Objective: To explore the effects of adiponectin receptor 1(AdipoR1) knockdown on the proliferation and apoptosis of human rheumatoid arthritis synovial fibroblast cell line(MH7A) induced by lipopolysaccharide(LPS). Methods: ①The interference efficiency of AdipoR1 silenced (sh-AdipoR1) MH7A cells was identified by immunofluorescence and Western blot techniques. ②The effects of LPS(100 ng/mL) on the proliferation and apoptosis of sh-AdipoR1 and sh-NC cells were detected by CCK8 kit and flow cytometry, respectively. ③ Besides, the expression levels of apoptosis associated genes: BCL-2, BCL-XL, BAX and BAK in sh-AdipoR1 and sh-NC cell lines stimulated by LPS, were detected by real-time polymerase chain reaction(real-time PCR) experiment. Groups of sh-NC and sh-AdipoR1 without LPS stimulation were set as controls. Results: ①The expression of fluorescent protein in MH7A cells transfected with lentivirus was nearly 100%, detected by fluorescence microscope. Moreover, the expression of AdipoR1 protein in sh-AdipoR1 group was significantly lower than that in sh-NC group(P<0.05), indicating that AdipoR1 silenced cells were successfully constructed. ②The cell proliferation rate and apoptotic cell rate of sh-AdipoR1 group had no obvious difference compared to sh-NC group without LPS stimulation. The cell proliferation rate of both sh-NC and sh-AdipoR1 groups increased after 24 and 48 hours LPS stimulation, and apoptotic cell rate of sh-NC and sh-AdipoR1 groups significantly increased after 48 hours LPS stimulation(P<0.05). The cell proliferation rate of sh-AdipoR1 group was significantly lower than that of sh-NC group after LPS stimulation for 24 and 48 hours (P<0.05). And the apoptotic cell rate of sh-AdipoR1 group was significantly higher than that of sh-AdipoR1 group after LPS stimulation for 48 hours(P<0.05). ③The mRNA expression levels of BCL-2 and BCL-XL of sh-AdipoR1 group had no significant difference compard to the sh-NC group without LPS stimulation. Neither did BAK and BAX mRNA expression levels. After LPS stimulation, BCL-2 and BCL-XL mRNA expression levels of both sh-NC and sh-AdipoR1 groups reduced, while BAK and BAX elevated(P<0.05). Compared with those in sh-NC group, the mRNA expression levels of BCL-2 and BCL-XL were significantly decreased while BAX and BAK were significantly increased in the sh-AdipoR1 group with LPS stimulation(P<0.05). Conclusion: Our research found that down-regulation of AdipoR1 gene could significantly inhibit the proliferation and promote the apoptosis of MH7A cells under LPS exposure. It indicates that adiponectin receptor-1 related signaling pathways may play a role in rheumatoid arthritis.