Based on Virtual Screening and Simulation Exploring the Mechanism of Plant-Derived Compounds with PINK1 to Postherpetic Neuralgia

Abstract

Recent studies have found that PINK1 mutation can mediate the dysfunction of mitochondrial autophagy in dopaminergic neurons; In order to reveal the role of PINK1 in the pathogenesis of PHN and nd new targets for PHN treatment. Purpose: Herein, we have employed a rigorous literature review pipeline to enlist 2801compounds from more than 200 plants from the Asian region. The virtual screening procedure helps us to shortlist the total compounds into 20 based on their better binding energy. Moreover, the Prime MM-GBSA procedure screened the compound data-set further, where Vitexin, Luteoloside, and 2'-Deoxyadenosine-5'-monophosphate had a score of (−59.439, −52.421 and − 47.544) kcal/mol, respectively. Finally, the immunohistochemistry and transmission electron microscopy (TEM) were conducted to verify the effective mechanism. The results of Immunohistochemical analysis showed that the rst two compounds had notable therapeutic effects on PHN mice, while compound 3 had no signi cant therapeutic effect. Meanwhile, the TEM result indicated that Vitexin showed the most signi cant microstructural adjustment on mitochondria. We concluded that Vitexin could alleviate PHN by regulating mitochondrial autophagy through PINK1. In this study, we observed the level of autophagy of mitochondria and the expression of PINK1 in dorsal horn neurons of PHN.