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目的:探讨凉膈散对内毒素(LPS)诱导急性肺损伤(ALI)大鼠信号转导与转录激活子3(STAT3)和磷酸化STAT3蛋白表达的影响。方法:SPF级健康雌性Wistar大鼠156只,随机分为对照组、LPS组、LPS+3个不同剂量凉膈散组、LPS+地塞米松组。LPS造模动物,又分为注射LPS后1、2、4、8、16h不同时相处死组,每组6只。各组大鼠在给生理盐水或LPS后相应的时间处死、取材,用WesternBlot法观察大鼠肺组织STAT3、P-STAT3含量的动态变化。结果:与对照组比较,LPS组大鼠尾ivLPS后,肺组织内STAT3、P-STAT3蛋白表达明显增强,其表达分别在1h、2h后达到峰值,随后逐渐下降。与LPS组相比较,凉膈散各剂量组与地塞米松干预组能显著抑制肺组织内STAT3、P-STAT3的表达。结论:内毒素致急性肺损伤时出现肺组织STAT3、P-STAT3异常表达,凉膈散可以抑制其异常表达,而发挥对内毒素ALI的保护作用。
Objective: To investigate the effect of Liangqi Powder on the expression of STAT3 and STAT3 in acute lung injury (ALI) rats induced by lipopolysaccharide (LPS). METHODS: A total of 156 healthy female Wistar rats with SPF were randomly divided into control group, LPS group, LPS+3 different doses of Liangqisan group and LPS+dexamethasone group. The LPS model animals were divided into different groups at the time of 1,2,4,8,16 h after injection of LPS, and 6 rats in each group. Rats in each group were sacrificed at the corresponding time after administration of physiological saline or LPS. The dynamic changes of STAT3 and P-STAT3 contents in lung tissue of rats were observed by Western Blot. RESULTS: Compared with the control group, the STAT3 and P-STAT3 protein expression in the lung tissue of the LPS group was significantly increased after tail iv LPS. The expression of STAT3 and P-STAT3 protein peaked at 1 h and 2 h after LPS and then gradually decreased. Compared with LPS group, Liangqi powder and dexamethasone intervention group could significantly inhibit the expression of STAT3 and P-STAT3 in lung tissue. Conclusions: The abnormal expression of STAT3 and P-STAT3 in lung tissue occurs during acute lung injury induced by endotoxin. Liangyu powder can inhibit its abnormal expression and play a protective role against endotoxin ALI.