Wang Yan-Lei, Jing You-Ling, Cai Qing-Yan, Cui Guo-Jin, Zhang Yi-Bing, Zhang Feng-Yu
Department of Physiology, Hebei United University, Tangshan 063000, China.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2012 Mar;43(2):170-3.
To investigate the relationship between apoptosis-related genes and lung injury induced by intestinal ischemia reperfusion and to explore the effects and its possible mechanism of sodium aescinate.
Rat model of intestinal I/R injury was established with clamping of the superior mesenteric artery for 60 min and then clamping was relieved for 60 min. Twenty-four SD rats were randomly divided into three groups with eight rats in each: sham group, intestinal ischemia/reperfusion group (I/R group) and sodium aescinate group (SA + I/R group). Lung wet/dry weight ratio, lung coefficient and Superoxide dismutase (SOD), malondialdehyde (MDA) in plasma and lung tissue were measured, as well as the expression levels of Bcl-2 and Bax proteins in lung tissue were examined using immunohistochemical method.
Compared with sham group, lung wet/dry weight ratio, lung coefficient and MDA in plasma and lung tissue were significantly increased, and while the activity of SOD in plasma and lung tissue were decreased significantly in I/R group. At the same time, the protein expression level of Bcl-2 and Bax were significantly increased. But Bax protein expression was much greater than that of Bcl-2, the ratio of Bcl-2 to Bax was decreased significantly in I/R group than that in sham group. Compared with I/R group, lung wet/dry weight ratio, lung coefficient and MDA in plasma and lung tissue were significantly decreased, and while the activity of SOD in serum and lung tissue were significantly increased in SA + I/R group. At the same time, Bax protein expression was significantly decreased, both Bcl-2 protein expression and the ratio of Bcl-2 to Bax were significantly increased in SA + I/R group than that in I/R group.
Lung injury induced by intestinal ischemia reperfusion is correlated with abnormal expression levels of Bcl-2 and Bax protein which is caused by oxidative injury. Sodium aescinate can protect the lung injury induced by intestinal ischemia/reperfusion (I/R), which may be mediated by inhibiting lipid peroxidation, upregulating Bcl-2 gene protein expression, improving the ratio of Bcl-2/ Bax to inhibit lung apoptosis.
探讨凋亡相关基因与肠缺血再灌注诱导的肺损伤之间的关系,并探究七叶皂苷钠的作用及其可能机制。
通过夹闭肠系膜上动脉60分钟,然后松开夹闭60分钟,建立大鼠肠缺血/再灌注损伤模型。24只SD大鼠随机分为三组,每组8只:假手术组、肠缺血/再灌注组(I/R组)和七叶皂苷钠组(SA + I/R组)。测量肺湿/干重比、肺系数以及血浆和肺组织中的超氧化物歧化酶(SOD)、丙二醛(MDA),并采用免疫组织化学方法检测肺组织中Bcl-2和Bax蛋白的表达水平。
与假手术组相比,I/R组肺湿/干重比、肺系数以及血浆和肺组织中的MDA显著升高,而血浆和肺组织中的SOD活性显著降低。同时,Bcl-2和Bax蛋白表达水平显著升高。但Bax蛋白表达远大于Bcl-2,I/R组中Bcl-2与Bax的比值显著低于假手术组。与I/R组相比,SA + I/R组肺湿/干重比、肺系数以及血浆和肺组织中的MDA显著降低,而血清和肺组织中的SOD活性显著升高。同时,Bax蛋白表达显著降低,SA + I/R组中Bcl-2蛋白表达以及Bcl-2与Bax的比值均显著高于I/R组。
肠缺血再灌注诱导的肺损伤与氧化损伤导致的Bcl-2和Bax蛋白表达异常有关。七叶皂苷钠可保护肠缺血/再灌注(I/R)诱导的肺损伤,其机制可能是通过抑制脂质过氧化、上调Bcl-2基因蛋白表达、提高Bcl-2/Bax比值来抑制肺细胞凋亡。