目的探讨木瓜苷(GCS)对佐剂性关节炎(AA)大鼠滑膜前列腺素受体表达的影响。方法采用弗氏完全佐剂(FCA)诱导大鼠AA模型,分离培养大鼠滑膜细胞,用四甲基噻唑蓝(MTr)法检测滑膜细胞的增殖能力,放射免疫法(RIA)测定滑膜细胞产生前列素E2(PGE2)和环磷酸腺苷(cAMP)的水平,Western blot法检测滑膜EP2和EP4的表达。结果GCS能显著抑制AA大鼠滑膜细胞的增殖,降低胞内的PGE2水平,升高cAMP水平,且GCS对滑膜细胞cAMP水平的提高与其抑制滑膜细胞增殖密切相关。GCS能上调滑膜EP2和EP4的表达。结论GCS影响EP2、EP4受体的表达,恢复滑膜细胞EP-G蛋白-cAMP信号的正常转导可能是其发挥作用的主要机制之一。
Objective To study the effect of glucosides of chaenomeles speciosa (GCS) on the expression of EP2 and EP4 in synovial tissues from rats with adjuvant arthritis. Methods Complete Freund's adjuvant (FCA) was used to induce adjuvant arthritis (AA) in rats. The synoviocytes from AA rats were collected and incubated. Synoviocytes proliferation was determined by 3-(4,5-dimethyhhiazal-2yl) 2,5-dipheny+ltetrazoliumbromide (MTT) assay. Levels of prostaglandins E2 (PGE2) and cAMP were determined by radioim-munoassay (RIA). The expression of EP2 and EP4 was detected by Western blot analysis. Results GCS significantly inhibited the proliferation of synovioeytes. GCS decreased the level of PGE2 and increased the level of cAMP. The results of correlation analysis demonstrated that GCS inhibited synovioeytes hyperplasia by increasing the level of cAMP in synoviocytes. The results of Western blot analysis demonstrated that GCS significantly improved the expression of EP2 and EP4. Conclusion These results suggest that restoring normal transduetion of the EP-G protein-cAMP signal pathway may be one of the most important mechanisms of GCS.