Effects Of Nicotine On Cerebral Ischemia And CD11b-IR Positive Cell Responses In Mice

Stroke is a popular nervous system disease. Cerebral arterial thrombosis is the most common type of stroke. Brain damage in the post-ischemia period accompanies with the activation of endogenous (microglia) and exogenous (polymorphonuclear leucocytes, neutrophil, monocyte) inflammatory cells. In view of the apparent controversial properties of nicotine in relation to brain ischemia, we have characterized the effects of nicotine in mice photothrombosis model by some methods. After intravenacaudalis injection of the photosensitive dye Rose Bengal B, subsequent focal illumination of the brain with a cold light source through the intact skull led to focal cortical infarcts of reproducible size, location and geometry. After 30 minutes of focal ischemia, we treated the mice with nicotine (0.5mg/kg) via intraperitoneal injection. In the positive control group, MK-801 was given intraperitoneally in a single dose of 1.0mg/kg body weight 30 min before induction of phototrombosis.The changes of behavior was measured by the movement capture system at different time points after ischemia. On excision, brains were stained with 2,3,5-triphenyltetrazolium chloride (TTC). Meanwhile, cryostat section were stained with Cresyl violet (Nissl) and immunohistochemistry(IHC). The food intake of the nicotine treatment mice grew down accompanying with the decrease of the motor function (P<0.05 vs. ischemia group). Acute nicotine administration induced significant nerve injury in a photothrombotic model of cerebral focal ischemia in mice. The infarction volume have significant difference between the nicotine treatment group and the ischemia group (P<0.01). The neuronal loss in nicotine treatment group is graver than standard ischemia group and it has significant difference(P<0.001). The activation of micoroglia has significant difference between the nicotine treatment group and the ischemia group. Conclusions (1)Nicotine can aggravate the infarction volume and motor degeneration of ischemia mice. (2)Nicotine can aggravate the pathophysiological process of the cerebral ischemia, the clinical value of nicotine remains controversial. (3)The activation of micoroglia has significant enhancement in the nicotine administration group. It is suggested that the neurovirulent process induced by nicotine may include inflammatory mechanisms. (4)MK-801 can diminish the infarction volume and motor degeneration of ischemia mice. It is commonly used in experiment.