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Abstract

Effects of Mecobalamin on Cerebral Ischemia-Reperfusion Injury of Spontaneously Hypertensive Stroke Prone Rats

Author(s): X. Zhang, Xuanjing Sun and W. Fu*
The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing 210023, Department of Acupuncture and Encephalopathy, Xuzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Xuzhou 221000, Department of Neurology, The Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, P. R. China

Correspondence Address:
W. Fu, Department of Neurology, The Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, P. R. China, E-mail: dr.wysh@163.com


We aimed to evaluate the effects of mecobalamin on the cerebral ischemia-reperfusion injury of spontaneously hypertensive stroke prone rats. 72 male rats were randomly divided into control group, model group, nimodipine group, high-dose mecobalamin group, middle-dose mecobalamin group and low-dose mecobalamin group (n=12). All groups were administrated intragastrically every morning once a day for 7 continuous days. The model of 2 h of focal cerebral ischemia and 24 h of reperfusion was established by blocking middle cerebral artery. Neurological deficits were graded with reference to the Longa method. Cerebral edema was determined using the wet-dry weighing method. The volume of cerebral infarction was measured by triphenyltetrazolium chloride staining and the levels of tumour necrosis factor alpha, interleukin-1 beta and interleukin-8 were measured by radioimmunoassay. High and middle-dose mecobalamin significantly reduced the volume of cerebral infarction, alleviated cerebral edema and improved nerve function compared with those of the model group (p<0.05). Compared with the model group, high and middle-dose mecobalamin significantly reduced the levels of tumour necrosis factor alpha, interleukin-1 beta and interleukin-8 in cerebral tissue (p<0.05). Mecobalamin protected spontaneously hypertensive stroke prone rats from cerebral ischemia-reperfusion injury, which may be related to the decreased levels of tumour necrosis factor alpha, interleukin-1 beta and interleukin-8 in cerebral tissue.

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