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目的研究烟酸对博莱霉素肺纤维化大鼠模型的干预影响以及可能的机制。方法54只清洁级SD大鼠随机分为3组:烟酸组(N组),模型组(B组),正常组(CN组)。烟酸组和模型组大鼠实验当天气管内滴入博莱霉素5 mg/kg,正常组气管内滴入等量生理盐水。在气管内滴药后第7,14,28天每组各处死6只动物,取肺组织称重计算肺系数,行HE、M asson染色并做肺泡炎、肺纤维化评分,比色法测羟脯氨酸含量,免疫组化法测转化生长因子-β1(TGF-β1),α-平滑肌肌动蛋白(α-SMA)水平表达。结果模型组TGF-β1,α-SMA蛋白表达明显高于正常组,烟酸组则低于模型组。模型组各时间点肺泡炎评分均高于同一时间点正常组和烟酸组;实验第14,28天肺纤维化程度,肺系数,羟脯氨酸含量也高于同期正常组及烟酸组。结论烟酸可以抑制博莱霉素肺纤维化的形成,可能与部分抑制肺组织TGF-β1,α-SMA蛋白表达有关。
Objective To study the effects of nicotinic acid on bleomycin-induced pulmonary fibrosis in rats and its possible mechanism. Methods Totally 54 clean SD rats were randomly divided into 3 groups: niacin group (N group), model group (B group) and normal group (CN group). In niacin group and model group, bleomycin 5 mg / kg was dripped in the trachea during the experiment, and normal saline was injected into the trachea of the normal group. Six animals were killed in each group on the 7th, 14th and 28th day after intratracheal instillation. The lungs were weighed to calculate the lung coefficient. HE and Masson staining were performed and alveolitis, pulmonary fibrosis score and colorimetry were measured Hydroxyproline content and expression of TGF-β1 and α-SMA were detected by immunohistochemistry. Results The expression of TGF-β1 and α-SMA in the model group was significantly higher than that in the normal group, while the nicotinic acid group was lower than the model group. The alveolitis score of model group was higher than that of normal group and nicotinic acid group at the same time point. On the 14th and 28th day, the degree of pulmonary fibrosis, pulmonary coefficient and hydroxyproline content were also higher than those of normal group and nicotinic acid group . Conclusion Niacin can inhibit the formation of bleomycin-induced pulmonary fibrosis, which may be related to the partial inhibition of the expression of TGF-β1 and α-SMA in lung tissue.