Effect of Polydatin on Neurological Function and the Nrf2 Pathway during Intracerebral Hemorrhage.

Abstract

This study investigates the effect of polydatin on the neurological function of cerebral hemorrhage rats and on the Nrf2 pathway of the endogenous antioxidant system in tissues around cerebral hematoma. Further, the study also aims to provide solid insights for clinical diagnosis and treatment. A total of 54 SPF grade male Wistar rats were divided into three groups: the sham group, model group, and polydatin group. Various parameters such as neurological deficit score, brain water content, pathological morphology, oxidative stress index content, Nrf2, NQO1, HO-1 mRNA expression, and the expression of HO-1, Nrf2, and kelch-like epichlorohydrin-1 (Keap1) protein were observed. Compared with the sham group, the mNSS score and brain water content of rats in the model group increased significantly after dosing (P < 0.05). When compared with the model group, the mNSS score and brain water content of rats in the polydatin group decreased significantly after dosing (P < 0.05). Compared with the other group, the serum NSE content of rats in the polydatin group decreased (P < 0.05). An increase was observed in the contents of NO, SOD, MDA, GSSG, and GSH in the brain tissue of rats in the model group when compared with the sham group. Compared with the model group, the contents of NO and MDA in the brain tissue of rats in the polydatin group decreased, while the contents of SOD, GSSG, and GSH increased (P < 0.05). The relative expressions of Nrf2, NQO1, and HO-1mRNA in the brain tissue of rats in the polydatin group was relatively high compared with both groups (P < 0.05). Polydatin can improve the neurological function of ICH rats and reduce the oxidative stress response by regulating the Nrf2-ARE pathway and downstream gene expression. This study preliminarily discussed the relevant mechanism of polydatin in the treatment of ICH rats, thus providing a theoretical reference to ICH treatment.