagosomes by transmission electron microscopy (scale bar = 200 µm) in the five groups, arrow: autophagosomes. Data are shown as mean ± standard deviation (n = 3 biological replicates). GAPDH was used as the loading control. + P < 0.05, +++ P < 0.001, versus HG; # P < 0.05, ### P < 0.001, versus HG + LY294002; ^^ P < 0.01, ^^^ P < 0.001, versus HG + Rg1. Akt, protein kinase B; p-Akt, phosphorylated Akt.

Journal: Scientific Reports

Article Title: Ginsenoside Rg1 alleviates HG-induced autophagy of retinal microvascular endothelial cells by activating ACE2/Ang1-7/Mas in vitro

doi: 10.1038/s41598-025-29344-0

Figure Lengend Snippet: Involvement of PI3K/Akt pathway in the mitigating effect of Rg1 on HG-caused dysfunctional HRMECs. ( A ) HRMECs were subjected to 48-h incubation with 30 mM glucose (HG group), followed by treatments with 10 μM Rg1 and/or 50 μM LY294002 (HG + Rg1, HG + LY294002 and HG + Rg1 + LY294002 groups). MTT assay was used to detect cell viability in the four groups. ( B and C ) Cell apoptosis was assessed with the flow cytometry experiment. ( D – H ) Western blot was performed to measure protein expressions of p-Akt/Akt, ACE2 and Mas in the four groups. ( I ) ELISA was utilized to detect Ang1-7 level in the four groups. ( J – L ) Western blot was conducted to measure protein expressions of LC3II/LC3I and P62 in the four groups. ( M ) and ( N ) Microstructural detection of autophagosomes by transmission electron microscopy (scale bar = 200 µm) in the five groups, arrow: autophagosomes. Data are shown as mean ± standard deviation (n = 3 biological replicates). GAPDH was used as the loading control. + P < 0.05, +++ P < 0.001, versus HG; # P < 0.05, ### P < 0.001, versus HG + LY294002; ^^ P < 0.01, ^^^ P < 0.001, versus HG + Rg1. Akt, protein kinase B; p-Akt, phosphorylated Akt.

Techniques: Incubation, MTT Assay, Flow Cytometry, Western Blot, Enzyme-linked Immunosorbent Assay, Transmission Assay, Electron Microscopy, Standard Deviation, Control

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