3-N-Butilftalit Rotenone-Induced Parkinson Hastalığı Modellerinde Nöroinflamasyonu CGas/STING Pathway ile zayıflatır

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Abstrat Neuroinflammation plays an important role in Parkinson’s disease(PD) and contribute to the onset and progression of degeneration of dopaminergic neurons.NBP is a widly used durg in the treatment of cerebrovascular disease,and recent studies shows that NBP can also inhibit ROS production,alleviate mitochondrial impairment in various PD models. Mitochondrial dysfunction,which may lead to mtDNA release,can activate the cGas/STING pathway and then induce an inflammatory cascade.Therefore,we put forward a hypothesis that NBP can protect PD by inhibiting the cGas/Sting pathway and inflammatory response of microglia.In the present study,we used rotenone induced BV2 cells and mice models.Our results shows the STING inhibitor,C-176,could reduce the rotenone induced inflammation in BV2 cells,indicating that the cGas/Sting pathway contributes to the inflammatory response in microglia.In addition,NBP can inhibit mitochondrial DNA leakage and activation of cGas/STING pathway,subsequently reduce the overactivation of microglia and the pruduction of proinflammatory factors in rotenone induced BV2 cells and PD mice.This study demonstrats that NBP can exert protective effect in PD through the downregulation of the cGas/STING signaling.This study will provide a novel insight into the potential role of NBP in PD therapy.

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