[Effect of electroacupuncture on autophagy in synovial tissues of rheumatoid arthritis rats]

To observe the effects of electroacupuncture (EA) on autophagosomes, unc-51-like autophage activating kinase 1 (ULK1), Beclin1, and microtubule-associated protein light chain 3 (LC3) expression, and synoviocyte ultrastructure in the synovial tissues of rheumatoid arthritis (RA) rats, and to explore the mechanism of EA in regulating the proliferation of synoviocytes via the autophagy pathway.

The SD rats were randomly divided into a normal group, a model group, a methotrexate (MTX) group, and an EA group, with 6 rats in each group. Following RA modeling with Freund's complete adjuvant, rats in the MTX group were treated with intragastric administration of 0.35 mg/kg MTX, twice a week, for 4 weeks, while those in the EA group received 20-min EA stimulation at "Zusanli" (ST36) and "Guanyuan" (CV4), once per day, for 4 weeks, with an interval of one day between weeks. The rat left hind toe volume was measured using the toe volume measuring instrument. HE staining was conducted for detecting the morphology of rat synovial tissues, followed by the observation of autophagosomes under the transmission electron microscope. The levels of serum interleukin (IL)-1 and tumor necrosis factor (TNF)-α were assayed by ELISA, and the protein expression levels of ULK1, Beclin1, and LC3 were detected by Western blot.

Compared with the normal group, the left hind toe volume of the model group increased significantly (P<0.01), while serum IL-1 and TNF-α (P<0.01), synovial ULK1, Beclin1, and LC3 protein expression (P<0.01, P<0.05) up-regulated. HE stain and electron microscope showed obvious synovial hyperplasia, and doublemembrane autophagosomes scattering in the synoviocytes. The comparison with the model group showed that MTX and EA remarkably decreased the left hind toe volume (P<0.01), serum IL-1 and TNF-α (P<0.01), down-regulated the protein expression levels of ULK1 and LC3 in synovial tissues (P<0.05, P<0.01), and inhibited the synovial hyperplasia, with no obvious autophagosomes observed in the synoviocytes. The protein expression of ULK1 in the EA group was significantly lower than that in the MTX group (P<0.01).

EA alleviates the joint swelling and synoviocyte injury of RA rats possibly by regulating the expression of ULK1, LC3, and Beclin1 and inhibiting the synoviocyte autophagy and proliferation.