The protective effect of cordyceps sinensis extract on cerebral ischemic injury via modulating the mitochondrial respiratory chain and inhibiting the mitochondrial apoptotic pathway
| Autor: | Tian-Yang Tan, Ru Ma, Yue Li, Ya-Fei Chen, Shuyan Wang, Yun-Xin Li, Zhenquan Liu, Qiang Li, Xue Bai |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Male Cerebral is chemic injury Mitochondrial respiratory chain Ischemia Apoptosis RM1-950 Pharmacology Neuroprotection Brain Ischemia Electron Transport Rats Sprague-Dawley 03 medical and health sciences Mice 0302 clinical medicine In vivo medicine Cytochrome c oxidase Animals Membrane Potential Mitochondrial biology Chemistry Plant Extracts Cytochrome c Infarction Middle Cerebral Artery Mitochondrial apoptotic pathway General Medicine medicine.disease Mitochondria Stroke Disease Models Animal 030104 developmental biology Neuroprotective Agents Cerebral blood flow 030220 oncology & carcinogenesis Cordyceps biology.protein Therapeutics. Pharmacology Cordyceps sinensis |
| Zdroj: | Biomedicine & Pharmacotherapy, Vol 124, Iss, Pp 109834-(2020) |
| ISSN: | 0753-3322 |
| Popis: | Cerebral ischemia is a common refractory brain disease, resulting from a reduction in the blood flow to the brain. Mitochondrial dysfunction leads to ischemic stroke and brain injury. Cordyceps sinensis (CS) is an important traditional Chinese medicine, which has been linked to neuroprotection in recent studies. In this study, we investigated the role of the mitochondrial respiratory chain and the mitochondrial apoptotic pathway on the protective effect of Cordyceps sinensis extract (CSE) against cerebral ischemia injury both in vivo and in vitro. In a murine middle cerebral artery occlusion (MCAO) model, administration of CSE relieved neuronal morphological damage and attenuated the neuronal apoptosis. CSE also reduced neurobehavioral scores and oxygen free radical (OFR), while improving the levels of ATP, cytochrome c oxidase (COX), and mitochondrial complexes I-IV. Furthermore, the mRNA expression of Bax, cytochrome c (Cyt c) and caspase-3 were down-regulated. In brain microvascular endothelial cells (BMECs) exposed to oxygen and glucose deprivation (OGD), CSE prevented OGD-induced cellular apoptosis, and recovered the reduction of mitochondrial membrane potential (MMP). Moreover, CSE treatment induced an increase of Bcl-2 protein expression and a decrease of Bax, Cyt c and caspase-3 protein expression. Meanwhile, the caspase-3, -8, and -9 activities were also inhibited. The results indicate that CSE can relieve cerebral ischemia injury and exhibit protective effects via modulating the mitochondrial respiratory chain and inhibiting the mitochondrial apoptotic pathway. |
| Databáze: | OpenAIRE |
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