Polygonatum sibiricum polysaccharides enhance pancreatic β-cell function in diabetic zebrafish by mitigating mitochondrial oxidative damage via the AMPK-SIRT1 pathway DOI Creative Commons
Lin Fan, Wenjing Yu, Ping Li

et al.

Frontiers in Nutrition, Journal Year: 2025, Volume and Issue: 12

Published: May 9, 2025

Background Mitochondrial oxidative damage in pancreatic β-cells is a key contributor to diabetes pathogenesis, particularly under hyperglycemic conditions. Polygonatum sibiricum polysaccharides (PSP) have demonstrated potential anti-diabetic effects; however, their precise mechanism, through the AMPK-SIRT1 pathway, remains unclear. Methods A diabetic zebrafish model was established by exposure 2% glucose for 28 days. Zebrafish were divided into control, model, low-dose PSP (50 μg/mL), medium-dose (100 high-dose (200 and metformin groups. Behavioral, biochemical, molecular analyses performed assess β-cell function, mitochondrial damage, inflammation. Network pharmacology analysis used predict targets, docking validated protein interactions. Immunofluorescence Western blotting (WB) conducted examine apoptosis-related expression. Results significantly improved swimming behavior, reduced blood fructosamine levels, enhanced ATP production ( p < 0.01). Antioxidant enzyme activities (SOD, CAT) increased, while stress markers (MDA) inflammatory cytokines (IL-1β, IL-6, TNF- α ) decreased treatment downregulated Cycs expression, alleviating damage. Moreover, upregulated AMPK SIRT1 expression 0.01), along with downstream regulators PGC-1α Nrf1/2 confirming pathway activation. identified 389 shared targets between diabetes-related pathways, implicating mechanisms of inflammation, insulin resistance, dysfunction. Molecular strong binding affinities SIRT1. WB showed cleaved caspase-3 levels apoptosis following Conclusion protects function mitigating via further highlight PSP’s as multi-target therapeutic agent diabetes.

Language: Английский

Polygonatum sibiricum polysaccharides enhance pancreatic β-cell function in diabetic zebrafish by mitigating mitochondrial oxidative damage via the AMPK-SIRT1 pathway DOI Creative Commons
Lin Fan, Wenjing Yu, Ping Li

et al.

Frontiers in Nutrition, Journal Year: 2025, Volume and Issue: 12

Published: May 9, 2025

Background Mitochondrial oxidative damage in pancreatic β-cells is a key contributor to diabetes pathogenesis, particularly under hyperglycemic conditions. Polygonatum sibiricum polysaccharides (PSP) have demonstrated potential anti-diabetic effects; however, their precise mechanism, through the AMPK-SIRT1 pathway, remains unclear. Methods A diabetic zebrafish model was established by exposure 2% glucose for 28 days. Zebrafish were divided into control, model, low-dose PSP (50 μg/mL), medium-dose (100 high-dose (200 and metformin groups. Behavioral, biochemical, molecular analyses performed assess β-cell function, mitochondrial damage, inflammation. Network pharmacology analysis used predict targets, docking validated protein interactions. Immunofluorescence Western blotting (WB) conducted examine apoptosis-related expression. Results significantly improved swimming behavior, reduced blood fructosamine levels, enhanced ATP production ( p < 0.01). Antioxidant enzyme activities (SOD, CAT) increased, while stress markers (MDA) inflammatory cytokines (IL-1β, IL-6, TNF- α ) decreased treatment downregulated Cycs expression, alleviating damage. Moreover, upregulated AMPK SIRT1 expression 0.01), along with downstream regulators PGC-1α Nrf1/2 confirming pathway activation. identified 389 shared targets between diabetes-related pathways, implicating mechanisms of inflammation, insulin resistance, dysfunction. Molecular strong binding affinities SIRT1. WB showed cleaved caspase-3 levels apoptosis following Conclusion protects function mitigating via further highlight PSP’s as multi-target therapeutic agent diabetes.

Language: Английский

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