虾青素对百草枯致大鼠肺纤维化的干预作用及机制

发布时间：2018-03-02 11:00

本文关键词： 百草枯肺间质纤维化虾青素　出处：《南京医科大学学报(自然科学版)》2017年04期 　论文类型：期刊论文

【摘要】：目的:观察虾青素(astaxanthin,AX)对百草枯(paraquat,PQ)诱导大鼠肺纤维化的影响,并进一步探讨肺纤维化可能的发病机制。方法:SD大鼠随机分为正常对照组、PQ模型组及虾青素干预组。模型组及干预组大鼠腹腔注射百草枯造模后,干预组第2天起给予虾青素灌胃,对照组及模型组给予相应溶剂。分别于给药后第7、14、28天处死大鼠,测定大鼠血清中羟脯氨酸(hydroxyproline,HYP)、基质金属蛋白酶(matrix metalloproteinase,MMP)1、MMP2、MMP9和基质金属蛋白酶组织抑制剂(tissue inhibitor of matrix metalloproteinase1,TIMP1)的含量,取固定部位肺组织切片行HE、Masson染色进行病理学观察,免疫组化法测定转化生长因子-β1(TGF-β1)的含量,对病理图像进行形态学测量分析。结果:(1)HE染色及Masson染色结果显示:干预组纤维化炎症程度明显低于模型组;(2)模型组大鼠中毒后羟脯氨酸较正常组增高(P0.05),虾青素干预后,大鼠鼠肺血清羟脯氨酸水平较模型组降低(P0.05);(3)PQ模型组在肺纤维化区域TGF-β1弱阳性表达,虾青素干预后,TGF-β1表达含量下降,第28天最为明显,差异有统计学意义(P0.05);(4)模型组与干预组MMP1、MMP2、MMP9表达含量均较正常对照组升高。MMP1、MMP2、MMP9在PQ中毒后表达量逐渐升高,第14天达到高峰后下降,但第28天含量仍高于对照组。与模型组相比,干预组MMP2、MMP9含量均有下降,第14、28天显著,其差异有统计学意义(P0.05)。TIMP1在干预期间与模型组及对照组无显著差异。结论:虾青素能够减弱肺纤维化大鼠肺组织病理的胶原沉积、减少肺组织中羟脯氨酸的含量、降低肺血清中MMP2、MMP9的含量,抑制肺组织中TGF-β1的分泌,从而减轻PQ引起的大鼠肺纤维化。
[Abstract]:Objective: To observe the effect of astaxanthin (astaxanthin, AX) on paraquat (paraquat, PQ) induced pulmonary fibrosis in rats, and to further explore the pathogenesis of pulmonary fibrosis. Methods: SD rats were randomly divided into normal control group, PQ model group and astaxanthin intervention group. The model group and intervention group rats by intraperitoneal injection paraquat after modeling, the intervention group from the second day to give intragastric administration of astaxanthin, control group and model group were given corresponding solvent respectively. All rats were killed on day 7,14,28 after administration, the determination of hydroxyproline in serum of rats (hydroxyproline, HYP), matrix metalloproteinases (matrix metalloproteinase, MMP MMP9 and MMP2, 1). Tissue inhibitor of matrix metalloproteinases (tissue inhibitor of matrix metalloproteinase1, TIMP1) the content of fixed parts of the lung tissue sections for HE, Masson staining for pathological observation, immunohistochemical determination of transforming growth factor beta 1 (TGF- beta 1) The content analysis of the pathological images were measured. Results: (1) HE staining and Masson staining showed that the inflammation degree of fibrosis in intervention group was significantly lower than the model group; (2) poisoning model of rats were higher than normal group (P0.05), astaxanthin after intervention decreased serum hydroxyproline levels compared with rat lung the model group (P0.05); (3) PQ in pulmonary fibrosis model group TGF- beta 1 weakly positive expression, astaxanthin intervention, TGF- beta 1 expression decreased. The twenty-eighth day was the most obvious, the difference was statistically significant (P0.05); (4) model group and intervention group MMP1, MMP2, MMP9 expression levels were compared with the normal control group increased.MMP1, MMP2, MMP9 expression in PQ after poisoning was gradually increased, reaching a peak at fourteenth days after twenty-eighth days of decline, but the content is still higher than the control group. Compared with the model group, the intervention group MMP2, MMP9 were decreased significantly after 14,28 days, the difference was statistically significant ( P0.05).TIMP1 during the intervention and the model group and the control group had no significant difference. Conclusion: astaxanthin can decrease pathological collagen deposition in lung tissue of pulmonary fibrosis rats, reduce the content of hydroxyproline in lung tissue, reduce lung MMP2 in serum, the content of MMP9, TGF- beta 1 inhibits the secretion of lung tissue, thereby reducing caused by PQ pulmonary fibrosis in rats.

【作者单位】：南京医科大学附属常州第二人民医院呼吸科;
【分类号】：R563

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