机构地区:[1]甘肃省人民医院急诊科,兰州730000 [2]兰州市第二人民医院急诊科,兰州730046
出 处:《中华急诊医学杂志》2017年第11期1252-1256,共5页Chinese Journal of Emergency Medicine
基 金:兰州市卫生科技发展项目(LZWSKY2014-2-18)
摘 要:目的观察姜黄素对百草枯中毒大鼠肺组织胶原面积及TNF-α、IL-6、NE表达的影响,以探讨姜黄素治疗百草枯中毒的可能机制。方法SPF级Wistar大鼠108只,随机(随机数字法)分为空白对照组(B组)、百草枯染毒组(PQ组)、姜黄素治疗组(PC组),PQ组及PC组给予百草枯(50 mg/ kg)(北京华都生物科技)一次性灌胃染毒复制中毒模型,同时空白对照组给予等量生理盐水灌胃;灌胃30 min后,PC组给予姜黄素(sigma公司)200 mg/kg一次性腹腔注射,B组、PQ组注射等体积生理盐水,常规饲养。于3 d、7 d、14 d,行HE染色、Masson染色观察肺组织病理形态学、胶原纤维的分布及变化,酶联免疫吸附法检测血清肿瘤坏死因子(TNF-α)、白介素(IL-6)含量,免疫组织化学法观察肺组织中性粒细胞弹性蛋白酶(NE)的表达及变化。结果与B组比较,PQ组各时间点肺组织均有不同程度的肺泡炎,以7 d时最为严重;肺组织弥漫性纤维化,大量胶原纤维沉积,14 d胶原纤维沉积最严重;NE表达明显增强,14 d最明显。血清TNF-α、IL-6含量亦显著升高(P<0.05,P<0.01);与PQ组比较,PC组各时间点肺泡炎及肺纤维化程度均有明显减轻,NE表达明显减弱,TNF-α、IL-6含量亦显著降低(P<0.05)。结论抑制炎症因子及NE的表达,降低大鼠的肺泡炎和肺纤维化程度,可能是姜黄素治疗百草枯中毒肺的作用机制之一。Objective To observe the effects of curcumin on the lung collagen area and the expression of TNF-α, IL-6 and NE in paraquat-poisoning rats at different intervals, and discuss the possible mechanism of curcumin antagonizing paraquat poisoning. Methods A total of 108 SPF Wistar rats were divided into three groups (random number) : blank group (B group) for control, paraquat poisonin group (PQ group) and cureumin-treatment group ( PC group). The rats of PQ group and PC group were given paraquat (50 mg/kg) by gavage, and the rats of B group were given equal volume of sterile saline solution at the same time. Thirty minutes later, the rats of PC group were given curcumin (200 mg/kg ) by intraperitoneal injection, and rats of B group and PC group were given equal volume of sterile saline solution instead. At 3 d, 7 d and 14 d after modeling, the distribution and pathological changes of lung tissue and collagen fiber were observed by HE and Masson staining. The concentration of tumor necrosis factor ( TNF-α) and interleukin-6 (IL-6) were detected by enzyme-immunoassay. The lung neutrophil elastase (NE) expression was observed by immuno-histochemical method. Result Compared with B group, PQ group had pulmonary alveolitis in different degrees at different intervals, and the most serious pulmonary alveolitis was observed at 7 d after modeling. Diffused pulmonary fibrosis of the lung tissue and a large area of collagen fiber deposition were observed especially at 14 d after modeling, as well as the expression of NE was observed obviously, especially at 14 d after modeling. The concentration of TNF-α, IL-6 in serum were significantly increased (P 〈 0. 05, P 〈 0. 01 ). Compared with PQ group, the pulmonary alveolitis and fibrosis obviously in PC group with obvious reduction in the expression of NE and significant descrease in the concentrations of TNF-α and IL-6 ( P 〈 0.05 ). Conclusion Inhabiting inflammatory factors to alleviate the seriousness of alveolar inflammation
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