鬼针草总黄酮对急性炎症的保护作用及可能机制研究

目的: 研究鬼针草总黄酮(TFB)对急性炎症的保护作用与可能机制。方法: 二甲苯诱导急性小鼠耳肿胀,检测耳肿胀度和血清TNF-α、IL-1、IL-6、IL-8含量;氟氏完全佐剂诱导佐剂性关节炎(AA)大鼠原发性炎症,检测足肿胀度和血清TNF-α、IL-1、IL-2、IL-6、IL-8含量,HE染色观察炎症关节病理学变化,免疫组织化学法检测关节软骨组织ASIC1a蛋白。结果: 小鼠急性耳肿胀和AA大鼠原发性炎症中,模型组动物血清TNF-α、IL-1、IL-6和IL-8含量均明显升高,TFB(100、200 mg/kg) 灌胃给药能降低小鼠耳肿胀度和血清TNF-α、IL-1、IL-6、IL-8含量,TFB(67、133 mg/kg)可以升高AA大鼠血清IL-2的含量。TFB灌胃给药可以使AA大鼠关节炎性细胞减少,改善病理变化。在AA大鼠原发性炎症中模型组大鼠关节软骨组织ASIC1a表达明显升高,TFB(67、133 mg/kg)组ASIC1a的表达明显降低。相关性分析结果显示,AA大鼠原发性炎症中ASIC1a与血清TNF-α、IL-1、IL-8含量呈正相关。结论: TFB对急性炎症具有保护作用,其抗炎机制可能与调节炎症介质释放有关。

Protective effects of total flavonoids of Bidens bipinnata L on acute inflammation and possible mechanism

AIM: To investigate the protective effects of total flavones of Bidens bipinnata L (TFB) on acute inflammation and its possible mechanism.METHODS: Mice ear edema model was induced by dimethylbenzene, and ear edema degree was measured 30 min later. Adjuvant arthritis (AA) rats model was established through intradermal injected with freund's complete adjuvant, and paw swelling degree was observed. Serum TNF-α, IL-1, IL-6, IL-8, and IL-2 contents were detected through enzyme linked immunosorbent assay (ELISA) in both models. Histopathological changes of knee joint were measured through hematoxylin-eosin staining, and the protein expression of ASIC1a in cartilage tissue was tested through immunohistochemistry.RESULTS: Compared with that of the model group, the ear edema degree and serum TNF-α, IL-1, IL-6, and IL-8 contents in the TFB (100, 200 mg/kg) groups were decreased. Compared with that of the AA model rats, the paw swelling degree and the protein expression of ASIC1a in cartilage tissue were lower in TFB (67, 133 mg/kg) groups, while serum IL-2 contents were elevated. The histopathological changes in the knee joint of AA rats including the number of inflammatory cells could be ameliorated by TFB(33, 67, 133 mg/kg). Results of Person correlation test demonstrated that ASIC1a protein was positively correlated with serum TNF-α, IL-1 and IL-8 concentrations.CONCLUSION: TFB has protective effects on acute inflammation, the mechanism might be associated with inhibitting the release of inflammatory mediators.