[Effect of eye-acupuncture on cerebral intracellular adhesion molecule-1 expression in rats with acute cerebral ischemia-reperfusion injury].

OBJECTIVE: To investigate the effect of the eye-acupuncture therapy on cerebral intercellular adhesion molecule-1 (ICAM-1) expression in rats with acute cerebral ischemia-reperfusion injury (CI/RI) so as to reveal its underlying mechanism.

METHODS: Forty male SD rats were randomly and equally divided into normal, sham operation (sham), model and eye-acupuncture groups. Acute CI/RI model was established by occlusion of the middle cerebral artery with a modified suture-blocking method. Filiform needles were inserted into the "Qan" (Liver Area), "Shangjiao" (Upper Energizer Area), "Xiajiao" (Lower Energizer Area), etc. of the eye-acupuncture acupoints, and retained for 20 min. The treatment was conducted twice daily, 7 times altogether. Seventy-two hours after Acute CI/RI, the neurological behavior was assessed by ZeaLonga neurophysical impairment scale. Cerebral ICAM-1 protein and ICAM-1 mRNA expression levels were detected by Western blot (Penumbra area of the right cerebral infarction region) and real time-polymerase chain reaction (PCR) methods, respectively.

RESULTS: After modeling, the neurophysical impairment score of the model group was increased from 0 to (2.63 +/- 0.92) points on the first day and (2.63 +/- 0.74) points 72 h following Acute CI/RI. Correspondingly, cerebral ICAM-1 protein and mRNA expression was up-regulated considerably in the model group than in the normal control group (P < 0. 01). In comparison with the model group, the neurologic impairment score, and cerebral ICAM-1 protein and mRNA expression levels of the eye-acupuncture group were down-regulated obviously (P < 0.01, P < 0.05). No significant differences were found between the normal control and sham groups in neurologic impairment score and the expression levels of the ICAM-1 protein and ICAM-1 mRNA(P > 0.05).

CONCLUSION: Eye-acupuncture therapy can improve the cerebral ischemia-reperfusion injury induced behavior changes, which may be related to its effects in down-regulating the expression of cerebral ICAM-1 protein and gene.