白芍总苷对大鼠佐剂关节炎抗炎作用及机制研究

目的 探讨白芍总苷(total glucosides of paeonia:TGP)对佐剂关节炎大鼠足爪组织中核转录因子NF-κB/p65蛋白表达的抑制作用和对大鼠足爪组织病理改变的影响及血清中血管内皮生长因子(VEGF)和白介素-17(IL-17)含量的影响.方法 建立Ⅱ型胶原诱导的佐剂关节炎大鼠模型,用免疫组化染色法检测足爪组织中NF-κB/p65蛋白的表达.病理切片观察不同剂量的TGP对佐剂关节炎大鼠的治疗效果.用ELISA法检测佐剂关节炎大鼠血清中VEGF和IL-17的含量.结果 大、中剂量组的胞浆内NF-κB/p65的阳性表达比模型对照组明显降低(P＜0.01),TGP大、中剂量治疗组与地塞米松组能明显改变佐剂关节炎大鼠皮下组织细胞排列、炎性细胞浸润及血管增生现象,TGP小剂量组对改善佐剂关节炎大鼠足部皮肤的病理状况无明显作用.中、大剂量的TGP组和地塞米松组血清VEGF和IL-17的含量明显降低(P＜0.01).结论 TGP能抑制佐剂关节炎大鼠的炎症反应,其机制可能是TGP可下调NF-κB/p65蛋白的表达,降低炎性细胞因子IL-17和血清VEGF的产生,最终抑制血管增生及炎性细胞浸润.

The anti-inflammatory effects and mechanisms study of TGP on rat adjuvant arthritis

OBJECTIVE To explore the inhibitory effect of total glucosides of paeonia(TGP) on the Nuclear factor-κB/p65(NF-κB/p65) protein expression in paws of Adjuvants arthritis rats,the histopathology change of the skin of the rats paws,and the level of the serum Vacular endothelial growth factor(VEGF) and Interleukin-17(IL-17).METHODS Type Ⅱcollageninduced arthritis model in SD rats was established successfully.The expression of NF-κB/p65 proteins in rat’s paw tissues was detected by immunohistochemical staining.The histopathology change of the skin of the rats paws was observed by microscope.The contents of serum VEGFand IL-17 were detected by ELISA.RESULTS The expression of NF-κB/p65 protein obviously decreased in 100 mg/kg and 50 mg/kg TGP groups comparised with 25mg/kg TGP group(P ﹤ 0.01).Compared with 25mg/kg TGP group,the cell arrangement,inflammatory cells infiltrating and vascular proliferation were significangly changer in 100 mg/kg and 50 mg/kg TGP groups,the contents of serum VEGF and IL-17 were obviously decreased in 100 mg/kg TGPand 50 mg/kg TGP group than in 25mg/kg TGP group(P﹤0.01).CONCLUSION The inhibitory effect of TGP on inflammation maybe related to decreasing the expression of NF-κB/p65 protein,inhibiting inflammatory cell infiltration and vascular proliferation,and suppressing the production of VEGFand IL-17in RA rats.TGP can inhibit the inflammation in adjuvant arthritis in rats,the mechanism may be reduced to decreasing the expression of NF-κB/p65 protein,inhibiting the protuction of inflammatory cytokine IL-17 and serum VEGF.Finally,vascular proliferation and inflammatory cell infiltration are suppressed.