Effect Of Bupivacaine On Spinal Glial Ceils In A Rat Model Of Inflammatory Pain

Objective：To observe the effect of intrathecal bupivacaine on Glial cells andinflammatory cytokine in the spinal cord in the inflammatory pain model.Methods：Seventy-two healthy male SD rats weighing200-220g were randomlydivided into4groups: sham operation group; inflammatory pain group；bupivacainegroup and saline group. subcutaneous injection of0.1ml saline reagent right foot atthe end of palm(sham operation group) and subcutaneous injection of0.1ml2.5%formalin reagent right foot at the end of palm (inflammatory pain group); Afterintrathecal injection of40μl saline(saline group)and intrathecal injection of40μL0.125%bupivacaine(bupivacaine group), inflammatory pain was induced bysubcutaneous injection of0.1ml2.5%formalin reagent right foot at the end of palm.The mechanical paw withdrawal threshold and Cumulative pain score weremeasured before and after operation. Six animals of each group were killed and L4-5segment of the spinal cord was removed at24h after operation for determination ofOX42and GFAP protein expression by Western blot method;and the six rats wereused for real-time quantitative PCR in IL-1β, IL-6and TNF-α gene secretion levels.Results： Formalin reagent increased MWT and Cumulative pain score, thensuppressed by intrathecal bupivacaine. Inflammatory pain increased OX42andGFAP expression in the spinal cord; Intrathecal bupivacaine attenuated Formalinreagent induced up-regulation of OX42and GFAP expression in the spinal cord.Inflammatory pain increased IL-1β, IL-6and TNF-α gene secretion levels;Intrathecal bupivacaine attenuated IL-1β and TNF-α levels,and had no effect on IL-6levels.Conclusion：In the inflammatory pain model, bupivacaine can inhibit the OX42andGFAP expression of spinal cord glial cell and inhibit the release of inflammatorycytokine IL-1β and TNF-α.