DHA对百草枯诱导大鼠肺纤维化的拮抗作用

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目的观察DHA对百草枯(paraquat,PQ)诱导肺纤维化的拮抗作用。方法 Wistar大鼠随机分为5组:正常对照组、染毒组、低剂量DHA(500 mg/kw.bw)+PQ联合组、高剂量DHA(1000 mg/kw.bw)+PQ联合组和DHA对照组(1000 mg/kw.bw),每组10只。低、高剂量DHA+PQ联合组和DHA对照组,分别经灌胃给予DHA,正常对照组和染毒组给予等体积玉米油,给予DHA的第8日,低、高剂量DHA+PQ联合组和染毒组一次性经灌胃给予50 mg/kg.bw PQ染毒,正常对照组和DHA对照组均给予等体积生理盐水。PQ染毒后,持续给予DHA,于染毒后第35日,处死动物,分别制备肺组织切片,并行HE、Masson染色,观察肺组织损伤和纤维化情况。称量肺组织湿重和干重,计算湿重/干重比值(wet-to-dry weight ratio,W/D),采用碱水解法测定肺组织中羟脯氨酸(hydroxyproline,HPY)含量。结果与正常对照组比较,染毒组大鼠肺组织W/D明显减小(P<0.05);肺组织中的HPY含量增加了18.3%,与正常对照组相比差异有统计学意义(P<0.05);病理检查可见肺组织明显纤维化。补充500 mg/kg.bw DHA,大鼠肺组织W/D增加,与染毒组相比差异有统计学意义(P<0.05),肺组织中的羟脯氨酸比染毒组减少了12.3%(P<0.05),与对照组差别不明显,病理观察显示,纤维化改变也明显减轻。高剂量DHA+PQ联合组与染毒组无明显差别。结论摄入适量的DHA能够拮抗PQ诱导的大鼠肺纤维化。 Objective To observe the antagonistic effect of DHA on pulmonary fibrosis induced by paraquat (PQ). Methods Wistar rats were randomly divided into 5 groups: normal control group, exposure group, low dose DHA (500 mg / kw.bw) + PQ combination group and high dose DHA (1000 mg / kw.bw) + PQ combination group DHA control group (1000 mg / kw.bw), 10 mice in each group. Low and high dose DHA + PQ combination group and DHA control group, respectively, by intragastric administration of DHA, normal control group and exposure group were given the same volume of corn oil, DHA on the 8th day, low and high dose DHA + PQ combination group The rats in the control group and the DHA control group were given equal volume of normal saline by intragastric administration of 50 mg / kg.bw PQ once a day. After PQ exposure, DHA was continuously administered. On the 35th day after the injection, animals were sacrificed and lung tissue sections were prepared for HE staining and Masson staining respectively. Lung injury and fibrosis were observed. The wet weight and dry weight of lung tissue were weighed and the wet / dry weight ratio (W / D) was calculated. The content of hydroxyproline (HPY) in lung tissue was determined by alkaline hydrolysis method. Results Compared with the normal control group, the W / D of lung tissue in the treated group was significantly decreased (P <0.05), and the content of HPY in the lung tissue increased by 18.3%, which was significantly different from that in the normal control group (P <0.05). Pathological examination showed obvious pulmonary fibrosis. Compared with the control group (P <0.05), the hydroxyproline in the lung tissue decreased by 12.3 % (P <0.05), but the difference with the control group was not obvious. The pathological observation showed that the changes of fibrosis were also significantly reduced. High-dose DHA + PQ combination group and exposure group no significant difference. Conclusion DHA intake can antagonize PQ-induced pulmonary fibrosis in rats.
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