On neuronal apoptosis after cerebral ischemia and Chinese medicine treatment pathway.docVIP

 PAGE \* MERGEFORMAT 20 On neuronal apoptosis after cerebral ischemia and Chinese medicine treatment pathway [Keywords:] cerebral ischemia, apoptosis, apoptosis pathway, medicine, review Cerebral ischemia caused by a biochemical cascade of neuronal apoptosis, resulting in the corresponding region of the brain dysfunction and trigger a series of ischemic symptoms. Therefore, looking for inhibition of neuronal apoptosis after cerebral ischemia of effective drugs, to improve the prognosis of ischemic stroke is particularly important. 1 pathway of apoptosis 1.1 The death receptor pathway Cell surface death receptors of tumor necrosis factor receptor (TNFR) superfamily. Mainly include: Fas (CD95), TNFR-1 [1], DR3 (death receptor 3) [2], DR4 (death receptor 4) [3], DR5 (death receptor 5) [4]. the present study is the most clearly Fas-Fas-L signaling pathway. Fas-L homologous trimer complex form [5]. Each trimeric Fas-L can be combined with three Fas molecules, leading to three Fas molecules intracellular DD (Death domain) in series with each other. Fas in the DD series with FADD (Fas-associated death domain) of the DD combination. And this combination has led to FADD’s DED (Death effect domain) and Caspase-8 DED zymogen similar regional integration, the region is CARD ( Caspase recruitment domain) a, to activate Caspase-8, Caspase-8 and further activation of downstream Caspase, eventually leading to apoptosis. Caspase-protease (cysteine #8203;#8203;containing aspartate specific protease) family, is now considered a central part of the implementation of apoptosis [6]. Apoptotic signal through activation of upstream activation of Caspase-then the downstream Caspase-, in the implementation phase of apoptosis by the downstream Caspase-(such as Caspase-3) for a specific substrate (the key enzyme for some more) for cutting, such as the activation of lamin, actin, etc. protease and endonuclease enzymes, inhibit DNA repair enzymes, thereby undermining t