Objective To observe the effect of Shenkangling on MAPK signaling pathway after oxidized lowdensity lipoprotein（ ox-LDL）-induced mesangial cell（ MC） proliferation and study the mechanism. Methods The MCs were randomized into the normal control group

ox-LDL group

ox-LDL + CXC-chemokine receptor 6（ CXCR6） group

Shenkangling low-concentration and high-concentration groups

and atorvastatin low-concentration and high-concentration groups. The protein contains of C-X-C chemokine ligand 16（ CXCL16） and CD36 and the phosphorylation levels of p38

ERK1 /2

SAPK / JNK and nuclear factor-κB（ NF-κB） p65 of MCs in all groups were observed. Results Comparing with the normal control group

the protein contains of CXCL16 and CD36 and the phosphorylation levels of p38

ERK1 /2

SAPK / JNK and NF-κB p65 of MCs in the ox-LDL + CXCR6 group were significantly increased（ P < 0. 01）. Comparing with the ox-LDL + CXCR6 group

the protein contains of CXCL16 and CD36 and the phosphorylation levels of p38

SAPK / JNK and NF-κB p65 of MCs were significantly decreased in the Shenkangling groups and atorvastatin groups（ P < 0. 01）

and the phosphorylation level of ERK1 /2 was significantly decreased in the Shenkangling groups and atorvastatin high-concentration group（ P < 0. 05 or P < 0. 01）. The protein contain of CXCL16 and the phosphorylation levels of SAPK / JNK and NF-κB p65 in the Shenkangling high-concentration group were significantly lower than those in the atorvastatin low-concentration group（ P < 0. 05 or P < 0. 01）. Conclusion Shenkangling can effectively inhibit the proliferation of MCs possibly by inhibiting the proteins such as p38

ERK1 /2 and SAPK / JNK associated with MAPK singling pathway

NF-κB p65

CXCL16 and CD36.