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目的探讨在百草枯(paraquat,PQ)中毒所致的大鼠急性肺损伤时黄芩甙(baicalin,Bai)对肺组织损伤和肺间质巨噬细胞肿瘤坏死因子(TNF-α)表达水平及肺组织中血红素氧合酶-1(HO-1)表达的影响。方法将SD大鼠随机分为对照组、PQ染毒组、Bai治疗组和Bai单纯对照组,每组10只。PQ染毒组腹腔注入PQ液(25 mg/kg)制造中毒模型；Bai治疗组对造模成功大鼠静脉注射Bai(300 ng·kg~(-1)·d~(-1)),共3 d；Bai单纯对照组是健康大鼠静脉注射Bai(300 mg·kg~(-1)·d~(-1)),共3 d；对照组给予等量生理盐水。均观察3 d后,取肺组织常规HE染色和电镜观察肺组织损伤情况,分离培养肺间质巨噬细胞(PIM)观察TNF-α的表达情况。用逆转录聚合酶链反应(RT-PCR)检测肺组织的HO-1 mRNA表达。用Western blot方法分析肺组织中HO-1蛋白表达。结果对照组和Bai单纯对照组肺组织结构基本正常,PQ染毒组肺组织损伤较对照组明显加重,Bai治疗组肺组织损伤较PQ组减轻。Bai治疗组的TNF-α表达水平[(484．2±39．5)μg/L]低于PQ染毒组[(790．2±35．0)μg/L],高于对照组[(121．6±19．2)μg/L],且差异均有统计学意义(P＜0．05),Bai治疗组肺组织的HO-1 mRNA和蛋白表达水平分别为59．8±5．40和122．0±31．98,明显高于PQ组(45．9±5．82和77．92±10．23),差异均有统计学意义(P＜0．05)。结论Bai减轻了大鼠PQ中毒所致的肺损伤,其机制可能与PIM的TNF-α表达水平降低及肺组织中HO-1基因和蛋白表达升高有关。
Objective To investigate the effects of baicalin (Bai) on the lung injury and the expression of tumor necrosis factor (TNF) in pulmonary interstitial macrophages in rats with acute lung injury induced by paraquat (PQ) Effect of Heme Oxygenase-1 (HO-1) Expression in Tissue. Methods SD rats were randomly divided into control group, PQ group, Bai treatment group and Bai simple control group, with 10 rats in each group. The rats in PQ group were injected intraperitoneally with PQ solution (25 mg / kg) to make the model of poisoning. Bai group was injected intravenously with Bai (300 ng · kg -1 · d -1) The control group was treated with Bai (300 mg · kg -1 · d -1) intravenously for 3 days. The control group was given the same amount of normal saline. After 3 days of observation, lung tissues were harvested for HE staining and electron microscopy for lung injury. TNF-α expression was isolated and cultured in pulmonary interstitial macrophages (PIMs). The expression of HO-1 mRNA in lung tissue was detected by reverse transcription-polymerase chain reaction (RT-PCR). Western blot analysis of HO-1 protein expression in lung tissue. Results The lung tissues in control group and Bai control group were basically normal. The lung injury in PQ group was more severe than that in control group. The lung injury in Bai group was less than that in PQ group. The level of TNF-α in Bai group was significantly lower than that in PQ group [(484.2 ± 39.5) μg / L [(790.2 ± 35.0) μg / L] 121.6 ± 19.2) μg / L, respectively, and the difference was statistically significant (P <0.05). The HO-1 mRNA and protein expression levels in lungs of Bai-treated group were 59.8 ± 5. 40 and 122.0 ± 31.98, respectively, which were significantly higher than those in PQ group (45.9 ± 5.82 and 77.92 ± 10.23, P <0.05). Conclusions Bai reduces the lung injury induced by PQ poisoning in rats. The mechanism may be related to the decrease of TNF-α and the expression of HO-1 gene and protein in lung tissue.