(2) EGF of different doses (50, 100, 500, and 1000ng/ml) added to the medium prior to acetaminophen could reduce hepatocyte injury in a dose-dependent manner.
Conclusion: The fragments of C 3 and C 5 in ZAHS can stimulate KC to secrete NO, by which they can mediate hepatocyte injury, which maybe the potential mechanism of liver injury mediated by complements in some pathological condition.
Cadmium (Cd)-induced cytotoxicity and intracellular Ca2+ alteration ([Ca2+]i) in hepatocytes and intervention with selenium (Se) were studied to discuss mechanism of Cd-induced hepatocyte injury and protective effect by Se.
There had significant difference between the contents of HBV-DNA copies and the severe degree of hepatocyte injury(P<0.05); The contents of HBV-DNA copies had no correlation with the severe degree of hepatocyte injury(P>0.05).
Study one The establishment of the hepatocyte injury model made on BRL-3 A rat hepatocyte induced by CCl4Methods: rat hepatocytes are divided into control group, 5mmol/L CCl4 group, 10mmol/L CCl4 group, 15mmol/L CCl4 group, 20mmol/L CCl4 group, the culture medium without serum is added into the control group cells, the CCl4 with corresponding concentration is added into cells.
Methods:40 male rats were divided into 4 groups, including group A、B、C and D. Acute hepatocyte injury was induced in all male rats by CCL4 administration about 4 weeks.
H2O2 positive precipitation on outer plasma membrane of hepatocytes was obviously increased at 3 h,and disappeared at 24 h but hepatocyte injury was very severe at this time,at 48 h hepatocyte recovered through regeneration.
Conclusion: The detection of serum glutamate dehydrogenase is of significance in early clinical diagnosis and prediction of hepatic disease, especially in hepatocyte injury and necrotic hepatopathy.
It was shown that PGI2 could circumvent the augmented catabolic rate of 4,5-phosphatidyl inositol-diphosphate (PIP2) in CCl4 induced hepatocyte injury.
Thus, our study demonstrates that the serum IL-6 level is a possible marker for identifying the clinical status in acute hepatitis and that this cytokine may have some roles in hepatocyte injury.
Furthermore, we found that a significant correlation between serum IL-6 level and prothrombin time existed in these patients and that the elevated serum IL-6 returned to a normal range after recovery from their hepatocyte injury.
To study the mechanisms of hepatocyte injury, we examined serum interleukin-6 (IL-6) level in acute hepatitis patients.
Oxidative stress may initiate significant hepatocyte injury in subjects with fatty liver.
To understand the relationship between the expression of HBV-markers andinjury of hepatocytes,we have examined HBsAg,HBcAg in liver tissue with PAPmethod and HBV-markers in serum with ELISA method of 70 patients with CH-B.The results showed that the expression patterns of HBsAg could be divided into 4types,those of HBcAg into 3 types.The positive percentages of HBsAg and HBcAgin CPH were higher than in CAH under which the expression patterns were notconsidered.When considering the expression patterns,positive...
To understand the relationship between the expression of HBV-markers andinjury of hepatocytes,we have examined HBsAg,HBcAg in liver tissue with PAPmethod and HBV-markers in serum with ELISA method of 70 patients with CH-B.The results showed that the expression patterns of HBsAg could be divided into 4types,those of HBcAg into 3 types.The positive percentages of HBsAg and HBcAgin CPH were higher than in CAH under which the expression patterns were notconsidered.When considering the expression patterns,positive percentages of mem-brane type of HBsAg and cytoplasmic membrane type of HBcAg in CAH were higherthan in CPH.It was suggested that the expressions of HBV-Ag of these types wereconsistent with the degree of hepatocytic injury.The combination positive percen-tages of HBsAg+HBeAg+Anti-HBc,and HBsAg+Anti-HBc in serum in CAH,which indicated HBV replication,were higher than in CPH.The positive percen-tage of HBeAg increased along with the increase of SGPT.It revealed that HBV-markers in serum which indicated HBV replication could also reflect the conditionof hepatocyte injury.Target antigen and relation between the expression of HBV-markers in liver tissue and in serum were discussed.
We studied the acetaminophen (AAP)-induced primary cultured rat hepatocyte injury and its mecha-nism. The results showed that in monolayer-culture condition, AAP-induced lactic dehydrogenase (LDH)escape from the hepotocytes happened only when intracellular GSH was significantly reduced. This sug-gested the intracellular GSH depletion might be the causc of AAP-induced hepatocyte injury. By directdetermination of GSH and [Ca~(2+)f]c synchronously, we demonstrated for the first time that AAP couldcause...
We studied the acetaminophen (AAP)-induced primary cultured rat hepatocyte injury and its mecha-nism. The results showed that in monolayer-culture condition, AAP-induced lactic dehydrogenase (LDH)escape from the hepotocytes happened only when intracellular GSH was significantly reduced. This sug-gested the intracellular GSH depletion might be the causc of AAP-induced hepatocyte injury. By directdetermination of GSH and [Ca~(2+)f]c synchronously, we demonstrated for the first time that AAP couldcause GSH depletion and [Ca~(2+)f]c elevation in suspensionn-cultured hepatocytes. Dithiothreitol (DTT)could prevent the GSH depletion induced by AAP and completely antagonize the AAP-induced elevat-ion of [Ca~(2+)]c. It indicated that [Ca~(2+)f]c elevation could be the direct cause of AAP-induced rathepatocyte injury and that the elevation of [Ca~(2+)f]c might be linked with GSH depletion.
We have studied pathologically 36 cases of carcinomas of extrahepatic bile ducts,ofwhich 27 were surgically removed,9 from a autopsy series.Of all 36 cases 24 were carcinomas aris-ing in the proximal portions of extrahepatic bile ducts.The gross appearence could be classified as inrta-luminal papillary and wall infiltrating carcinomas respectiverly.Histoloigcally,it is classified as 4types:(1)papillary adnocarcinoma with intraluminal growth;(2)well differentiated adnocarcino-ma;(3)poorly differentiated adenocarcinoma;(4)carcinoma...
We have studied pathologically 36 cases of carcinomas of extrahepatic bile ducts,ofwhich 27 were surgically removed,9 from a autopsy series.Of all 36 cases 24 were carcinomas aris-ing in the proximal portions of extrahepatic bile ducts.The gross appearence could be classified as inrta-luminal papillary and wall infiltrating carcinomas respectiverly.Histoloigcally,it is classified as 4types:(1)papillary adnocarcinoma with intraluminal growth;(2)well differentiated adnocarcino-ma;(3)poorly differentiated adenocarcinoma;(4)carcinoma simplex.The latter 3 all showed infil-trating growth into the duct wall.Invasion of nerves were observed in 24 cases.Carcinomas arising inthe proximal portion of the bile ducts may extend into the liver.In 9 cases intrahepatic bile stasis wasfound in partially removed liver tissue which also showed various degrees of hepatocyte injury(atro-phy,degeneration and necrosis).The pathological features of the carcinomas of extrahepatic bileducts,their biological behavior and clinico-pathological correlation was discussed.
hepatocyte injury
肝细胞损伤
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