摘要
目的 探索大黄素对脂多糖(lipopolysaccharide,LPS)诱导的新生大鼠急性肺损伤的保护作用.方法 新生大鼠腹腔注射LPS制作建立急性肺损伤模型,每天腹腔注射不同剂量大黄素(emodin,EMD),连续治疗7 d,对照组腹腔注射等体积生理盐水.通过HE、Masson染色进行组织病理学检测,免疫组织化学检测肺组织平滑肌肌动蛋白(α-SMA)表达水平,原位末端标记法(TUNEL)检测肺组织细胞凋亡水平,Western Blot检测肺组织I型胶原蛋白(Collagen I)、III型胶原蛋白(Collagen III)、裂解的天冬氨酸特异性半胱氨酸蛋白酶3(cleaved Caspase 3)、白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)蛋白表达水平.结果 脂多糖使大鼠肺损伤评分、肺纤维化程度、α-SMA平均光密度、TUNEL阳性率、Collagen I、Collagen III、cleaved Caspase3、IL-1β、TNF-α蛋白表达水平较对照组显著增加,大黄素处理能剂量依赖性抑制脂多糖引起的上述变化.结论 大黄素对LPS诱导的新生大鼠急性肺损伤具有保护作用.
Abstract
Objective To explore the protective effect of emodin on acute lung injury induced by lipopolysaccharide(LPS)in neonatal rats.Methods Neonatal rats were intraperitoneally injected with LPS to establish an acute lung injury model.Different doses of emodin(EMD)were administered intraperitoneally every day for 7 days,while the control group was injected with an equal volume of saline.Tissue pathology was examined through HE and Masson staining,the expression level of α-smooth muscle actin(α-SMA)in lung tissues was detected by immunohistochemistry,the level of cell apoptosis in lung tissues was detected by terminal deoxynucleoti-dyl transferase dUTP nick end labeling(TUNEL),and the expression levels of type I collagen(Collagen I),type III collagen(Collagen III),cleaved caspase-3,interleukin-1β(IL-1β),and tumor necrosis factor-α(TNF-α)in lung tissues were detected by Western blot.Results LPS significantly increased lung injury scores,the degree of pulmonary fibrosis,the average immunoreactivity of α-SMA,the TUNEL positive rate,and the expression levels of Collagen I,Collagen III,cleaved Caspase-3,IL-1β,and TNF-α in rats compared to the control group,which could be inhibited by emodin treatment in a dose-dependent manner.Conclusion Emodin has a protective effect on acute lung injury induced by LPS in neonatal rats.
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