Sinensetin ameliorates high glucose-induced diabetic nephropathy via enhancing autophagy in vitro and in vivo

Diabetic nephropathy (DN) affects around 40% of people with diabetes, the final outcome of which is end-stage renal disease. The deficiency of autophagy and excessive oxidative stress have been found to participate in the pathogenesis of DN. Sinensetin (SIN) has been proven to have strong antioxidan...

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Veröffentlicht in:Journal of biochemical and molecular toxicology 2023-10, Vol.37 (10), p.e23445-e23445
Hauptverfasser: Kong, Zili, Lv, Wenshan, Wang, Yunyang, Huang, Yajing, Che, Kui, Nan, Huiqi, Xin, Yu, Wang, Jiaxuan, Chen, Jintao, Wang, Yangang, Chi, Jingwei
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container_issue 10
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container_title Journal of biochemical and molecular toxicology
container_volume 37
creator Kong, Zili
Lv, Wenshan
Wang, Yunyang
Huang, Yajing
Che, Kui
Nan, Huiqi
Xin, Yu
Wang, Jiaxuan
Chen, Jintao
Wang, Yangang
Chi, Jingwei
description Diabetic nephropathy (DN) affects around 40% of people with diabetes, the final outcome of which is end-stage renal disease. The deficiency of autophagy and excessive oxidative stress have been found to participate in the pathogenesis of DN. Sinensetin (SIN) has been proven to have strong antioxidant capability. However, the effect of SIN on DN has not been studied. We examined the effect of SIN on cell viability and autophagy in the podocyte cell line, MPC5 cells, treated with high glucose (HG). For in vivo studies, DN mice models were established by intraperitoneal injected with streptozotocin (40 mg/kg) for 5 consecutive days and fed with a 60% high-fat diet, and SIN was given (10, 20, and 40 mg/kg) for 8 weeks via intraperitoneal injection. The results showed that SIN could protect MPC5 cells against HG-induced damage and significantly improve the renal function of DN mice. Moreover, SIN remarkably restored the autophagy activity of MPC5 cells which was inhibited under HG conditions. Consistent with this, SIN efficiently improved autophagy in the kidney tissue of DN mice. In brief, our findings demonstrated the protective effect of SIN on DN via restoring the autophagic function, which might provide a basis for drug development.
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The deficiency of autophagy and excessive oxidative stress have been found to participate in the pathogenesis of DN. Sinensetin (SIN) has been proven to have strong antioxidant capability. However, the effect of SIN on DN has not been studied. We examined the effect of SIN on cell viability and autophagy in the podocyte cell line, MPC5 cells, treated with high glucose (HG). For in vivo studies, DN mice models were established by intraperitoneal injected with streptozotocin (40 mg/kg) for 5 consecutive days and fed with a 60% high-fat diet, and SIN was given (10, 20, and 40 mg/kg) for 8 weeks via intraperitoneal injection. The results showed that SIN could protect MPC5 cells against HG-induced damage and significantly improve the renal function of DN mice. Moreover, SIN remarkably restored the autophagy activity of MPC5 cells which was inhibited under HG conditions. Consistent with this, SIN efficiently improved autophagy in the kidney tissue of DN mice. 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subjects Animal models
Animal tissues
Autophagy
Cell viability
Damage
Diabetes
Diabetes mellitus
Diabetic nephropathy
Drug development
Glucose
High fat diet
In vivo methods and tests
Kidneys
Nephropathy
Oxidative stress
Pathogenesis
Recovery of function
Renal function
Streptozocin
title Sinensetin ameliorates high glucose-induced diabetic nephropathy via enhancing autophagy in vitro and in vivo
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