雷公藤甲素调节TLR3蛋白减轻大鼠急性肺损伤

Triptolide Alleviates LPS-induced Acute Lung Injury in Rats by Regulating TLR3 Protein

目的研究观察雷公藤甲素对脂多糖诱导的急性肺损伤大鼠的影响。方法将30只雄性SD大鼠随机分为3组:对照组、模型组和加药组。HE染色分析肺病理损伤;Masson染色检测肺组织原纤维沉积;检测动脉血氧分压(PaO2);ELISA检测血清炎性因子的水平;检测Toll样受体3(Toll-like receptors3,TLR3)的mRNA和蛋白表达。结果与对照组比较,模型组出现明显的病理损伤、胶原沉积、PaO2降低、血清炎性因子升高和TLR3表达增加。与模型组比较,加药组病理损伤和胶原沉积减少、PaO2提高、炎性因子和TLR3表达降低。结论TPL降低炎性因子水平,抑制TLR3的表达,减轻LPS诱导的大鼠All症状。

Objective To explore the effect of Triptolide (TPL) on rats with lipopolysaccharide (LPS)-induced acute lung injury ( ALI) and its potential mechanism. Methods Thirty male SD rats were randomly divided into three groups: control group, model group and treatment group. Lung pathological injury was analyzed by HE staining. Masson staining was used to detect fibril deposition. Arterial partial blood oxygen pressure (PaO2) was detected. Serum levels of inflammatory cytokines were detected by ELISA. Toll-like receptor 3 ( TLR3 ) mRNA and protein expression levels were detected. Results Compared with the control group, the model group showed obvious pathological damage, collagen deposition, decreased PaO2, increased inflammatory cytokines and TLR3 expression. Compared with the model group, treatment group showed reduced pathological damage, collagen deposition, increased PaO2 decreased inflammatory cytokines and TLR3 expression. Conclusion TPL reduces the levels of inflammatory cytokines, inhibits the expression of TLR3 , and alleviates the symptoms of LPS-induced ALI in rats.