红景天苷对低压低氧诱发大鼠脑损伤的保护作用

Protective effect of salidroside against high altitude hypoxia-induced brain injury in rats

目的观察红景天苷对低压低氧暴露大鼠脑损伤的保护作用,初步探讨红景天苷预防低压低氧脑损伤的可能机制。方法利用低压低氧小动物模拟实验舱,模拟海拔6000 m急性暴露,制备低压低氧脑损伤大鼠模型。检测各组大鼠呼吸频率改变,利用末端脱氧核苷酸转移酶介导的脱氧尿苷缺口末端标记法(TUNEL)检测大鼠海马齿状回(DG)区细胞凋亡情况,利用Western blot法检测海马DG区Ras同源分子家族成员A(Rho A)的表达和磷酸化的细胞外信号调节激酶(p-ERK)、c-Jun氨基端激酶(p-JNK)的水平变化。结果模拟海拔6000 m急性暴露后,大鼠呼吸频率显著增加,低压低氧脑损伤引起大鼠海马DG区神经元发生凋亡,大鼠海马DG区组织中Rho A表达下降,ERK和JNK蛋白磷酸化水平下降;红景天苷干预可显著减少海马DG区神经元凋亡,并逆转Rho A蛋白表达和ERK和JNK蛋白的磷酸化水平。结论急性低压低氧暴露引起海马DG区神经细胞凋亡,红景天苷对低压低氧暴露诱发神经细胞凋亡起到保护作用。

Objective To observe the protective effect of salidroside against brain injury in rats exposed to hypobaric hypoxia, and investigate the molecular mechanism of salidroside in the prevention of hypobaric hypoxia-induced brain injury. Methods Rats were placed in experiment module simulating 6000 m altitude to establish acute hypobaric hypoxia-induced brain injury models. Their respiratory frequency was observed and recorded. Cell apoptosis in the hippocampal dentate gyrus （DG） was detected by TUNEL assay; the expressions of Ras homolog family member A （RhoA）, phosphorylated extracellular signal-regulated kinase （p-ERK） and phosphorylated c-Jun N-terminal kinase （p-JNK） were detected by Western blotting. Results After acute exposure to 6000 m altitude, the respiratory frequency of the rats increased remarkably. The simulation of hypobaric hypoxia induced cell apoptosis in hippocampal DG region, and salidroside intervention inhibited the process of cell apoptosis. The expressions of RhoA, p-ERK, p-JNK decreased after hypobaric hypoxia exposure. Salidroside intervention reversed RheA expression and raised the levels of p-ERK and p-JNK. Conclusion Acute exposure to hypobaric hypoxia can induce cell apoptosis in rat hippocampal DG, and salidroside can protect the cells from the exposure-induced apoptosis.