OBJECTIVETo observe the effect of electroacupuncture (EA) on the expressions of CD36 gene and protein in peritoneal macrophages of atherosclerotic rabbits, and to explore the mechanism of acupuncture regulation of atherosclerosis.

METHODSA total of 26 male New Zealand rabbits were randomly divided into a blank group (7 rabbits) and a model group (19 rabbits). The rabbits in the blank group were fed with common feedstuff, and those in the model group were applied with high fat diet and arteria carotis communis bullon injury. One rabbit was sacrificed after 8 weeks to observe the morphological changes of carotid atherosclerotic plaques by HE staining to verify model establishment separately in the blank group and model group. The model rabbits were randomized into a control group, an EA group and a western medication group, 6 rabbits in each one. Common feedstuff was used in the blank group and high fat feed in the other groups. No intervention except grabbing and fixation as the EA group was in the blank group and control group. Rabbits in the EA group were treated with acupuncture at bilateral "Neiguan" (PC 6), "Zusanli" (ST 36), "Guanyuan" (CV 4), and EA with sparse-dense wave was connected at bilateral "Neiguan" (PC 6) and "Zusanli" (ST 36) for 20 min, 4 Hz/20 Hz and 1 mA. 20 mL suspension of 1mg/kg/d atorvastatin calcium tablets were prescribed by intragastric administration in the western medication group for 4 courses, 6 d as one course with 1 d between two courses, once a day. The expression of CD36 protein in peritoneal macrophages was detected by Western blot. Reverse transcription (RT) of RNA and polymerase chain reaction (PCR) of cDNA were used to detect the expression of CD36 mRNA in peritoneal macrophages.

RESULTSIn the blank group, the vascular wall thickness was uniform and the endothelium was intact. There was no accumulation of foam cells and atherosclerotic plaques. In the model group, the intima of the artery obviously thickened; the intima was damaged; the atherosclerotic plaque and inflammatory cell infiltration were found in the intima, and the foam cells were seen. After treatment, the expressions of CD36 protein and CD36 mRNA in the control group, EA group and western medication group were higher than those in the blank group (all<0.01). Those in the EA group and western medication group were lower than the expressions in the control group (all<0.01). There was no statistical significance for the expressions of CD36 protein and CD36 mRNA between the EA group and the western medication group (both>0.05). .

CONCLUSIONEA can reduce the expressions of CD36 protein and CD36 mRNA in peritoneal macrophages of atherosclerotic rabbits, which may be one of the mechanisms of EA treatment of atherosclerosis.