Li Lei, Li Yan, Miao Cheng, Liu Yi, Liu Rui
Department of Neurology, Xinxiang Central Hospital, Xinxiang, China.
Clinical Medical College of Tianjin Medical University, Tianjin, China.
Ann Transl Med. 2020 Sep;8(18):1168. doi: 10.21037/atm-20-5759.
This study aims to investigate the regulation of herbal polysaccharide, Coriolus versicolor polysaccharides (CVP), on neuronal apoptosis in a rat cerebral ischemia-reperfusion injury (CIRI) model. We also intend to explore the mechanisms and effectiveness of CVP in the treatment of neuronal apoptosis in CIRI rats, including neurological function, cerebral infarction volume, inflammatory factors, and the p38 mitogen-activated protein kinase (p38MAPK) signaling pathway as well as its downstream protein cleaved-Caspase-3.
A CIRI model was established in rats using the Longa method of middle cerebral artery occlusion. Neurological function scores and cerebral infarction volumes were measured in CIRI rats. Annexin V-fluorescein isothiocyanate (FITC) were used to measure neuronal apoptosis in CIRI rats. The levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in CIRI rats were determined using enzyme-linked immunosorbent assay (ELISA). A western blot assay was used to measure the protein expression levels of p38MAPK, phospho-p38MAPK (p-p38MAPK), Bcl-2, Bax and cleaved-Caspase-3 in brain tissue of CIRI rats.
CVP can effectively improve the neurological function of rats after 6, 12, 24, and 48 h of CIRI. It can also improve the behavioral test, reduce the cerebral infarction volume and inhibit the apoptosis of nerve cells in CIRI rats. The protein expression levels of p-p38MAPK and cleaved-Caspase-3 exhibited a decreasing trend following CVP administration.
CVP can significantly reduce the pathological characteristics of CIRI in rats and inhibit the apoptosis of nerve cells around the lesions. The mechanism of its effectiveness is related to inhibiting the activation of the p38MAPK signaling pathway.
本研究旨在探讨中药多糖云芝多糖（CVP）对大鼠脑缺血再灌注损伤（CIRI）模型中神经元凋亡的调控作用。我们还打算探究CVP治疗CIRI大鼠神经元凋亡的机制和效果，包括神经功能、脑梗死体积、炎症因子、p38丝裂原活化蛋白激酶（p38MAPK）信号通路及其下游蛋白裂解型半胱天冬酶-3（cleaved-Caspase-3）。
采用大脑中动脉闭塞的Longa法在大鼠中建立CIRI模型。测量CIRI大鼠的神经功能评分和脑梗死体积。用膜联蛋白V-异硫氰酸荧光素（FITC）检测CIRI大鼠的神经元凋亡情况。采用酶联免疫吸附测定（ELISA）法测定CIRI大鼠白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）的水平。用蛋白质免疫印迹法检测CIRI大鼠脑组织中p38MAPK、磷酸化p38MAPK（p-p38MAPK）、Bcl-2、Bax和裂解型半胱天冬酶-3的蛋白表达水平。
CVP能有效改善CIRI 6、12、24和48小时后大鼠的神经功能。它还能改善行为测试，减少脑梗死体积，并抑制CIRI大鼠神经细胞的凋亡。给予CVP后，p-p38MAPK和裂解型半胱天冬酶-3的蛋白表达水平呈下降趋势。
CVP可显著减轻大鼠CIRI的病理特征，并抑制损伤周围神经细胞的凋亡。其作用机制与抑制p38MAPK信号通路的激活有关。
