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Published on: June 9, 2017
Ghrelin protects MES23.5 cells against rotenone via inhibiting mitochondrial dysfunction and apoptosis
Jianhan Yu1, Huamin Xu1, Xiaoli Shen1
1Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College of Qingdao University, Qingdao, 266071, China.
Abstract:
Ghrelin is an endogenous ligand for the growth hormone secretagogue (GHS) receptor and has several important physiological functions. Recently, particular attention has been paid to its neuroprotective effect. Rotenone is used to investigate the pathogenesis of Parkinson's disease (PD) for its ability to inhibit mitochondrial complex I. The current study was carried out to investigate the neuroprotective effects of ghrelin against rotenone in MES 23.5 dopaminergic cells and explored the possible mechanisms underlying this protection. Our results showed that rotenone induced significant decrease in cell viability which was counteracted by ghrelin treatment. In addition, rotenone challenge reduced mitochondrial membrane potential, inhibited the activity of mitochondrial complex I and depressed cytochrome C release from mitochondria. This mitochondrial dysfunction was reversed by ghrelin treatment. Furthermore, our results demonstrated that ghrelin protected MES23.5 cells against rotenone-induced apoptosis by inhibiting activation of caspase-3. Overall, our findings showed ghrelin provided protective effects on MES23.5 dopaminergic cells against rotenone via restoring mitochondrial dysfunction and inhibiting mitochondrial dependent apoptosis.
Insights
Ghrelin protects dopaminergic cells from rotenone-induced damage by preserving mitochondrial function and inhibiting apoptosis. This neuroprotective effect highlights ghrelin
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Ghrelin is an endogenous ligand for the growth hormone secretagogue (GHS) receptor.
- Ghrelin exhibits neuroprotective effects, making it a potential therapeutic agent.
- Rotenone, a mitochondrial complex I inhibitor, is used to model Parkinson's disease pathogenesis.
Purpose of the Study:
- To investigate the neuroprotective effects of ghrelin against rotenone-induced toxicity in MES 23.5 dopaminergic cells.
- To elucidate the mechanisms underlying ghrelin's protective action against rotenone.
Main Methods:
- MES 23.5 dopaminergic cells were challenged with rotenone.
- Ghrelin treatment was administered to assess its protective effects.
- Cell viability, mitochondrial membrane potential, mitochondrial complex I activity, cytochrome C release, and caspase-3 activation were measured.
Main Results:
- Rotenone significantly decreased cell viability and mitochondrial function, including membrane potential and complex I activity.
- Rotenone induced cytochrome C release and caspase-3 activation, indicative of apoptosis.
- Ghrelin treatment counteracted rotenone's effects, restoring cell viability and mitochondrial function while inhibiting apoptosis.
Conclusions:
- Ghrelin demonstrates significant neuroprotective effects against rotenone-induced damage in dopaminergic cells.
- Ghrelin protects cells by restoring mitochondrial dysfunction and inhibiting mitochondrial-dependent apoptosis.
- Ghrelin's mechanisms involve preserving mitochondrial integrity and preventing caspase-3 activation.
