Objective To investigate the effect of miR-155 on the PI3K/Akt/mTOR signaling pathway in rheumatoid arthritis (RA) rats by targeting PIK3R1. Methods SD rats were randomly divided into control group, model group, miR-155 agomir group, miR-155 antagomir group, and miR-155 negative control group. RA model was induced in rats. After treatment with drugs, joint symptoms were observed. The arthritis index and hind toe volume were measured. HE staining was used to observe the pathological morphology of rat joint tissues. Levels of inflammatory factors IL-6, IL-17, and IL-18 in rat joint tissues was detected with the kits. PI3K/Akt/mTOR signaling pathway protein expression in rat joint tissues was detected with Western blotting. qRT-PCR experiment was used to detect the levels of miR-155 and PIK3R1 mRNA in rat joint tissues. Dual luciferase reporter gene experiment was used to detect the targeted regulation of miR-155 on PIK3R1. Results Compared to those in the control group, the symptoms of arthritis in the model group were obvious, the arthritis index, hind toe volume, joint tissue inflammatory factors IL-6, IL-17, and IL-18 levels, joint tissue p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR levels, joint tissue miR-155 level increased significantly (P<0.05), and the PIK3R1 mRNA level reduced significantly (P<0.05). Compared to those in the model group and the miR-155 negative control group, the above indexes of miR-155 antagomir group were significantly improved (P<0.05). The trend in miR-155 agomir group was opposite to that in miR-155 antagomir group (P<0.05). Conclusion MiR-155 targets to down-regulate the expression of PIK3R1, to activate PI3K/Akt/mTOR signal, to aggravate the joint damage of RA rats, and to down-regulate the expression of miR-155. It inhibits the activation of PI3K/Akt/mTOR signal and the occurrence and development of inflammation, and relieves the symptoms of arthritis. |