[AMPK over-expression inhibits proliferation, matrix synthesis and inflammation response of glomerular mesangial cells in pristine-induced lupus mice].

Objective To explore the effects of AMP-activated protein kinase (AMPK) over-expression on the proliferation, matrix synthesis and inflammatory cytokine production in glomerular mesangial cells from pristane-induced systemic lupus erythematosus (SLE) mice. Methods C57BL/6 mice were randomly divided into control group and model group. The SLE mouse model was established by the treatment with pristane. The levels of autoantibodies were detected by ELISA. The primary glomerular mesangial cells were isolated from the mice of the control and model groups. The primary glomerular mesangial cells of the model mice were divided into model subgroup, empty vector subgroup and over-expression subgroup. The pEGFP-C1-vector and pEGFP-C1-MPK were transferred into the cells of the empty vector and over-expression subgroups, respectively. The expression of AMPK was tested by Western blotting. After AMPK was successfully over-expressed, cell apoptosis was detected by flow cytometry. The expressions of AMPK, cyclin D1, proliferating cell nuclear antigen (PCNA), P21, P27, fibronectin (FN), collagen IV (Col4), interleukin 6 (IL-6) and interleukin 1β (IL-1β) were measured by Western blotting. Results The levels of serum dsDNA IgG, dsDNA IgM, Sm IgG, Sm IgM significantly increased in the model group compared with the control group, indicating that the mouse model used in this study successfully imitated the pathological process of SLE. In addition, over-expression of AMPK promoted the apoptosis of mesangial cells from the SLE mice. Moreover, the expressions of cyclin D1, PCNA, P21, FN, Col4, IL-6 and IL-1β were markedly depressed, whereas the level of P27 protein was raised in these cells after AMPK over-expression. Conclusion AMPK over-expression can inhibit the cell proliferation, matrix synthesis and inflammatory response of mesangial cells in pristane-induced SLE mice.