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Astragaloside IV rescues MPP+-induced mitochondrial dysfunction through upregulation of methionine sulfoxide
Yue Liu1, Li Chong1, Xiaoqing Li1
1Department of Neurology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710068, P.R. China.
Abstract:
Methionine sulfoxide reductase (Msr) repairs oxidatively damaged proteins through acting as an antioxidant. Oxidative stress has been postulated to cause the mitochondrial dysfunction that is associated with aging and certain diseases, including Parkinson's disease (PD). The present study investigated the protective effects of astragaloside IV (AS-IV) on 1-methyl-4-phenylpyridinium (MPP+)-induced mitochondrial dysfunction through MsrA in PC12 cells. This revealed that oxidative stress reduced the expression of MsrA following MPP+ treatment. AS-IV was demonstrated to protect PC12 cells from MPP+-induced oxidative damage through upregulating MsrA. MsrA expression was dependent on the Sirt1-FOXO3a signaling pathway. In addition, knockdown of MsrA reduced the protective effects of AS-IV, indicating that the antioxidant effects of AS-UV occurred through MsrA. These results suggest that AS-IV exerts antioxidant effects and regulates mitochondrial function. Thus, AS-IV may serve as an effective therapeutic agent for aging and PD.
Insights
Astragaloside IV protects against oxidative stress and mitochondrial dysfunction by upregulating Methionine sulfoxide reductase A (MsrA). This suggests AS-IV may be a therapeutic for aging and Parkinson's disease.
Area of Science:
- Biochemistry
- Neuroscience
- Pharmacology
Background:
- Oxidative stress contributes to mitochondrial dysfunction, implicated in aging and Parkinson's disease (PD).
- Methionine sulfoxide reductase (Msr) enzymes act as antioxidants by repairing oxidatively damaged proteins.
Purpose of the Study:
- To investigate the protective effects of astragaloside IV (AS-IV) against 1-methyl-4-phenylpyridinium (MPP+)-induced mitochondrial dysfunction in PC12 cells.
- To elucidate the role of MsrA and the Sirt1-FOXO3a pathway in AS-IV's protective mechanism.
Main Methods:
- PC12 cells were treated with MPP+ to induce oxidative stress and mitochondrial dysfunction.
- The expression of MsrA was analyzed following MPP+ treatment and AS-IV administration.
- The involvement of the Sirt1-FOXO3a signaling pathway was investigated.
- MsrA knockdown was performed to assess its role in AS-IV's protective effects.
Main Results:
- MPP+ treatment reduced MsrA expression, indicating oxidative damage.
- AS-IV treatment upregulated MsrA expression, protecting PC12 cells from MPP+-induced damage.
- AS-IV's effect on MsrA was dependent on the Sirt1-FOXO3a signaling pathway.
- Knockdown of MsrA diminished the protective effects of AS-IV.
Conclusions:
- AS-IV exerts antioxidant effects and regulates mitochondrial function primarily through the upregulation of MsrA.
- The Sirt1-FOXO3a pathway mediates AS-IV's action on MsrA.
- AS-IV shows potential as a therapeutic agent for age-related conditions and Parkinson's disease.
