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Autophagy modulation in resveratrol protective effects on steroidogenesis in high-fat diet-fed mice and
Ping Wang1, Mengyu Lin1, Chao Chen1
1Department of Histology and Embryology, Anhui Medical University, Hefei, 230032, China.
Background:
Autophagy dysregulation and oxidative stress play critical pathophysiological roles in developing obesity-related metabolic health disorders. This study aims to investigate how autophagy modulation is related to resveratrol (RSV) antioxidant activities and preventive effects on steroidogenesis decline associated with a high-fat diet (HFD) and oxidative damage.
Methods And Results:
Eight-week-old C57BL/6 J male mice were fed with HFD with or without supplement RSV (400 mg/kg/day) by gavage for 16 weeks. The control group was fed with a standard diet with no RSV or the same amount of RSV. Mouse Leydig cell line TM3 cell was used for in vitro studies. Oxidative stress was induced in TM3 cells with H2O2, followed by RSV treatment plus autophagy activator rapamycin or autophagy inhibitor 3-methyladenine, respectively. RSV supplement could upregulate proteins level of StAR and mitochondrial proteins COX4 and mtTFA, indicating the amelioration of steroidogenesis decline and mitochondrial dysfunction caused by HFD. Antioxidants such as GPx4 and SOD2 were improved by RSV as well. The observation of autophagosomes and the changes in expressions of LC3II/I, Beclin1, and Atg7 indicated that RSV could reverse the autophagy defect associated with HFD. 3-methyladenine inhibition of autophagy partially abolished RSV protection on mitochondrial function and steroidogenesis in H2O2-challenged TM3 cells. However, the combination use of rapamycin and RSV did not improve protection on Leydig cells against oxidative damage.
Conclusions:
The stimulation of autophagy by RSV is closely linked to its antioxidant actions and positive impact on steroidogenesis in HFD mice. The findings suggest RSV is protective against obesity-related Leydig cell impairment.
Insights
Resveratrol (RSV) protects against obesity-related Leydig cell damage by stimulating autophagy and reducing oxidative stress, thereby improving steroidogenesis and mitochondrial function in mice fed a high-fat diet.
Area of Science:
- Endocrinology
- Metabolic Health
- Cellular Biology
Background:
- Autophagy dysregulation and oxidative stress are key factors in obesity-related metabolic disorders.
- High-fat diets (HFD) can impair steroidogenesis and mitochondrial function in Leydig cells.
- Resveratrol (RSV) possesses antioxidant properties that may counteract these effects.
Purpose of the Study:
- To investigate the relationship between autophagy modulation, resveratrol's antioxidant activity, and its protective effects on steroidogenesis decline.
- To determine if RSV can prevent HFD-induced and oxidative damage-related impairment in Leydig cells.
Main Methods:
- Mice were fed HFD with or without RSV supplementation for 16 weeks.
- In vitro studies used TM3 Leydig cells treated with H2O2, RSV, rapamycin (autophagy activator), or 3-methyladenine (autophagy inhibitor).
- Evaluated protein levels (StAR, COX4, mtTFA, GPx4, SOD2), autophagosome formation, and autophagy-related protein expressions (LC3II/I, Beclin1, Atg7).
Main Results:
- RSV supplementation improved steroidogenesis and mitochondrial function in HFD-fed mice by upregulating StAR, COX4, and mtTFA.
- RSV enhanced antioxidant proteins (GPx4, SOD2) and reversed HFD-induced autophagy defects.
- In vitro, autophagy inhibition partially blocked RSV's protective effects against oxidative damage in TM3 cells.
Conclusions:
- RSV's stimulation of autophagy is linked to its antioxidant effects and positive impact on steroidogenesis.
- RSV demonstrates protective effects against obesity-related Leydig cell impairment.
- Autophagy modulation plays a significant role in RSV's beneficial actions on Leydig cells.
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