Objective: To observe the effect of electroacupuncture (EA) on changes of cyclooxygenase (COX)-2 mRNA and protein expression after inflammation occurrence at the back by application of human recombinant IL-1beta (hr IL-Ibeta) plus air-pouch in rats, so as to analyze the relativity between EA-induced changes of COX-2 expression and proinflammatory cytokines regulative pathway.
Methods: Ninety female Wistar rats were randomized into control, model, and EA groups with 30 cases in each. Inflammatory model was established by subcutaneous implantation of a sterilized hollow teflon cylinder (sac, 1.5 mi in volume) at the back and intrasaccal injection of hr IL-1beta (10 ng/ml). EA (2 Hz, 1 mA) was immediately applied to "Quchi" (LI 11) for 30 min. Exudate in the sac was withdrawn at various intervals after hr IL-1beta-injection for assaying COX-2 mRNA expression with RT-PCR and protein expression with Western Blotting.
Results: In comparison with control group, one hour (h) after hr IL-1beta-injection, COX-2 mRNA and protein expression levels were up-regulated significantly in model group (P < 0.01); while compared to model group, COX-2 mRNA and protein expression levels in EA group were down-regulated considerably (P < 0.05). 5 h and 24 h after hr IL-1beta-injection, COX-2 mRNA expression in model and EA groups was significantly higher than that in control group (P < 0.01), and no significant differences were found between model and EA groups in COX-2 mRNA expression levels (P > 0.05). On the contrary, 5 h after administration of hr IL-1beta, COX-2 protein expression in model group was significantly higher than that in control group (P < 0.05). On the 24 h after hr Ibeta-1beta-injection, no significant differences were found in COX-2 protein expression levels among control, model and EA groups (P > 0.05).
Conclusion: EA can effectively suppress hr IL-1beta-injection induced up-regulation of COX-2 mRNA and protein expression in the rats, suggesting a close relativity between the regulation of proinflammatory cytokines and EA-induced inhibition of COX-2 mRNA and protein expression.