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目的探讨紫苏水提物(PLE)对白细胞介素6(IL-6)与其受体(IL-6R)结合的拮抗作用。方法建立IL-6/IL-6R结合的ELISA模型,观察PLE(0.0625～2mg·L-1)对两者结合的影响。PLE(0.3和3mg·L-1)预处理肝癌HepG2细胞,Western blotting方法检测PLE对rhIL-6诱导Stat3磷酸化的影响。建立急性酒精性肝损伤小鼠模型,免疫组化方法观察PLE(3g·kg-1)对小鼠肝组织的形态学影响;同时检测IL-6mRNA在肝组织的表达及Stat3磷酸化的水平。结果ELISA检测显示,PLE(0.0625～2mg·L-1)可显著抑制IL-6/IL-6R结合。PLE(0.3和3mg·L-1)可下调IL-6诱导的HepG2细胞中Stat3的磷酸化水平。与对照组相比,PLE(3g·kg-1)组小鼠肝细胞变性、坏死,炎性细胞浸润均有明显改善,且肝组织IL-6mRNA表达及Stat3的磷酸化水平亦显著下降。结论PLE可能阻断IL-6/IL-6R结合,抑制IL-6生物活性。
Objective To investigate the antagonistic effect of Perilla fruticosus (PLE) on the binding of interleukin-6 (IL-6) to its receptor (IL-6R). Methods The IL-6/IL-6R binding ELISA model was established to observe the effect of PLE (0.0625-2 mg·L-1) on the binding of the two. Hepatocellular carcinoma HepG2 cells were pretreated with PLE (0.3 and 3 mg·L-1) and Western blotting was used to detect the effect of PLE on rhIL-6-induced Stat3 phosphorylation. A mouse model of acute alcoholic liver injury was established. Immunohistochemistry was used to observe the morphological effects of PLE (3g·kg-1) on liver tissue in mice. Simultaneously, IL-6 mRNA expression and Stat3 phosphorylation were detected in liver tissue. Results ELISA showed that PLE (0.0625-2 mg·L-1) significantly inhibited IL-6/IL-6R binding. PLE (0.3 and 3 mg·L-1) down-regulated phosphorylation of Stat3 in IL-6-induced HepG2 cells. Compared with the control group, hepatocyte degeneration, necrosis, and inflammatory cell infiltration were significantly improved in the PLE (3g·kg-1) group, and the expression of IL-6 mRNA and Stat3 phosphorylation were also significantly decreased in the hepatic tissue. Conclusion PLE may block IL-6/IL-6R binding and inhibit IL-6 biological activity.