| IntroductionCerebral infarction is one of important diseases that result in human death and disability. Cigarette smoking is an important risk factor of Cerebral infarction , which can increase the expression of ICAM-1 on VEC by damaging it. By mediating adhesion of monocyte-endothelial cell, ICAM-1 may aggravate brain injury and affect prognosis of cerebral infarction.Subjects and methodsSubjects were assigned into four groups; (1) CI smoker ( 2) CI non-smoker. CI patients were selected within 3 days who had attacks. Diagnostic criterion was accorded with the fourth national cerebrovascular disease meeting revised criterion. All patients underwent brain CT or MRI examination. Infarction volume was calculated with formula presented by pullicino. ( 3 ) Healthy smokers (4) Healthy non-smokers. According to smoking criterion regulated by World Health Organization (WHO) : smoker is one who smokes one cigarette per day and continuously for one year. None of the subjects had a history of recent infections disease or had clinical evidence of any cardiovascular events or kidney or liver disease or had hypertension or diabetes, mellitus and so on.Venous blood was drawn in the morning after an overnight fast. Blood sample was then centrifuged and serum was retained. Determination of serum sl-CAM-1 concentrations was performed in duplicate with an ELISA. Statistical analyses were performed with SPSS11. 0 Software, and one-way analysis of variance (ANOVA) N students t test was employed.ResultsThe level of serum sICAM-1 in case of smokers with Cerebral infarctionis was higher than that of non-smokers with Cerebral infarctionis ( P < 0. 05 ) and obviously higher than that of healthy non-smokers ( P < 0.01) , The level in healthy smokers was higher than that of healthy non-smokers (P <0.05).The level in severe smokers was higher than that of mild smokers ( P < 0.01) , the level in moderate smokers was higher than that of mild smokers( P < 0.05).DiscussionICAM-1 is the ligand of LFA-1 and Mac-1, which belongs to immunoglobu-lin super family (IGSF). Usually, 1C AM is expressed on VEC weakly. But the expression is significantly enhanced when VECs are injured. ICAM-1 can shed into blood from surface of VEC to become into sICAM-1, which still have the function of binging with ligand. Recent studies demonstrated, the level of serum sICAM-1 in patients with acute cerebral thrombosis was significantly higher than that of healthy controls, which had also strongly expression in patients after cerebral ischemia reperfusion. Our study demonstrated, the level of serum sICAM-1 in case of smokers with CI was higher than that of non-smokers with CI , The level in healthy smokers was higher than that of healthy non-smokers. All above indicates that high level of sICAM-1 caused by cigarette smoking may accelerate occurrence and development of CI. Animal experiment demonstrated significantly increased expression of ICAM-1 mRNA and ICAM-1 on cerebral VEC in smoking rats. The CI volumes of middle cerebral artery in smoking rats was bigger than that of nonsmoker, which was correlated with cigarette index. Our studies showed, cigarette smoking could affect CI volumes. All above indicates smoking may aggravate cerebral damage. However the underlying mechanism is unclear.Cigarette smoke contains about 4000 kinds of ingredients including nicotine , CO and tar which are harmful. The three ingredients can injured VECheavily and change its structure and function by different pathways. Meanwhile ICAM-1 is expressed strongly by VEC. Animal experiment demonstrated, long term massive smoking changed VEC ultra-structure in rats, leading to dysfunction of VEC, to increase expression of ICAM-1 mRNA ICAM-1 on VEC. It was demonstrated that increased expression of ICAM-1 on VEC was mainly due to being stimulated by cytokines, such as IL-1, TNF-a, IFN-'y and so on. Animal experiment had also shown that the expression of TNF-a in VEC was significantly enhanced because of smoking. Subsequently molecular mechanism indicated PKC route mi...
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