| Objective: Acute liver injury refers to the sudden occurrence of massive liver cell damage in a short period of time by radiation injury,drug intoxication,immune injury,viral infection and other causes in patients without original chronic liver disease leading to impaired liver function,which may subsequently lead to adverse consequences such as liver failure,coagulation dysfunction,hepatic encephalopathy,etc.Acute liver injury induced by D-aminogalactose(D-Gal N)is similar to human The pathomorphological features of viral hepatitis are very similar.In this study,we investigated whether Epimedium(ICT)has a hepatoprotective effect on D-Gal N-induced acute liver injury and how its action is related to the PI3K/AKT signaling pathway to provide a new strategy for the treatment of acute liver injury.Methods: Thirty-five SD male rats were randomly divided into 5 groups of 7 rats each(normal group,model group,silymarin 120 mg/kg group,ICT1 mg/kg group and ICT2 mg/kg group)with D-Gal N hydrochloride aq modeling.The drug was administered by transoral gavage,and the three dosing groups were given the corresponding drug at the standard of 10 ml/kg,and the other two groups were given distilled water requiring the same volume of drug as that given to the first three groups for 9days.After 2 h of the last administration,the other four different groups excluding the normal group were injected intraperitoneally with D-aminogalactose hydrochloride solution(500 mg/kg)at 5 ml/kg to establish an acute liver injury model in rats,and some liver tissues were collected and serum was extracted from the blood of the eyes.Pathological histology was scored according to the following scoring rules: 0 points for no abnormalities in morphological structure;slightly enlarged hepatocyte cord gap,and the inflammatory cell infiltration in the pool area was scored as 1 point;the hepatocellular cord gap was moderately enlarged,and a small number of inflammatory cell infiltrates appeared in the sink area was scored as 2 points;the hepatocellular cord gap was significantly enlarged,and the inflammatory cell infiltration such as more neutrophils appeared in the mandula region was scored as 3 points;the hepatocellular cord gap was significantly enlarged,and a large number of inflammatory cell infiltrates such as neutrophils appeared in the mantle area were scored as 4 points.The levels of ALT,AST,ALP,TBIL,γ-GT in serum,MDA,ROS,SOD,CAT and GSH-Px in liver tissue were measured by biochemical method;and the contents of TNF-α,IFN-γ,IL-1β,IL-6 and NO in serum were measured by ELISA kit.;AKT,PI3 K,p-PI3 K and other protein expression levels in liver tissues were measured by western blot.Immunohistochemical staining verifies the expression of Bcl-2 with Bax in liver tissue.Results:Compared with the model group,the serum levels of ALT,AST,TBIL,ALP and γ-GT were significantly decreased in ICT treated rats(P < 0.05 or P < 0.01);the activities of MDA and ROS in the liver tissue of ICT treated rats were significantly decreased(P < 0.05 or P < 0.01);the activities of SOD,GSH-Px and CAT in the liver tissue of ICT treated rats were significantly increased(P < 0.05 or P < 0.01);the contents of TNF-α,IL-1β,IL-6,IFN-γ and NO in the serum of ICT treated rats were significantly decreased;the protein expression levels of p-PI3 K,p-AKT and Bax in the liver tissue of ICT treated rats were decreased,and the expression of Bcl-2 was increased.Among them,Immunohistochemical staining results are the same as above,the ICT 2 mg/kg group had the best results.Conclusions: It is evident that ICT has antioxidant and apoptosis-reducing effects on acute liver injury induced by D-Gal N hydrochloride aq in SD rats,and the rationale for this effect may be related to the inhibition of PI3K/AKT signaling pathway. |
PDF Full Text Request