| Objective: By setting up the model of Paraquat Poisoning rats to explore and promote the protection function and mechanism of liver cells auxin(p HGF)on acute chemical liver injury rats.Methods: Selecting 90 healthy SD rats(male and female equal)into three groups randomly: normal group,model group and treatment group,30 rats each.Model group and treatment group were injected PQ(25mg/kg)for one time,and treatment group was given p HGF(50g/kg)intraperitoneal injection once a day for up to the seventh day after the above process.The general situation of rats in each group was observed.On the first,the third and the seventh day time,the same number of rats were given intraperitoneal injection,rats were sacrificed after left ventricular injection,the samples of arterial blood,liver were collected to detect erum ALT,AST,SOD,TNF-? and NO.The pathological changes and expression of apoptosis related protein Bcl-2 and Bax in rat liver tissues were observed.Results:(1)General situation: the model group had poisoning symptoms after 1 to 2 hours,the most obvious poisoning performance happened in the third day,symptoms gradually eased in the seventh day.The p HGF poisoning symptoms in treatment group decreased after intervention compared with model group.(2)Serum ALT,AST value change: compared with the normal group,the ALT and AST levels in model group were significantly increased at different time points,and the difference was statistically significant(p<0.01).Compared with the model group,the ALT and AST levels in treatment group were decreased at different time points,and the difference was statistically significant(p<0.05),especially on the third day(p<0.01).(3)The levels of SOD,TNF-? and NO: compared with normal group,the serum SOD level in model group at each time point were significantly decreased,the difference was statistically significant(p<0.01).Compared with model group,the serum SOD level in treatment group at each time point increased,the difference was statistically significant(p< 0.05),especially in the third day(p<0.01).Compared with the normal group,the level of serum TNF-? was significantly increased at different time points,and the difference was statistically significant(p<0.01).Compared with model group,the serum TNF-? level in treatment group was significantly decreased,the difference was statistically significant(p<0.01).Compared with normal group,the level of serum NO was significantly increased at different time points,and the difference was statistically significant(p<0.01).Compared with model group,the serum NO level in treatment group was no statistical difference in the first days(P >0.05),and decreased in the third day and the seventh day(p<0.05).(4)The liver tissue HE staining results: the cell size,morphology,the structure of hepatic lobule and hepatic cord arrangement were normal in normal group.Liver cell swelling was obviously,and visible eosinophilic cytoplasm and vacuoles degeneration,local cell apoptosis and liver cells dotted and focal necrosis in model group.Compared with model group,The liver tissue pathology in treatment group reduced to some degrees,and no focal necrosis in the liver.(5)The liver tissue Bax,Bcl-2 protein expression: small amount of Bax protein could express in the in the liver sinus and central vein in normal liver tissue,small amount of Bax protein could invisible in the in the liver sinus and liver cell plasma.Compared with normal group,the Bax and Bcl-2 protein expression level in model group at each time point were significantly increased,the difference was statistically significant(p<0.01).Compared with model group,the Bax protein expression level was increased and the Bcl-2 protein expression level in treatment group was decreased at each time point,both the difference were statistically significant(p<0.05).Conclusions: p HGF has protective effects on acute chemical liver injuries induced by paraquat poisoning in rats,and its mechanism may be related to reduce the degree of injury by reducing oxidative damage,reducing inflam Mation and inhibiting apoptosis. |
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