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目的研究三羟异黄酮预先给药对内毒素诱导大鼠急性肺损伤的保护作用及其机制。方法 32只雄性Wistar大鼠,随机分为4组,每组8只:对照组(C组)、三羟异黄酮组(G组)分别腹腔注射生理盐水1 ml／kg、三羟异黄酮50 mg／kg,30 min后,静脉注射生理盐水1 ml／kg;内毒素组(L组)、三羟异黄酮预预先给药组(Gpre组)分别腹腔注射生理盐水1 ml／kg、三羟异黄酮50 mg／kg,30 min后,静脉注射脂多糖6 mg／kg。注射脂多糖后4 h处死动物。测定支气管肺泡灌洗液(BALF)中蛋白浓度、髓过氧化物酶(MPO)活性及中性粒细胞(PMN)数。检测肺组织湿干重比(W／D)、丙二醛(MDA)含量、MPO 活性、肿瘤坏死因子-α(TNF-α)和血红素氧合酶-1(HO-1)mRNA、蛋白表达。观察肺组织病理学的改变。结果与C组比较,L组肺损伤严重、BALF中蛋白、MPO、PMN水平和肺组织W／D、MDA及MPO水平及TNF-α和HO-1 mRNA、蛋白表达水平升高(P<0．05或0．01),G组上述指标差异均无统计学意义(P >0．05);与L组比较,Gpre组除HO-1 mRNA、蛋白表达水平升高(P<0．05)外,其他指标均降低(P< 0．05或0．01)。结论三羟异黄酮预先给药对内毒素诱导大鼠急性肺损伤有一定的保护作用,与抑制PMN在肺组织的聚集、激活,TNF-α表达下调及HO-1表达上调有关。
Objective To study the protective effect of genistein on acute lung injury induced by endotoxin in rats and its mechanism. Methods Thirty-two male Wistar rats were randomly divided into 4 groups with 8 rats in each group: control group (C), genistein group (G) were injected intraperitoneally with normal saline (1 ml / kg), genistein mg / kg, 30 minutes later, intravenous injection of normal saline 1 ml / kg; endotoxin group (L group), genistein preconditioning group (Gpre group) were injected with normal saline 1 ml / Isoflavone 50 mg / kg, 30 min after intravenous injection of lipopolysaccharide 6 mg / kg. Animals were sacrificed 4 h after injection of lipopolysaccharide. The protein concentration, myeloperoxidase (MPO) activity and neutrophil count (PMN) in bronchoalveolar lavage fluid (BALF) were determined. The W / D, MDA, MPO, TNF-αand HO-1 mRNA and protein expression. Observe the pathological changes of lung tissue. Results Compared with group C, the lung injury in group L was severe. The levels of protein, MPO and PMN in BALF and the levels of W / D, MDA and MPO and the mRNA and protein expressions of TNF-α and HO-1 in BALF were increased .05 or 0.01). There was no significant difference in the above parameters between G group and G group (P> 0.05) ), Other indicators were lower (P <0.05 or 0.01). Conclusion Preconditioning of genistein can protect rat from acute lung injury induced by endotoxin, which is related to the inhibition of PMN accumulation and activation in lung tissue, the down-regulation of TNF-α and the up-regulation of HO-1.