Chun-lai Liao1, Li Tong, Yu-yao Chen. 1. TCM and New Drug Research Laboratory, Department of Traditional Chinese Medicine, First Military Medical University, Guangzhou 510515, China. liaochunlai0314@sina.com
Abstract
OBJECTIVE: To observe the effect of Buyanghuanwu decoction (BYHWD) on neuronal nitric oxide synthase (nNOS) immunoreactivity after permanent focal cerebral ischemia in rats. METHODS: The rats were randomized into normal control group, cerebral ischemia model groups (with ischemia for 1, 4, and 10 h respectively), and corresponding ischemia groups treated with BYHWD. Focal cerebral ischemia was produced by permanent middle cerebral artery occlusion (MCAO) with nylon suture inserted through the internal carotid artery. Brain nNOS in different brain regions was assayed by SABC immunohistochemistry at different time points ranging from 1 to 10 h after occlusion. RESULTS: nNOS activity in the cerebral tissues was enhanced in the ischemic hemisphere as the time following ischemia prolonged. Pretreatment with BYHWD group significantly decreased nNOS activity to 170.80+/-21.71 and 189.20+/-18.53 in the striatum cortex 18a region and to 127.33+/-19.83, 215.20+/-38.80, and 191.20+/-22.39 in the caudate putamen, in comparison with the untreated cerebral ischemia model group (244.60+/-12.44 and 363.00+/-24.82 in the striatum cortex 18a region and 138.67+/-13.99, 266.40+/-29.25, and 373.20+/-31.55 in the caudate putamen, P<0.05), and this effect began to be observed in the early stage of ischemia and gradually high-lighted as the ischemia time increased. CONCLUSION: BYHWD significantly restrains the up-regulated activity of nNOS after focal cerebral ischemia to protect the cerebral ischemic lesion from the early stage following the onset of ischemia.
OBJECTIVE: To observe the effect of Buyanghuanwu decoction (BYHWD) on neuronal nitric oxide synthase (nNOS) immunoreactivity after permanent focal cerebral ischemia in rats. METHODS: The rats were randomized into normal control group, cerebral ischemia model groups (with ischemia for 1, 4, and 10 h respectively), and corresponding ischemia groups treated with BYHWD. Focal cerebral ischemia was produced by permanent middle cerebral artery occlusion (MCAO) with nylon suture inserted through the internal carotid artery. Brain nNOS in different brain regions was assayed by SABC immunohistochemistry at different time points ranging from 1 to 10 h after occlusion. RESULTS:nNOS activity in the cerebral tissues was enhanced in the ischemic hemisphere as the time following ischemia prolonged. Pretreatment with BYHWD group significantly decreased nNOS activity to 170.80+/-21.71 and 189.20+/-18.53 in the striatum cortex 18a region and to 127.33+/-19.83, 215.20+/-38.80, and 191.20+/-22.39 in the caudate putamen, in comparison with the untreated cerebral ischemia model group (244.60+/-12.44 and 363.00+/-24.82 in the striatum cortex 18a region and 138.67+/-13.99, 266.40+/-29.25, and 373.20+/-31.55 in the caudate putamen, P<0.05), and this effect began to be observed in the early stage of ischemia and gradually high-lighted as the ischemia time increased. CONCLUSION: BYHWD significantly restrains the up-regulated activity of nNOS after focal cerebral ischemia to protect the cerebral ischemic lesion from the early stage following the onset of ischemia.