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目的:探讨甜牛大力总黄酮(TFRMS)和苦牛大力总黄酮(TFRMC)对小鼠急性肺损伤(ALI)模型的作用,并观察TFRMS和TFRMC抗炎作用的差异。方法:采用脂多糖(LPS)致小鼠ALI模型,观察TFRMS和TFRMC对小鼠ALI模型的抗炎作用,测定小鼠肺泡灌洗液(BALF液)中白细胞数(WBC)和总蛋白量(Pro),免疫组化法测定小鼠肺组织中核转录因子-κB p65(NF-κB p65)的表达,酶联免疫吸附试验(ELISA)测定肺组织中白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)含量,实时荧光定量PCR法测定IL-6,TNF-αmRNA的表达量,苏木素-伊红(HE)染色观察肺组织病理形态的改变。结果:与正常组比较,模型组WBC数,Pro,IL-6和TNF-α水平显著增加(P<0.01),肺组织有炎症改变;与模型组比较,TFRMS和TFRMC可明显减少小鼠急性肺炎BALF液的WBC数量,Pro渗出量(P<0.05,P<0.01),显著降低肺组织NF-κB p65蛋白水平(P<0.01),抑制IL-6,TNF-αmRNA表达(P<0.05,P<0.01),减少肺组织中IL-6和TNF-α水平(P<0.05,P<0.01);从组织病理学的角度上观察到,TFRMS和TFRMC各剂量组均可减轻LPS引起的急性肺损伤。结论:TFRMS和TFRMC均具有明显的抗炎作用,TFRMC和TFRMS作用效果相似,其抗炎作用机制可能是通过干扰NF-κB p65途径,减少IL-6,TNF-αmRNA表达,从而抑制IL-6和TNF-α炎症介质的生成。
Objective: To investigate the effect of TFRMS and TFRMC on acute lung injury (ALI) in mice and to observe the difference of anti-inflammatory effects between TFRMS and TFRMC. Methods: The anti-inflammatory effects of TFRMS and TFRMC on mouse ALI model were observed by lipopolysaccharide (LPS). The white blood cell count (WBC) and total protein in BALF were measured Pro). The expression of nuclear factor-κB p65 (NF-κB p65) was detected by immunohistochemistry and the levels of interleukin-6 (IL-6) and The levels of tumor necrosis factor-α (TNF-α) and IL-6 and TNF-α mRNA were detected by real-time fluorescence quantitative PCR. The pathological changes of lung tissue were observed by hematoxylin-eosin staining. Results: Compared with the normal group, the levels of WBC, Pro, IL-6 and TNF-αin the model group were significantly increased (P <0.01), and the inflammation in the lung tissue was changed. Compared with the model group, TFRMS and TFRMC significantly reduced the acute (P <0.05, P <0.01), significantly decreased the level of NF-κB p65 protein in lung tissue (P <0.01) and inhibited the expression of IL-6 and TNF-α mRNA , P <0.01), and decreased the levels of IL-6 and TNF-α in lung tissues (P <0.05, P <0.01). From the histopathological point of view, Acute lung injury. CONCLUSION: Both TFRMS and TFRMC have obvious anti-inflammatory effects. The anti-inflammatory effects of TFRMC and TFRMS are similar. The anti-inflammatory mechanism may be through inhibiting the NF-κB p65 pathway, decreasing the expression of IL-6 and TNF- And TNF-α production of inflammatory mediators.