The Effect Of Smoking On The Expression Of C-fos,bax In The Brain Of Rat

IntroductionSmoking is harm to health. Cigarette smoking is a risk factor for the development of atherosclerosis, particular coronary heart disease and peripheral vascular disease. Gunther find that the endothelial cells are activated by substance found in smoking, so that leukocytes adhere to and interact with them.Cigarette contains many kinds of harmful substances. It can induce protein peroxidized, DNA damage, cell dead. It also leads to cell in mammal apoptosis and necrosis. There are many clinical cases about smoking and cerebral ischemia, but we dont find the research a-bout smoking causing cerebral cell apoptosis. My study build up the smoking rat model to discuss the expression of c - fos and bax so as to find its mechanism. Gene c - fos is a number of IEGs, It is a nuclear transcription factor involved in differentiation and cell death. Transient expression of c - fos can stimulate cell, persistent c - fos elevation is a harbinger of cell death. Bax is a pro - apoptotic member of the bcl - 2 family, the expression of protein bax represent cell apoptosis. Cell can apoptosis in the induction of excited amino acid and ischemic damage.My study observed the expression of c - fos , bax in the rat brain and cellular ultramicrostructure in different condition so as to research the effect of cigarette in brain.Materials and Methods1. Animal and group dividing : health adult wistar rats is divided into five groups; normal group, no - smoking group, giving up smoking group, long - term group, short - term group.2. Reagent and instrument; c - fos, bax SABC immunohisto-chemical stain reagent, cigarette, transmission electron microscope, light microscope , chipping machine.3. Make the model of smoking rat, fixing, dewatering, embodying in wax, HE dying, observing the ultramicrostructure, c - fos, bax immunohistochemical SABC stain.4. Statistical dealing; the data were expressed as mean + sd and analyzed by SSPS 10. 0 statistical package. I use t - text compared different groups.ResultsA small quantity expression of c - fos, bax in cerebral cortex and hippocampus in normal group and no - smoking group. Expression of c - fos, bax increased in short - term group ( P <0. 05 ) . The expression in giving up smoking group are less than that of short - term group. The ultrastructures of nerve were destructive in rat model.DiscussionCigarette contains many kinds of harmful substances, including CO, nicotine, pix. Smoking can induce protein peroxidize, DNAdamage, cell dead. Vayssier think smoking can cause mammals cell apoptosis and necrosis. My study shows that there are no significant difference between no smoking group and normal group, while there are significant difference between smoking group and normal group. The results show that smoking change cellular structure.iEGs are related many kings of pathological damage, c - fos is a number of lEGs family. It can express quickly when cell suffer from harmful stimulus. My study show that there are significant difference between the smoking group and no smoking group. Giving up smoking group restore a little, the expression of long - term group are less than the short - term group, the difference may be contribute to the expressive period of c - fos. Curran considers transient c - fos expression can stimulate cell and persistent c - fos elevation is a harbinger of cell death.My study finds there are positive protein c - fos in cerebral cortex and hippocampus after smoking, c - fos may be stimulated in the pathological changes in the ischemic nerve. The mechanism of expression in protein c - fos may be NMD A receptor and Ca2+ stimulated. Some article reported smoking can cause local cellular ischemia. The increasing of c - fos may be related to vascular spasm. Bax is a pro -apoptotic number of the bcl - 2 family , its expression represent cellular apoptosis. My study show that there are significant difference between the smoking group and no smoking group. Giving up smoking group restore a little, th...