The Impact Of Macrophage Cycle Of Burned Rat Skin Intervened By Hydrogen Sulfide

Objective: To explore the effect of H2 S for burned rats skin macrophages cycle. Method: Macrophages after burn wound in rats were the research object, 78 health y SD rats were divided into 13 groups(normal control group, normal saline group 1, 2, 3, Na HS group 1, 2, 3, PPG group 1, 2, 3, Na HS + PPG group 1, 2, 3, the normal control group received no intervention, the rest of the groups were form ed model of 5% partial thickness burns, the rats in the blank control group we re timely intraperitoneal injected saline one time every day; the rats in the Na HS group were timely intraperitoneal injected Na HS solution one time every d ay;the rats in PPG group were timely intraperitoneal injected propargylglycine one time daily;the rats in Na HS+PGG group were timely intraperitoneal injecte d Na HS solution and propargylglycine one time daily. On the day of 3,7,14 to take macrophage from the burned rats to culture, applied flow cytometry instru ment to analyze the change of macrophages cycle in the wound tissue.Results: The percentage of macrophages at the G1 phase of normal group were higher than normal saline groups, there was statistically significant differenc e; At the same point in time, the significantly difference statistically between Na HS g roup(N3, N7, N14) and normal saline group(NS3, NS7, NS14); At the same time point, there was significantly difference statistically between PPG group(P3, P7, P14) and normal saline group(NS3, NS7, NS14);At the same time point, there was si gnificantly difference statistically between Na HS group(N3, N7, N14) and Na HS + P GG group(N + P3, N+ P7, N + P14); At the same time point, there was significant ly different statistically between PPG group(P3, P7, P14) with Na HS + PPG grou p(N + P3, N + P7, N + P14). Conclusion: Wound macrophages will accelerate apoptosis after burn; Small dose of exogenous H2 S could reduce the apoptosis of macrophage on burned wound; PPG could increase the apoptosis of macrophages on burned wound through inhibiting the generation of endogenous H2 S.