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目的:探讨川芎嗪对大鼠急性肺部撞击伤所致异常凋亡抑制作用及其机制。方法:健康雄性SD大鼠72只,随机分为正常对照组(C组,n=24)、肺部撞击伤模型组(T组,n=24)、川芎嗪治疗组(L组,n=24)。C组无特殊处理,L组在撞击后立即腹腔注射川芎嗪80mg/kg 1次。细胞凋亡原位检测(TUNEL)法测定肺组织内细胞凋亡;检测肺水肿程度和肺血管通透性以检测肺功能改变,免疫组织化学检测肺组织Bcl-2、Bax和Caspase-3的表达;光镜和电镜下观察肺组织病理改变。结果:T组肺组织内细胞凋亡指数及肺组织损伤程度明显增高(均P<0.05);肺血管通透性增强(P<0.05),肺水肿程度增加(P<0.05);Caspase-3、Bax、Bcl-2表达较C组升高(P<0.05),Bcl-2/Bax比值降低。L组相对于T组肺组织内细胞凋亡指数及肺组织损伤程度降低(P<0.05),肺血管通透性破坏降低(P<0.05),肺水肿程度减轻(P<0.05);Caspase-3、Bax表达下降(P<0.05),而Bcl-2表达增强,Bcl-2/Bax比值增加(P<0.01)。结论:川芎嗪可通过抑制肺组织细胞凋亡减轻肺损伤,其机制可能是提高Bcl-2/Bax的比值,降低Caspase-3的表达水平来实现的。
Objective: To investigate the inhibitory effect of ligustrazine on abnormal apoptosis induced by acute lung injury in rats and its mechanism. Methods: Seventy two healthy male Sprague Dawley rats were randomly divided into four groups: normal control group (n = 24), model group with pulmonary injury (n = 24), ligustrazine treatment group (n = twenty four). C group without special treatment, L group immediately after the impact of tetramethylpyrazine 80mg / kg 1. The degree of pulmonary edema and pulmonary vascular permeability were detected by TUNEL method to detect lung function changes. The expressions of Bcl-2, Bax and Caspase-3 in lung tissue were detected by immunohistochemistry The pathological changes of lung tissue were observed under light microscope and electron microscope. Results: The apoptotic index and the degree of pulmonary injury were significantly increased in group T (all P <0.05), pulmonary vascular permeability (P <0.05) and pulmonary edema (P <0.05). Caspase-3 , Bax and Bcl-2 expressions were significantly higher than those in C group (P <0.05), and the ratio of Bcl-2 / Bax was decreased. Compared with the T group, the apoptotic index of lung tissue and the degree of lung injury decreased (P <0.05), the destruction of pulmonary vascular permeability decreased (P <0.05) and the degree of pulmonary edema alleviated (P <0.05) 3, Bax decreased (P <0.05), while the expression of Bcl-2 increased and the ratio of Bcl-2 / Bax increased (P <0.01). CONCLUSION: Tetramethylpyrazine can relieve lung injury by inhibiting apoptosis of lung tissue. Its mechanism may be to increase the ratio of Bcl-2 / Bax and decrease the expression of Caspase-3.