期刊
METABOLIC BRAIN DISEASE
卷 37, 期 8, 页码 2965-2978出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11011-022-01061-x
关键词
Cerebral ischemia; reperfusion; Salidroside; Nrf2; Trx1; Oxidative stress; Apoptosis
资金
- National Natural Science Foundation of China [82173961]
- Key Laboratory of polysaccharide bioactivity evaluation of TCM of Liaoning Province, Liaoning Distinguished Professor Project for Ying Jia
- Highlevel innovation and entrepreneurship team of Liaoning Province [XLYC2008029]
- Liaoning Provincial Department of Education Fund [LJKZ0911, LJKZ0950]
This study investigates the protective mechanism of Salidroside (SAL) on cerebral ischemia reperfusion injury (CIRI) through regulating the Nrf2/Trx1 axis. Results showed that SAL effectively alleviates infarction rate, improves histopathological changes, and reduces apoptosis and oxidative stress in CIRI rats and PC12 cells. It also inhibits ASK1/MAPK and activates Nrf2/Trx1 signaling pathway.
Cerebral ischemia reperfusion injury (CIRI) is still a serious problem threatening human health. Salidroside (SAL) is a natural phenylpropanoid glycoside compound with antioxidant, anti-inflammatory, and anti-ischemic properties. This study investigated the protective mechanism of SAL on middle cerebral artery occlusion (MCAO)- and oxygen-glucose deprivation/reoxygenation (OGD/R) model-induced CIRI via regulating the nuclear factor erythroid 2-related factor 2 (Nrf2)/thioredoxin 1 (Trx1) axis. The results indicated that SAL (50 mg/kg or 100 mg/kg, intraperitoneal injection) not only effectively alleviated infarction rate, improved histopathological changes, relieved apoptosis by strengthening the suppression of cleaved caspase-3 and Bax/Bcl-2 proteins and decreased malondialdehyde (MDA) formation, but also increased superoxide dismutase (SOD) and catalase (CAT) activities and upregulated the expressions of Nrf2 and Trx1 on MCAO-induced CIRI rats. SAL also efficiently inhibited apoptosis and decreased oxidative stress in OGD/R-stimulated PC12 cells. Furthermore, blocking the Nrf2/Trx1 pathway using tretinoin, an Nrf2 inhibitor, significantly reversed the protective effect of SAL on OGD/R-induced oxidative stress. Moreover, SAL reduced the expression of apoptosis signal-regulating kinase-1 (ASK1) and mitogen-activated protein kinase (MAPK) family proteins. These results demonstrated that SAL inhibited oxidative stress through Nrf2/Trx1 signaling pathway, and subsequently reduced CIRI-induced apoptosis by inhibiting ASK1/MAPK.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据