Effect Of Endogenous Carbon Monoxide Against Apoptosis Of PC12

Mechanism of Dealayed Encephalopathy After Acute Carboon Monoxide Poisoning(DEACMP)is very complicated, many theories such as ischemia or hypoxia, Cytotoxicity, reperfusion injury and free radical, excitatory amino acids, apoptosis, et al are believed to relatived to DEACMP. Some study reveal the level of co among rabbits'blood not only rise apparently but also relative to degree of brain injury,it is rather deserved to investigate whether endogenic CO take part in DEACMP as a new cell messenger. In this paper,we detected the develop of CO and the effect of CO to PC12 cells after hypoxia culture. WE hope it can offer experiment base to explaining the pathogenesis of DEACMP. PC12 cells systemm , namely pheochromocytoma clone, become important tool cells in neuroscience disbody investigation because of its quality of obtaining and cell uniform. It is used extensively in the aspect of function, differention, auxano and death of nerve cell. PC12 cells anoxic culture model and Zinc protoporpphyrin IX (ZnPP-9) disposal model was used to discuss the effect of endogenic CO after PC12 cells hypoxia and ischemia. Specyrophotography was used to detect the content of COHb among culture medium and flow cytometer was used to detect apoptosis cells. The results were as follows: 1.Expression of HO: Cell surface didn't express HO-1 when cell was cultured under normal oxygen but expressed significantly while hypoxia; thus HO-2 expressed both normal oxygen and hypoxia. 2.Testing of COHb: Biwave-length was used to detect the absorbency of COHb insteaded the relative amount of CO.COHb was significantly higher in hypoxia group after one hour than that in normal oxygen group and;COHb after 24 hour was at normal level, and the levels in hypxia/ZnPP group decreased and was significantly lower than those in hypoxia group. 3.Testing of apoptosis cells: Apooptosis cells reached the peak at 1 hour following hypoxia and significantly higher than normal oxygen; but apoptosis cells decreased in hypxia/ZnPP group Conclusion: 1.PC12 cells could produce endogenic CO by hypoxia, thus ZnPP could make CO decrease. 2.Endogenic could cause most cells apoptosis by hypoxia earlier period; thus ZnPP might protect nerve cell by inhibiting HO and decreasing CO.