【Abstract】Objective To explore the distribution and migration of oval cells in progressive hepatic injury. Methods Sixty SD rats were divided into the control group (n=20) and experimental group (n=40). After the establishment of hepatic carcinoma models, C-kit was continuously detected by immunohistochemistry and the liver pathologic changes were regularly observed by optical microscopy.Results The hepatic surface was smooth with eumorphism in histology in the control group. The C-kit positive cells were occasionally found. In the experimental group, the oval cells with C-kit positive were initially discovered in the portal regions in the second week, and these cells proliferated along the bile duct epithelia. With the hepatic injury becoming more serious, the oval cells extended into the hepatic lobular regions from the portal regions. When hepatocellular carcinoma occurred，the majority were mixed carcinomas, and the oval cells were found inside and outside the carcinoma nodes. In this period, the most of C-kit positive cells still located in the portal regions. Conclusion ①The oval cells are the most sensitive cells for the hepatic injury. ②The oval cells which migrate unruly participate in the formation of hepatic pseudolobules. ③The oval cells play an important role in hepatocarcinogenesis.
Objective To explore the regulating mechanism of hepatic injury in obstructive jaundice (OJ). Methods①Rat hepatocytes were isolated by in situ collagenase perfusion and primary culture. Hepatocytes were pretreated with various concentrations of protein kinase C (PKC) agonist parsmeae (PMA) and inhibitor chelerythrine for 20 min. After pretreatment, 50 μmol/L glycochenodeoxycholate (GCDC) was added. Cells were next detected by FCM and TUNEL.②Experimental obstructive jaundice was induced by double ligation of the bile duct (BDL), BDL for 3, 7, 14, 21days.We detected apoptotic status in liver with TUNEL and PKC protein in liver with immunohistochemistry method. Results①PMA increased GCDCinduced apoptosis and chelerythrine decreased GCDCinduced apoptosis in a concentrationdependent manner. ②The apoptotic rate of liver was related to time of OJ. Apoptosis index (AI) was the highest in 14day bile duct ligation. The ber PKC expression, the more number of apoptotic cells in OJ.Conclusion PKC takes part in the regulation and the occurrence and progression of hepatic injury in OJ.
To investigate the mechanisms of hepatic injury after biliary obstruction. After a rat model of complete biliary obstruction(CBO) was induced, hepatocyte mitochondria was isolated and the calcium content of mitochondria, the contents of liver malondialdyhyde (MDA) and superoxide dismutase (SOD), the levels of serum T-Bil, ALT, ALP and GGT were measured in each group. Results: After CBO, mitochondrial calcium content, liver MDA and serum T-Bil, ALT, ALP, GGT became increased progressively, compared with control group (Ｐ＜0.05); the liver SOD was decreased markedly (Ｐ＜0.05). Mitochondrial calcium content was highly positively correlated with liver MDA content, serum ALT and ALP, r values were 0.967, 0.924 and 0.919 respectively (Ｐ＜0.01). The liver MDA content was highly positively correlated with serum ALT and ALP, r values were 0.949 and 0.843 respectively (Ｐ＜0.01). Conclusions: Mitochondrial calcium overload and liver lipid peroxidation may be the important mechanisms of hepatic injury induced by biliary obstruction.
【Abstract】Objective To study the expression of cyclooxygenase-2 (COX-2) in hepatic inflammatory reaction of rats with sepsis, and to explore a new way of protecting hepatic cell. Methods Fifty-four Wistar rats were randomly divided into 3 groups: sham operation group, sepsis group and NS398 group. All rats were subjected to cecal ligation and puncture (CLP) or sham operation. RT-PCR was used to determine COX-2 mRNA expression, serum IL-6, TNF-α and IL-10 were determined by ELISA; and ALT and AST and liver pathological changes were determined in 3 groups and at different times (3, 6, 12 and 24 h) respectively. Results ①The expression of COX-2 mRNA of hepatic tissue was low in sham operation group. It obviously enhanced after CLP at 3 h and peaked at 6 h. High expressions were showed at 12 and 24 h. In NS398 group, it was lower than that of sepsis group at the same time, but higher than that of sham operation group. ②Serum ALT, AST and IL-6, TNF-α were increased in sepsis group than those of sham operation and NS398 group (P＜0.05)； Serum IL-10 was higher in NS398 group than that of sham operation and sepsis group (P＜0.05). ③Hepatic pathological injury extenuate after injected with NS398. Conclusion COX-2 may play an important role in hepatic injury with sepsis.
Objective To report the progression of breviscapine’s protective effect to hepatic ischemia-reperfusion injury. Methods Pertinent literatures and journal articles published in recent years were reviewed, and the progression of breviscapine protecting hepatic ischemia-reperfusion injury in the experimental and clinical research were analyzed and summarized. Results The role of breviscapine is considerable extensive. It can protect hepatic ischemia-reperfusion injury by anti-oxyradical and anti-lipid peroxidation, inhibiting mitochondrial damage, intracellular calcium overload, intra-thromboxane and apoptosis, improving microcirculation, and so on. Conclusion Breviscapine plays a protective role in hepatic ischemia-reperfusion injury, and it will be of great value to application and research.
ObjectiveTo investigate pathological changes of liver and risk factors for hepatic injury after trauma, in order to provide the instructions for clinical liver transplantation and accumulate the pathological data. MethodsWe retrospectively analyzed the clinical data of 142 patients who died after trauma between January 2010 and December 2014. Based on whether the patients had acute liver damage before dying, they were divided into two groups. The observation group had liver damage before dying, while the control group had not. Combined with the details of trauma, clinical data and autopsy results, we statistically analyzed the pathological changes of liver and risk factors for acute liver damage, including age, gender, trauma kind, trauma site, interval between trauma and hospitalization, damage degree, length of hypotension, the use of more than two vasopressors, large amount of blood transfusion, and complication of shock, infection, or underlying diseases. According to injury severity score (ISS) system, the damage degree was divided into mild damage (ISS<16), moderate damage (ISS≥16 and<25), and severe damage (ISS≥25). ResultsAmong the 142 patients, there were 45 in the observation group with varying degrees of liver cell necrosis, among whom there were 8 mild cases, 14 moderate and 23 severe. There were 97 patients in the control group without acute liver damage, and no significant changes were found in their hepatic tissue. Liver damage was not correlated with age, gender, damage kind, damage site, or pre-hospital time (P>0.05), while it was corrected with the degree of damage, time of hypotension (≥0.5 hour), the use of more than two vasopressors, large amount of blood transfusion (2 000 mL/24 hours), and combination of shock, infection, and other disease except for cardiac and pulmonary diseases (P<0.05). ConclusionWhen using donor livers from patients dying from trauma for transplantation, physicians should be alert to the factors discussed previously which can increase the risk of hepatic injury. Biopsy is useful to assess the suitability of donor livers prior to transplantation.