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目的:观察血必净对百草枯(PQ)所致肺纤维化过程中Smads蛋白的影响,初探血必净对肺纤维化的干预机制。方法:将SPF级C57BL/6J小鼠分为1正常对照组:予以腹腔注射等量生理盐水;2模型组(PQ组):腹腔一次注射18mg/kg剂量PQ;3血必净干预组:腹腔一次注射18mg/kg剂量PQ;0.5h后小鼠尾静脉注射50ml/kg血必净注射液(以后1次/d)。分别于第3、7、14天处死小鼠采集标本进行检测。苏木精-伊红染色观察肺组织病理改变;Western blot检测肺组织Smad2/3、p-smad2/3、Smad7蛋白的表达;RT-PCR检测Smad7mRNA表达。结果:1正常组小鼠肺组织苏木精-伊红染色肺泡结构正常,肺泡及间质区域无充血或炎性细胞浸润;模型组肺泡闭塞,肺泡腔面积减少,存在片状实变区域;血必净干预3d组肺组织弥漫性出血减少,有少量胶原沉积在细支气管周围;血必净干预7d组肺组织充血及出血较严重,部分闭塞,肺泡壁增厚明显,可见纤维细胞增殖、胶原沉积于血管及支气管周围;血必净干预14d组肺结构破坏明显,形成纤维块或纤维束,说明血必净早期干预对肺组织改善的效果明显;2模型组Samds信号蛋白p-smad2/3、Smad7表达上调,血必净干预后可不同程度地下调p-smad2/3高表达,增强Samd7的表达,血必净干预3d组作用较为显著。结论:成功构建百草枯所致小鼠肺纤维化模型,血必净可作用于Smads信号转导通路正、负反馈环路中的Smad2/3、Smad7关键信号蛋白,早期部分阻抑百草枯所致肺纤维化的进展。
Objective: To observe the effect of Xuebijing on Smads protein during paraquat-induced pulmonary fibrosis, and to explore the mechanism of Xuebijing on pulmonary fibrosis. Methods: SPF-grade C57BL / 6J mice were divided into 1 normal control group, intraperitoneal injection of normal saline, 2 model group (PQ group): intraperitoneal injection of PQ 18mg / kg; 3 Xuebijing intervention group: One injection of 18mg / kg dose of PQ; mice after 0.5h injection of 50ml / kg Xuebijing injection (after 1 / d). Mice were sacrificed on the 3rd, 7th and 14th day respectively to collect the specimens for detection. The expression of Smad2 / 3, p-smad2 / 3 and Smad7 in lung tissue was detected by Western blot. The expression of Smad7 mRNA was detected by RT-PCR. Results: 1 The lung tissue of normal mice showed normal alveolar structure and no hyperemia or inflammatory cell infiltration in alveolar and interstitial regions. Alveolar occlusion and alveolar area were reduced in model group, Serum bilirubin intervention 3d group decreased diffuse hemorrhage of lung tissue, a small amount of collagen deposition in the bronchioles around; blood clotting intervention 7d group pulmonary congestion and bleeding more serious, partial occlusion, alveolar wall thickening significantly, showing fibroblast proliferation, Collagen deposition in the blood vessels and bronchial circumference; serum creatinine intervention 14d obvious lung damage, the formation of fiber blocks or fiber bundles, indicating that the early intervention of Xuebijing significant effect on lung tissue improvement; 2 model group Samds signaling protein p-smad2 / The expression of Smad7 was up-regulated. After intervention with Xuebijing, the expression of p-smad2 / 3 was down-regulated and the expression of Samd7 was enhanced. The effect of Xuebijing on 3d group was significant. CONCLUSION: Paraquat-induced mouse model of pulmonary fibrosis is successfully constructed. Xuebijing can act on Smad2 / 3, Smad7 key signaling proteins in the positive and negative feedback loops of Smads signaling pathway, inhibit early paraquat Cause of pulmonary fibrosis.