论文部分内容阅读
目的研究脂多糖(lipopolysaccharide,LPS)所致急性肺损伤(acute lung injury,ALI)的病理过程,探讨吡咯烷二硫代氨基甲酸盐(pyrroli dinedithiocarbamates,PDTC)对LPS所致ALI的保护作用及机制。方法96只SD雄性大鼠分为对照组、模型组,PDTC预防组。静脉注射LPS(6mg/kg)复制ALI动物模型,分别于注射后2、4、8、12h活杀。PDTC预防组在注射LPS前30min予以PDTC(120mg/kg)腹腔注射。测定肺湿/干质量比(W/D),石蜡包埋切片经HE染色行肺组织病理评分,TUNEL法测肺泡巨噬细胞(alveolar macrophages,AM)凋亡率,免疫组化法检测核因子-κBp65(nuclear factor-κBp65,NF-κBp65)表达,RT-PCR法检测AM的sPLA2ⅡA、Bcl-2、Bax基因的表达。结果与对照组比较,模型组肺W/D、肺组织病理评分、AM的NF-κBp65表达及凋亡、AM的sPLA2ⅡA基因表达增加(P<0.05),AMBcl-2、Bax基因的表达下降(P<0.05)。与模型组比较,PDTC预防组上述改变得以逆转,肺损伤程度明显减轻(P<0.05)。结论预防性予以PDTC可抑制AMNF-κB活化,抑制sPLA2ⅡA基因表达,促进Bcl-2基因表达,抑制AM凋亡,对LPS所致的ALI有一定的保护作用。
Objective To investigate the pathological process of acute lung injury (ALI) induced by lipopolysaccharide (LPS) and to investigate the protective effect of pyrrolydine dithiocarbamates (PDTC) on ALI induced by LPS, mechanism. Methods 96 SD male rats were divided into control group, model group and PDTC prevention group. LPS (6mg / kg) was injected into the animal model of ALI intravenously and killed at 2, 4, 8 and 12h after injection respectively. The PDTC prophylaxis group was intraperitoneally injected with PDTC (120 mg / kg) 30 min before LPS injection. The lung wet / dry weight ratio (W / D), the pathological score of lung tissue were determined by HE staining, the apoptosis rate of alveolar macrophages (AM) was measured by TUNEL method, and the nuclear factor The expression of sPLA2ⅡA, Bcl-2 and Bax gene in AM was detected by RT-PCR, and the expression of NF-κBp65 and NF-κBp65 was detected by RT-PCR. Results Compared with the control group, the lung W / D, lung histopathological score, the expression of NF-κBp65 in AM and the expression of sPLA2ⅡA in AM increased (P <0.05) and the expression of AMBcl-2 and Bax decreased P <0.05). Compared with the model group, the changes in the PDTC prevention group were reversed, and the degree of lung injury was significantly reduced (P <0.05). Conclusion PDTC can prevent the activation of AMNF-κB, inhibit the expression of sPLA2ⅡA gene, promote the expression of Bcl-2 gene, inhibit the apoptosis of AM, and protect ALI induced by LPS.