文献类型：期刊文献

英文题名：Zhongfeng Capsules protects against cerebral ischemia-reperfusion injury via mediating the phosphoinositide 3-kinase/Akt and toll-like receptor 4/nuclear factor kappa B signaling pathways by regulating neuronal apoptosis and inflammation

作者：Yan, Chunlu[1];An, Fangyu[2];Wang, Jiayu[1];Shi, Yao[3];Yuan, Lingqing[3];Lv, Donghui[1];Zhao, Yanzhen[1];Liu, Yongqi[3];Wang, Yongfeng[3]

第一作者：颜春鲁

通信作者：Yan, CL[1];Wang, YF[2]

机构：[1]Gansu Univ Chinese Med, Sch Tradit Chinese & Western Med, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Univ Chinese Med, Teaching Expt Training Ctr, Lanzhou 730000, Gansu, Peoples R China;[3]Gansu Univ Chinese Med, Sch Basic Med, Lanzhou 730000, Gansu, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Sch Tradit Chinese & Western Med, Lanzhou 730000, Gansu, Peoples R China;[2]corresponding author), Gansu Univ Chinese Med, Sch Basic Med, Lanzhou 730000, Gansu, Peoples R China.|[10735]甘肃中医药大学;

年份：2022

卷号：27

期号：7-8

起止页码：561

外文期刊名：APOPTOSIS

收录：;Scopus(收录号：2-s2.0-85131574054);WOS:【SCI-EXPANDED(收录号:WOS:000807916500001)】；

基金：This work was supported by the Natural Fund of Gansu Province (1610RJZA061), the Improvement Project of College Students' Employment and Entrepreneurship Ability of Gansu Province (6-1), and the Open Project of Gansu Research Center of Traditional Chinese Medicine (zyzx-2020-07).

语种：英文

外文关键词：Zhongfeng Capsules; Cerebral ischemia-reperfusion injury; Apoptosis; Inflammatory reactions; Neuroprotective effect

摘要：Inflammatory reaction and neuronal apoptosis are the major pathophysiological mechanisms involved in cerebral ischemia-reperfusion injury (CI/RI). It has been reported that Zhongfeng Capsules (ZFCs), which contain Panax notoginseng, Hirudo, Red ginseng, Eupolyphaga sinensis, Pangolin scales, Rhubarb, and Radix Salvia miltiorrhizae, have a definite therapeutic effect on CI/RI. However, the specific molecular mechanisms of ZFCs are unclear. In this study, the effects of ZFCs on middle cerebral artery occlusion were investigated in rats. Our results showed that neurological impairment and neuronal apoptosis were alleviated in ZFC-treated rats. Additionally, infarct volume and cerebral edema decreased and there was an improvement in histopathological features. Furthermore, the expression levels of IL-1 beta, IL-6, and TNF-alpha were downregulated in ZFC-treated rats. TLR 4, NF-kappa B, Bax, and Caspase-3 expression also tended to decrease, whereas the expression of Bcl-2, p-PI3K, p-Akt, and I-kappa B alpha increased. The results indicate that the ZFCs effectively protected the rats against CI/RI possibly via the TLR4/NF-kappa B signaling pathway. Additionally, the formulation regulated the transcriptional activity of NF-kappa B, secretion of downstream inflammatory factors, and the expression of Bcl-2-Bax proteins in the PI3K/Akt pathway. Our findings suggest that ZFCs suppress neuronal apoptosis and inflammatory reaction via the PI3K/Akt and TLR4/NF-kappa B signaling pathways, respectively. Moreover, activation of the PI3K/Akt pathway may result in the inhibition of proinflammatory cytokine secretion, which may be another mechanism by which ZFCs alleviate CI/RI.