Protective Role of against Flies' Neurodegeneration with Improved Mitochondrial Function.

Adenosine 5'-monophosphate-activated protein kinase ()'s effect in -induced kinase 1 () mutant Parkinson's disease (PD) transgenic flies and the related mechanism is seldom studied. The classic PD transgenic flies was utilized to generate the disease characteristics specifically expressed in flies' muscles, and Western blot (WB) was used to measure the expression of the activated form of to investigate whether activated alters in PD flies. was used to drive overexpression in flies to demonstrate the crucial role of in PD pathogenesis. The abnormal wing posture and climbing ability of PD transgenic flies were recorded. Mitochondrial morphology via transmission electron microscopy (TEM) and ATP and NADH: ubiquinone oxidoreductase core subunit S3 (NDUFS3) protein levels were tested to evaluate the alteration of the mitochondrial function in PD flies. Phosphorylated AMPK dropped significantly in flies compared to controls, and overexpression rescued flies' abnormal wing posture rate. The elevated dopaminergic neuron number in PPL1 via immunofluorescent staining was observed. Mitochondrial dysfunction in flies has been ameliorated with increased ATP level, restored mitochondrial morphology in muscle, and increased NDUFS3 protein expression. Conclusively, overexpression could partially rescue the PD flies via improving flies' mitochondrial function.