Objective: To observe the influence of acupuncture intervention on expression of protein kinase A (PKAP in the cerebrocortex of rats with focal cerebral ischemia-reperfusion injury(CI/RI), so as to explore its underlying neuroprotection mechanism on cerebral ischemia.

Methods: Ninety male SD rats were randomly and evenly divided into sham-operation (sham), model and acupuncture groups which were further randomized into 3, 7 and 14-days (d) subgroups (10 rats/subgroup). CI/RI model was established by occlusion of the left middle cerebral artery for 2 hours and reperfusion. Manual acupuncture stimulation was applied to "Baihui" (GV 20) and "Shuigou" (GV 26), as well as the right "Quchi" (LI 11), "Hegu" (LI 4), "Neig (PC 6), "Zusanli" (ST 36),"Sanyinjiao"(SP 6) and "Taichong" (LR 3) for 30 min, once daily for 3, 7 and 14 d respectively. Rats of the sham and model groups were restrained for 30 min each day. Neurological defects were assessed by ethologic scoring according to Bederson's neurologic assessment scales. Cellular apoptosis in the ischemic cortex was detected by flow cytometry and PKA expression determined by immunohistochemistry for calculating its PKA immunoreaction (IR)-positive cell rate, respectively.

Results: Compared with the sham group, the neurologic scores, cortical cellular apoptosis rates and PKA IR-positive cell rates of the model group were significantly increased at the time-points of day 3, 7 and 14 post-treatment (P<0. 05). In comparison with the model group, the neurologic scores and cortical cellular apoptosis rates of the acupuncture group at the time-points of day 3, 7 and 14 post-treatment were considerably down-regulated (P<0. 05), and the cortical PKA IR-positive cell rates of the acupuncture group were remarkably increased (P<0. 05). In addition, along with the increase of acupuncture treatment sessions, lower apoptosis rates and more PKA IR-positive cells were found, suggesting a cumulative effect.

Conclusion: Acupuncture intervention can lower cellular apoptosis rate of the ischemic cerebrocortex and up-regulate cortical PKA expression level in CI/RI rats, which may be responsible for its effect in improving neurologic deficits.

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