Objective To explore possible mechanism of external application of compound Tripterygium Wilfordii in treating rheumatoid arthritis. Methods Randomly divided 30 SD rats into normal group

model group and compound Tripterygium Wilfordii external application group

with 10 rats in each group. Except for the normal group

the other two groups adopted type Ⅱ collagen-induced rat model with arthritis. Rats in the compound Tripterygium Wilfordii external application group were given compound Tripterygium Wilfordii topical agent 50 g/（kg · d） for external application on bilateral legs from the 14 th day after primary immune

once per day

for 28 days. The model and normal groups were not treated. Measured the volume of rats’ metapodium in each group every week. At the end of the experiment

examined the levels of interleukins1β（IL-1β）

tumor necrosis factor α（TNF-α）

vascular endothelial growth factor（VEGF） and angiogenin 1（Ang-1） in serum and synovial tissues. Examined the expression of proteins of extracellular signal regulated protein kinase（ERK） pathway in synovial tissues and conducted pathological examination on articular tissues. Results Volume of metapodium

level of each cytokine（except for VEGF） in serum and synovial tissue of rats in the model group remarkably increased compared with the normal group and the expression of p-ERK1/2 in synovial tissue also increased（P < 0. 05 or P < 0. 01）. Large amount of inflammatory cell infiltration

severe injury of articular cartilage and surface

bone substance erosion and structure disorder could be seen in pathological articular section. However

levels of IL-1β

TNF-α and Ang-1 of rats in the compound Tripterygium Wilfordii external application group decreased and each cytokine level and mRNA expression in synovial tissue decreased. P-ERK1/2 expression decreased（P < 0. 05 or P < 0. 01）; Pathological results showed compound Tripterygium Wilfordii external application had good effect in inhibiting synovial proliferation

decreasing inflammatory cell infiltration

and postponing bone and cartilage injury. Conclusion Compound Tripterygium Wilfordii external application could inhibit synovial proliferation

decrease angiogenesis and pannus formation in synovial tissues by decreasing inflammatory cytokines levels in synovial tissue and activation of ERK pathway in arthritis.