OBJECTIVETo observe the morphological changes of photoreceptor cells in rats with retinitis pigmentosa (RP) induced by N-methyl-N-Nitrosourea (MNU) and the effects of acupuncture against it.

METHODSA total of 16 SD rats were treated with one-time intraperitoneal injection of MNU (50 mg/kg) to induce RP, and randomly divided into an acupuncture group and a model group, 8 rats in each one. In addition, 4 rats were selected as a control group. After model establishment, rats in the acupuncture group were treated with acupuncture at "Xinming-1" (Extra) and "Jingming" (BL 1) for 30 min, once a day for 7 days; rats in the model group and control group received no treatment, and the feeding conditions and fixation were identical as the acupuncture group. 2 h after the end of intervention, rats were sacrificed by cervical dislocation to observe the morphological changes of rhodopsin, rod terminals and rod bipolar cells.

RESULTSDue to the loss of retina photoreceptor cells induced by MNU in rats, in the model group the rhodopsin was stained in residual cell bodies, and there were sporadic rod terminals and little rod bipolar cells; outer segments, inter segments, cell bodies and cell terminals were all affected at different levels. The distribution of rhodopsin was also changed in the acupuncture group, showing more bodies of photoreceptor cells, and the residual rod terminals and rod bipolar cells were more than those in the model group; the injury of retina was less than that in the model group.

CONCLUSIONMNU could lead to a comprehensive injury to the morphology of photoreceptor cells, however, acupuncture is capable of inhibiting morphological changes of photoreceptor cells induced by MNU.

Acupuncture Therapy ; Animals ; Humans ; Male ; Photoreceptor Cells ; cytology ; Rats ; Rats, Sprague-Dawley ; Retinitis Pigmentosa ; physiopathology ; therapy

OBJECTIVE: To explore the effect of delta-opioid receptor (DOR) in electroacupuncture (EA) protecting the brain against acute ischemic injury. METHODS: Fifty-one rats were randomly divided into sham ischemia group, ischemia group, sham EA group, EA group, and EA+DOR antagonist (naltrindole) group. Transient focal cerebral ischemia (1 hour) was induced in rat brain by middle cerebral artery occlusion (MCAO) method. EA was applied on Shuigou (GV 26) and Neiguan (PC 6) for 30 min, starting immediately after the onset of reperfusion. Neurological deficit scores and volume of cerebral infarction were detected after 24-hour reperfusion. Other 12 rats were randomly divided into sham ischemia group, ischemia group, EA group and EA + naltrindole group. DOR protein expressions were assessed by Western blotting after 24-hour reperfusion. RESULTS: In comparison with the ischemia group and sham EA group, EA significantly reduced ischemic infarction and neurological deficits (P<0.05); EA significantly increased the expression of 60 kD DOR protein (P<0.05) and tended to increase that of 36 kD DOR protein (P>0.05). When naltrindole was combined with EA, the naltrindole completely abolished the EA-induced protection in ischemic infarction and neurological deficits, and also arrested the expression of DOR. CONCLUSION: EA can up-regulate DOR expression and protect the brain from ischemia-reperfusion injury.