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目的:探讨龙血竭(LXJ)对博莱霉素肺损伤大鼠肺间质过度修复及其TGFβ1mRNA表达的调控作用。方法:60只健康SD大鼠,随机分为生理盐水组(NS)、博莱霉素肺损伤组(BLM)及龙血竭组(LXJ),每组20只,再分成两亚组,每亚组10只,通过博莱霉素一次性气管内滴入复制肺损伤修复大鼠模型,并在肺损伤修复过程中予龙血竭灌胃干预,分别于14和28天取大鼠肺组织,运用组织芯片,进行HE、胶原纤维染色及免疫组化分别定量肺内炎性细胞数、胶原蛋白、I型胶原,用实时荧光定量RT-PCR技术定量转化生长因子beta(TGFβ1)mR-NA的表达。结果:龙血竭对两时相肺组织的炎症程度和胶原(IOD分别从0.5492±0.2105和0.9578±0.3756降至0.2749±0.1592和0.3181±0.1210)及28天的I型胶原过度沉积(IOD从0.9348±0.3774降至0.5045±0.2796)皆有明显抑制作用(P<0.05),对两时相TGFβ1mRNA表达(从0.0219±0.0110和0.0170±0.0157分别降至0.0083±0.0024和0.0062±0.0051)有明显下调的作用(P<0.05)。结论:龙血竭具有抑制炎症性肺损伤促进修复,并可通过抑制胶原尤其是I型胶原的过度沉积而调控肺损伤肺间质过度修复之作用,后者可能主要与下调肺组织TGFβ1mRNA的表达有关。
Objective: To investigate the regulation effect of dragon’s blood (LXJ) on pulmonary interstitial over-repair and TGFβ1 mRNA expression in bleomycin-induced lung injury in rats. Methods: Sixty healthy SD rats were randomly divided into saline group (NS), bleomycin-induced lung injury group (BLM) and dragon’s blood group (LXJ), with 20 rats in each group. Subgroup of 10 rats were treated with bleomycin in a single intratracheal instillation of lung injury to repair the rat model, and in the process of lung injury repair to Dragon’s Blood Gavage intervention, respectively, at 14 and 28 days to take rat lung tissue The number of inflammatory cells, collagen and type I collagen in the lung were quantified by HE staining, collagen staining and immunohistochemistry. The expression of TGF-β1 (TGFβ1) mR-NA was quantified by real-time fluorescence quantitative RT- expression. Results: The degree of inflammation of DRG and the collagen (IOD decreased from 0.5492 ± 0.2105 and 0.9578 ± 0.3756 to 0.2749 ± 0.1592 and 0.3181 ± 0.1210, respectively) and type I collagen over-deposition (IOD from 0.9348 ± 0.3774 to 0.5045 ± 0.2796) (P <0.05), and significantly downregulated the expression of TGFβ1 mRNA at two time points (from 0.0219 ± 0.0110 and 0.0170 ± 0.0157 to 0.0083 ± 0.0024 and 0.0062 ± 0.0051, respectively) (P <0.05). CONCLUSION: DRG can inhibit the inflammatory lung injury and promote the repair, and it can regulate lung interstitial over-repair by inhibiting the excessive deposition of collagen, especially type I collagen, which may mainly and down-regulate the expression of TGFβ1 mRNA in lung tissue related.