H2S对急性脑梗死大鼠神经功能的保护作用及机制

目的 探讨H2S对急性脑梗死大鼠神经功能的保护作用以及相关机制.方法 将48只健康雄性SD大鼠随机分为假手术组、模型组、生理盐水组和H2S干预组.采用改良Longa法制备大鼠急性脑梗死模型,建模前25min,H2S干预组给予腹腔注射NaHS 28μmol/kg,生理盐水组给予等量生理盐水,分别于苏醒后和术后72h,评估各组大鼠的神经功能缺损.采用TTC染色法检测各组大鼠脑梗死面积,TUNEL法检测各组大鼠脑组织中细胞凋亡情况,Western blot法检测各组大鼠脑组织中PI3K、p-PI3K、Akt、p-Akt、Bcl-2、Bax蛋白的表达.结果 与模型组和生理盐水组相比,H2S干预组大鼠神经功能缺损程度评分、脑梗死面积和细胞凋亡指数均降低,差异均有统计学意义(P<0.05).与模型组和生理盐水组相比,H2S干预组大鼠脑组织中PI3K、Akt、Bcl-2蛋白相对表达量均升高,而p-PI3K、p-Akt、Bax蛋白相对表达量均降低,差异均有统计学意义(P<0.05).结论 H2S可能通过抑制PI3K/Akt信号通路而改变Bcl-2/Bax比例,减小急性脑梗死大鼠脑梗死面积及细胞凋亡指数,保护神经功能.

Protective effect and mechanism of H2S on neurological function in rats with acute cerebral infarction

Objective To investigate the protective effect of H2S on neurological function in rats with acute cerebral infarction and the possible mechanism. Methods Totals of 48 healthy male SD rats were ran-domly divided into sham operation group, model group, saline group and H2S intervention group. The model of rat acute cerebral infarction was established by modified Longa method. 25 min before modeling, rats in the H2S intervention group were given intraperitoneal injection of NaHS 28 μmol/kg, while in the saline group were giv-en the same amount of saline. After awakening and 72 h after operation, the neurological defects in rats of each group were evaluated. TTC staining was used to detect the cerebral infarct size in each group. TUNEL method was used to detect the cell apoptosis in brain tissue in each group. Western blot was used to detect the expressions of PI3K, p-PI3K, Akt, p-Akt, Bcl-2 and Bax proteins in the brain tissue. Results Compared with the model group and the saline group, the neurological defect score, the area of cerebral infarction and the apoptotic index in brain tissue in H2S intervention group were decreased, the differences were statistically significant (P<0.05). Com-pared with the model group and the saline group, the relative expression levels of PI3K, Akt and Bcl-2 proteins in brain tissue in H2S intervention group were increased, while the relative expression levels of p-PI3K, p-Akt and Bax proteins were decreased, the differences were statistically significant (P<0.05). Conclusions H2S might change the ratio of Bcl-2/Bax by inhibiting PI3K/Akt signaling pathway to reduce cerebral infarct size and apoptosis in-dex and protect neurological function in rats with acute cerebral infarction.