Stady On CBS Of Mice's Brain After Carbon Monoxide Poisoning

Background: The carbon monoxide (carbon monoxide, co) is one kind of achromatic color, tasteless, not smelly, non-irritant virulent gas. It is in the life and the production causes the toxic death , the most common asphyxiating gas.It may cause organism multi-system harm, exhausts oneself by the cerebrum seriously; especially on central nervous system and cardiovascular system.Besides may create the acute toxic brain damage, have a part of patients to alleviate, consciousness after the toxicant symptom restores normally, probably experience 2-60 days performance normal or the basic normal dormant period, can appear a series of symptoms, including dementia,amentia and extrapyramidal system's symptom, is called the Delayed encephalopathy after carbon monoxide poisoning (DEACMP). The disease rate is 10-30% in civil,0.8-43% in abroad. The clinical manifestation is a group by the acute stupid primarily energetic nerve function disorder, is CO poisoned the most serious type. The related CO poison and the hangfire brain illness pathogenesis research, proposed until now some hypotheses but its pathogenesis still not extremely clear.20th Century lately, hydrogen sulfide(H₂S) was founded as the third gas of endogenous neuromodulator after NO and CO.It has important physiological action in brain. H₂S specifically potentiate the activity of NMDA receptor and alter the induction of long-term potentiation(LTP) in the hippocampus. H₂S can regulate the release of corticotropin-releasing hormone from the hypothalamus. H₂S acts as a vasorelaxant, to relax smooth muscle cells. H₂S has anti-oxidation function. Cystathionine- beta- synthase(CBS)and cystathionine-gamma-lyase(CSE) are key enzymes of the trans-sulfuration pathway but can also use L-cysteine as an alternative substrate to form H₂S. Both enzymes are pyridoxal-5-phosphate dependent enzymes .CBS seems to be the main H₂S-forming enzyme in the CNS. H₂S formation by brain CBS can be controlled. Calmodulin(CaM) is the fast regulated pathway to activate CBS and enhance H₂S formation. H₂S,NOandCO have similar property in many Pathophysiologiy processes and form complex regulating networks of gas signal in body.At present, the animal experimentation confirmed that H₂S was protective in cerebral ischemia model . But after the CO poison the H₂S of brain situation still not was explicit reported. We observed the expression of CBS and CaM in the mice brain tissue after carbon monoxide poisoning to study the mechanism of delayed encephalopathy after carbon monoxide poisoning.Objective: This experiment draws up in establishes the CO poison mouse model in the foundation, dynamic observes CBS expression change rule from the protein horizontal level,. to study the mechanism of delayed encephalopathy after carbon monoxide poisoning.Methods: 162 healthy male Kunming mice, body weight (18-22)g,were divided into the air control group stochastically (54), the contamination group (54), the butylphthalide group, each group divided into 6h, 1d, 2d, 3d, 4d, 7d, 14d, 21d, and 28d,9 subnit again.The contamination group according to the 170ml/kg dosage, establishes the CO poison mouse model through the single abdominal cavity injection 99.9% co gas law, the butylphthalide group given abdominal cavity butylphthalide injection(1ml/Kg,bid) after the CO poison mouse model, the air control group by the same level dosage air injection. After makes the CO poison mouse model the corresponding time spot, the execution mouse, beheads takes the brain, conventional. Use the immunity organization reduction to examine each group of CBS and CaM expression.Result1,The air control group mouse hippocampus area CBS expression is no difference. The contamination group mouse hippocampus area CBS IHS value starts in the contamination latter 6 hours to reduce, 2d to the lowest point, lower than the air control group. Then raising, the highest point at 14d. Then lower again. The butylphthalide group reduced gradually, 2d to the lowest point but higher than the air control group and the contamination group. Then raising gradually, 7d to the highest point value Then lower again. The air control group and CO group 6h,7d,14d,21d and 28d IHS value comparison has statistics difference (P<0.05). CO group and the butylphthalide group 1d,2d and 14d IHS value comparison has statistics difference (P<0.05).2,The air control group mouse hippocampus area CaM is no difference. The CO group mouse hippocampus area CaM presents two stages the changes, first reduce,2d to the lowest point, then raising , 14d to the highest point, then reduce again,gradually.. The butylphthalide group reduced gradually, then raised, 3d to the first peak, 4d reduced. 7d to the highest point, then reduced again. The air control group and CO group1d,2d,4d and 28d IHS value comparison has statistics difference (P<0.05). CO group and the butylphthalide group 6h,2d,4d,14d and 21d IHS value comparison has statistics difference (P<0.05).Conclusion1,CBS and CaM are expressed in normal mouse hippocampus area, after the CO poison High concentration H₂S is protective for the brain in the early period, but it is harmful in the later period if the concentration of H₂S is higher. Thereforce H₂S maybe participate the mechanisms of DEACMP.2,CaM is the fast regulated pathway to activate CBS, but they chang nonsynchronically.The reason maybe other factors participate the regulation of CBS. High concentration CBS is feedback inhibited the expression of CaM.3,Butylphthalide is protective for the brain, H₂S maybe participate the mechanisms of protection.