Objective: To observe the influence of scalp-acupuncture on the expression of acid-sensing ion channels (ASICs) 1 a and 2 b of hippocampal CA 1 region in cerebral ischemia (CI) rats, so as to investigate its mechanism underlying improvement of ischemic stroke.
Methods: Thirty-two male SD rats were randomly allocated to normal control, model, scalp-acupuncture and Amiloride group (n=8 in each group). The model of focal CI was established by middle cerebral artery occlusion (MCAO). Scalp acupuncture stimulation was applied to bilateral Dingnieqianxiexian (MS 6) and Dingniehouxiexian (MS 7), once daily for 7 days. Rats of the Amiloride group were fed with Amiloride solution, twice a day for 7 days, and those of the normal control and model groups were grabbled and fixed in the same way with the acupuncture and Amiloride groups. The neurological deficit score was given according to Longa's method. The expression of hippocampal ASIC 1 a and ASIC 2 b was detected by immunohistochemistry, and the Ca2+ concentration in the hippocampal tissue assayed using flowing cytometry.
Results: After the intervention, the neurological deficit score of both the scalp-acupuncture and Amiloride groups were significantly decreased in comparison with pre-treatment (P<0.01), and the effect of scalp-acupuncture was markedly superior to that of Amiloride in reducing neurological deficit score (P<0.05). The expression of ASIC 1 a and ASIC 2 b in the hippocampal CA 1 region and hip-pocampal Ca2+ concentration were significantly up-regulated in the model group compared with the normal control group (P<0.01), and obviously down-regulated in both scalp-acupuncture and Amiloride groups (P<0.01, P<0.05),without significant differences between the two treatment groups in the ASIC 1 a and ASIC 2 b expression and Ca2+ concentration (P>0.05).
Conclusions: Scalp-acupuncture stimulation can improve neurological function in CI rats, which may be related to its effects in suppressing the increased expression of hippocampal ASIC 1 a and ASIC 2 b proteins and in reducing calcium overload in hip-pocampal neurocytes.