Therapeutic Effect of Electroacupuncture on Chronic Inflammation in Collagen-induced Arthritic Rats and Its Selective Inhibitory Action on COX-2 / 浙江中医药大学学报

ABSTRACT

[Objective]The intervention of electroacupuncture (EA) on chronic inflammation and cyclooxygenase-1/-2 mRNA expressions in rats with II collagen-induced arthritis was observed in vivo, so as to discuss the effect of EA on chronic inflammation and its pivotal mechanism. [Method]Wistar rats immunized intradermally with bovine type II collagen, were served as the animal models of chronic inflammation. EA stimulation, begun on day 11 after the injection, was applied at the acupoint equivalent to ST36 for continuous 10 times. Indomethacin and refecoxib were used respectively as the control treatments of NSAID inhibitor and COX-2 selective inhibitor. The arthritic index, swelling volume of paw and concentrations of prostaglandin E_2 (PGE_2) of local tissue were investigated. Furthermore, we investigated the impact of EA on the levels of COX-1 mRNA and COX-2 mRNA in synovial tissues and gastric mucosa of inflammatory rats by using reverse transcriptase-polymerase chain reaction (RT-PCR). [Results]All collagen-injected rats developed chronic inflammation of paws. EA remarkably reduced the paw swellings of rats on day 16 and day 21 and attenuated the severity of arthritis from the day 14 to day 21. The levels of PGE_2 in the inflammatory tissues of swollen paws were also lowered by EA. EA stimulation obviously down-regulated the expression of COX-2 mRNA in synovial tissue, but did not influence the level of COX-1 mRNA expressed in gastric mucosa. Indomethacin and refecoxib also strongly down-regulated COX-2 expression in synovial tissue. However, either indomethacin or refecoxib strongly affected the COX-1 mRNA expressions in gastric mucosa. [Conclusion] EA has a pronounced anti-inflammatory effect on collagen-induced arthritis, and the pivotal mechanism and also the advantage of its therapeutic result may be due to selective suppression of COX-2 gene activation, without destroying COX-1 activity in stomach.