Abstract: Objective To observe the effect of heat-sensitive moxibustion on the expression of CD11b in focal cerebral ischemia/reperfusion (I/R) injury model rats. Methods Fifty-one male SD rats were randomly divided into three groups, sham- operated group (n=10), I/R injury group (n=14) and moxibustion group (n=27). According to changes of tail temperature before and after moxibustion, moxibustion group was subdivided into non heat-sensitive moxibustion group (n= 13) and heat- sensitivel moxibustion group (n=14). Focal cerebral ischemia- reperfusion injury was induced by middle cerebral artery occlusion for 2 hours and reperfusion for 3 days. Behavioral performance was tested using neurologic deficit scores. Tail-flick latency was determined with tail flick analgesia meter. Infarct areas were examined using TTC staining, and cortical expression of CD11b was measured using immunohistochemical staining. Results After 3 d of operation, the tail- flick latency was significantly shorter in non heat- sensitive moxibustion group (9.32 ± 1.11) s and heat- sensitive moxibustion group (8.69±0.51) s than that of model group (12.21±1.04) s. The area of cerebral infarction was smaller in non heat-sensitive moxibustion group (20.59±2.25)% and heat-sensitive moxibustion group (13.18±3.50)% than that in model group (32.22 ± 14.20)% . Compared with model group, the expression of CD11b was significantly decreased in non heatsensitive moxibustion group and heat-sensitive moxibustion group (P＜0.05). Conclusion Heat-sensitive moxibustion can reduce the damage of cerebral inchemia-reperfusion, which might be through decreasing expression of CD11b.

Key words: Moxa Cone Moxibustion, brain ischemia, reperfusion injury, antigens, CD11b, rats, Sprague-Dawley, tailflick latency