Regulatory effect of ginsenoside compound K on apoptosis/autophagy in fibroblast-like synoviocytes of adjuvant arthritis rats
Objective To investigate the regulatory effects of ginsenoside compound K(CK)on apoptosis and autophagy in fibroblast-like synoviocytes(FLS)through PKM2/mTOR pathway.Methods SD rats were divided into normal group(n=10),model group(n=10),CK group(n=10)and methotrexate(MTX)group(n=10).,The 0.1 mL complete Freund's adjunct(CFA,10 mg/mL)was injected into the right hind metatarsal foot pad of rats to induce the adjuvant arthritis(AA)model.From day 15 after immunization,the rats in CK group were intragastrically given CK(80 mg/kg)for 18 consecutive days,and the rats in MTX group were administered with 0.5 mg/kg MTX every three days.Weight,arthritis global assessment,arthritis index,paw swelling,spleen and thymus index were evaluated every three days in every group.Apoptosis/autophagy-related and PKM2/mTOR pathway-related proteins were measured by Western blot.FLS autophagic flux was detected by overexpressed plasmids and the apoptosis of FLS was tested by flow cytometry.Results Compared with AA group,systemic inflammation score,arthritis index,paw swelling and spleen index were significantly attenuated in CK group and MTX group(P＜0.05),Bax,p62,and p-mTOR protein levels were significantly upregulated(P＜0.05),Beclin1,Bcl-2,and PKM2 protein levels were significantly downregulated(P＜0.05),the apoptosis rate of FLS was increased(P＜0.05),and FLS autophagic body was decreased(P＜0.05).There was no significant difference in systemic inflammation score,arthritis index,paw swelling and spleen index between CK group and MTX group(P＞0.05).Conclusion CK can alleviate the joint inflam-mation through regulating the apoptosis/autophagy of FLS by PKM2/mTOR pathway in AA rats.
万方数据
维普
