RÉSUMÉ
Objective: To investigate the effect of baicalin on the autophagy of the synovial RSC-364 cells of the rats induced by lipopolysaccharide (LPS) through Pl3k/Akt/mTOR signal pathway, and to clarify its mechanism. Methods: The rat synovial RSC-364 cells in logarithmic growth phase were divided into control group, model group. dexamethasone (DXMS) group. 10/imol • L 1 baicalin group. 20/imol • L 1 baicalin group and 40/imol • L baicalin group. The RSC-364 cells in control group were only supplemented with culture medium, and the RSC-364 cells in the other groups were stimulated with 1 mg • L 1 LPS for 12 h to make the inflammatory cell models. The survival rates of RSC-364 cells were detected by MTT assay, and the expression levels of P13k. Akt, mTOR. Beclinl. and LC3-II mRNA in the RSC-364 cells in various groups were detected by RT-PCR method; Western blotting method was used to detect the expression levels of Beclinl. Atg5. Atg7. Atgl2. microtubule-associated protein-light chain 3-II (LC3-II ). and P62 proteins in the RSC-364 cells in various groups. Results: Compared with control group, the survival rate of RSC-364 cells in model group was significantly increased ( P-'-CO. 01). the expression levels of P13k. Akt. mTOR mRNA and P62 protein in the RSC-364 cells in model group were significantly decreased (P<0. 05 or P<0. 01). and the expression levels of Atg5. Atg7. Atgl2. LC3-II . Beclinl mRNA and proteins were significantly increased ( P<0. 01) ; compared with model group, the survival rates of RSC-364 cells in different concentrations of baicalin groups were significantly decreased (P<0. 05 or P<0. 01). the expression levels of P13k. Akt. mTOR mRNA and P62 protein in the RSC-364 cells in different concentrations of baicalin groups were significantly increased (P-'-CO. 05 or P<0. 01). and the expression levels of Atg5. Atg7. Atgl2. LC3-II and Beclinl mRNA and proteins were decreased ( P<0. 05 or P<0. 01). Conclusion: Baicalin may inhibit the LPS-induced autophagy of the RSC-364 cells by activating the Pl3k/Akt/mTOR signaling pathway.