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Pinoresinol diglucoside alleviates ischemia/reperfusion‐induced brain injury by modulating neuroinflammation and oxidative stress
Author(s) -
Zhang Yi,
Lei Yuanbiao,
Yao Xiaoxi,
Yi Jiping,
Feng Ganghua
Publication year - 2021
Publication title -
chemical biology and drug design
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.59
H-Index - 77
eISSN - 1747-0285
pISSN - 1747-0277
DOI - 10.1111/cbdd.13956
Subject(s) - oxidative stress , pharmacology , neuroinflammation , nissl body , ischemia , brain ischemia , reperfusion injury , medicine , inflammation , chemistry , anesthesia , pathology , staining
Abstract Brain ischemia/reperfusion (I/R) injury is a common pathological process after ischemic stroke. Pinoresinol diglucoside (PDG) has antioxidation and anti‐inflammation activities. However, whether PDG ameliorates brain I/R injury is still unclear. In this study, middle cerebral artery occlusion (MCAO) model was established with male C57BL/6 mice, and the mice were treated with 5 and 10 mg/kg PDG via intravenous injection, respectively. The neurological deficit, infarct volume, and brain water content were then evaluated. HE staining and Nissl staining were used to analyze neuron injury. Besides, enzyme‐linked immunosorbent assay and colorimetry assay were used to examine the level of inflammatory markers and oxidative stress markers, and Western blot was used to detect the expressions of p‐p65, Nrf2, and HO‐1. It was revealed that PDG could significantly alleviate the MCAO‐induced neurological dysfunction of the mice and reduce the infarct volume, brain water content, and neuron injury. PDG treatment decreased the levels of TNF‐α, IL‐1β, IL‐6, NO, ROS, and MDA, and significantly increased the activities of SOD, GSH, and GSH‐Px in the brain tissue of the mice. Additionally, PDG could repress the activation of p65 and promote Nrf2 and HO‐1 expressions. In conclusion, PDG exerts anti‐inflammatory and antioxidation effects via regulating the NF‐κB pathway and Nrf2/HO‐1 pathway, thereby reducing the I/R‐induced brain injury of mice.