Effects of Naringenin on inflammation in complete freund's adjuvant-induced arthritis by regulating Bax/Bcl-2 balance.

Naringin (COG) is a flavanone with various bioactivities including an expectorant effect, antitussive effect, and inhibitory effect on asthma and acute lung injury. The aims of the present study were to investigate the antiarthritis activities of COG and elucidate the underlying mechanisms with regard to its molecular basis of action for the best combination. Arthritis was induced by intradermal injection of complete Freund’s adjuvant. Sprague–Dawley rats were randomly divided into five groups with 10 rats in each group: (1) control group, (2) AA group, (3) AA + dexamethasone (AA + Dex, 2 mg/kg), (4) AA + COG (20 mg/kg), (5) AA + COG (40 mg/kg). Paw swelling was measured, and the production of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 was detected by enzyme-linked immunosorbent assay (ELISA) in serum. Pathological changes of joints tissues were observed by hematoxylin and eosin (HE) staining. Apoptosis of synovial tissues was measured by terminal dUTP nick-end labeling (TUNEL) assay. The expressions of apoptosis-related molecules, including Bcl-2 and Bax, were determined by Western blotting. In both COG and Dex treatments, COG and Dex significantly suppressed paw swelling in AA rats. Moreover, COG and Dex significantly suppressed the production of TNF-α, IL-1β, and IL-6 in serum. HE staining study demonstrated that COG and Dex significantly suppressed pathological changes of joints tissues; TUNEL assay demonstrated that COG and Dex induced apoptosis of AA via regulation of the protein expression of Bcl-2 and Bax. These data suggest that COG may have therapeutic potential for RA.