从外泌体MALAT1调节Cav-1/PI3K/AKT/mTOR轴探讨补阳还五汤促脑缺血后神经再生的机制

内源性神经再生是中风康复的潜在治疗方法，但调控机制尚未明确。外泌体作为细胞间通讯的载体，将内含lncRNA等物质传递并作用于靶细胞，调控神经再生。MALAT1作为热点lncRNA，近年来发现其参与了脑发育和脑损伤保护，并可影响PI3K/Akt/mTOR通路，是中风后一个关键调节因子。Cav1既是外泌体摄入的受体，又可与RNA结合蛋白转运RNA，还是PI3K/Akt/mTOR通路的上游分子，MALAT1是否通过Cav1-PI3K/Akt/mTOR影响脑缺血后神经再生？补阳还五汤能调节Cav1- PI3K/Akt/mTOR信号轴，促进神经再生，还影响血外泌体MALAT1表达，那么，补阳还五汤是否通过影响外泌体MALAT1而调控Cav1-PI3K/Akt/mTOR轴而发挥治疗作用？项目拟从Cav1-PI3K/AKT/mTOR轴探讨MALAT1对神经再生的作用及补阳还五汤促神经再生的机理。

Endogenous neurogenesis is is a potential treatment for stroke rehabilitation, but the regulatory mechanism is not clear. As a carrier of intercellular communication, exosomes transfer lncRNA and others to target cells and regulate neurogenesis. More and more attention has been paid to the role of lncRNA. In recent years, Malat1, as a research hotspot, has been found to be involved in brain development and brain protection in recent years, and can affect PI3K / Akt / mTOR pathway, so Malat1 is regarded as a key regulator after stroke.Cav1 is not only a receptor that mediates exosomes intake, but transports RNA with RNA binding protein, and regulates PI3K / Akt / mTOR pathway as a upstream molecule. So, does malat1 affect neurogenesis after cerebral ischemia through cav1- PI3K / Akt / mTOR axis? Buyang Huanwu Decoction(BYHWD) can regulate PI3K / Akt / mTOR signal via Cav1, promote neurogenesis, and affect the expression of malat1 in exosome of patients. Does BYHWD play a therapeutic role by influencing the level of malat1 and the axis of cav1- PI3K / Akt / mTOR? This project aims to explore the effect of malat1 on neurogenesis and the mechanism of BYHWD in promoting neurogenesis, then reveal the new mechanism of neurogenesis regulation, and provide a new basis for the treatment of stroke with traditional Chinese medicine.