Department of Encephalopathy, Jinan Municipal No.2 Hospital of Traditional Chinese Medicine, Jinan 250200, China.
Cell Mol Biol (Noisy-le-grand). 2020 May 15;66(2):87-92.
Cerebral infarction is an acute cerebrovascular disease caused by abnormal blood circulation in the brain. In the present study, we investigate the effect of astragaloside IV on cognitive dysfunction in cerebrally infarcted rats via transforming growth factor-β (TGF-β) / Smad signaling pathway. For this purpose, 45 rats were divided into three groups including astragaloside, model, and control. 30 of 45 healthy adult male SD rats were randomly selected to establish an acute cerebral infarction model. 15 modeled rats were enrolled as a model and astragaloside group, and another 15 rats as a blank control group. The rats in the astragaloside group were fed with astragaloside IV according to 1.08 g/kg body weight, and those in the blank group and model group were given matching normal saline. The levels of TGF-β, Smad1, Smad3 and Smad7 of TGF-β/Smad signaling transduction pathway at T0 (week 0), T1 (week 3) and T2 (week 6) were determined by enzyme-linked immunosorbent assay (ELISA). The modified neurological severity score (mNSS) was used to evaluate the improvement of cognitive dysfunction in rats. The mNSS of rats with cerebral infarction in the astragaloside group was lower than that in the control group and model group (P< 0.05). While the levels of TGF-β, Smad1, Smad3 and Smad7 in the astragaloside group were higher than those in the control group and model group (P< 0.05). Astragaloside IV plays an important role in improving cognitive dysfunction in rats with cerebral infarction while affecting the levels of TGF-β, Smad1, Smad3 and Smad7 and activating TGF-β / Smad signaling pathway.
脑梗死是一种由于大脑血液循环异常引起的急性脑血管病。本研究通过转化生长因子-β（TGF-β）/ Smad 信号通路探讨黄芪甲苷对脑梗死大鼠认知功能障碍的影响。为此，将 45 只大鼠分为黄芪甲苷组、模型组和对照组，其中 45 只健康成年雄性 SD 大鼠中 30 只为造模组，随机抽取 15 只为模型组，另外 15 只为空白对照组。黄芪甲苷组大鼠按 1.08 g/kg 体质量灌胃黄芪甲苷，空白组和模型组大鼠给予等容量生理盐水。采用酶联免疫吸附法（ELISA）检测 TGF-β/Smad 信号转导通路中 TGF-β、Smad1、Smad3 和 Smad7 在 T0（0 周）、T1（3 周）和 T2（6 周）时的水平，采用改良神经功能缺损评分（mNSS）评估大鼠认知功能障碍的改善情况。黄芪甲苷组脑梗死大鼠的 mNSS 评分低于空白组和模型组（P<0.05），而黄芪甲苷组的 TGF-β、Smad1、Smad3 和 Smad7 水平均高于空白组和模型组（P<0.05）。黄芪甲苷 IV 通过影响 TGF-β、Smad1、Smad3 和 Smad7 水平并激活 TGF-β/Smad 信号通路，在改善脑梗死大鼠认知功能障碍方面发挥重要作用。
