Objective To summarize the role of nuclear factor kappa B (NF-κB) in the occurrence and progression of various sorts of liver injury. Methods Literatures on the structures, property of molecular biology and function of NF-κB, as well as its relationships with liver injury were collected and reviewed. Results NF-κB was an important nuclear factor existed in cells widely distributed in most cell types. The activation of NF-κB was induced by various sorts of liver injury. The activated NF-κB could affect the liver injury by regulating cytokines, adhesion molecules, and activating factor involving in immunologic reaction， inflammatory reaction and the apoptosis. Conclusion NF-κB plays an important role during the occurrence and progression of liver injury， and may become a new target in the treatment of liver injury.
【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.
目的探讨合并肝后静脉损伤的严重肝损伤时损伤静脉的显露和修复的方法。 方法本组肝右叶切除2例，肝右叶切除并直接修补肝后段下腔静脉1例，直接修补肝中静脉和肝正中裂2例，改良式全肝血流阻断修补肝和肝静脉8例，未发现出血部位行盲目修补2例。结果本组合并肝后静脉损伤15例，其中死于术中大出血4例，死于术后不可逆休克1例，痊愈10例。结论合并肝后静脉损伤时术前复苏、术中对损伤静脉的正确显露与修复是治疗的关键，改良式全肝血流阻断对修复肝后静脉损伤是一种有效方法。
The experimental models of chronic hepatic lesion of 40 rabbits were made by intra-abdominal injection of thioacetamide.The chronic hepatic lesion was confirmed by pathological examination and hepatectomies were performed in accordance with different measurements on each rabbit.The observations included indocyanine green retention rate,hepatic resection volume,and the outcomes of operations.The results showed that the mortality was correlative with the change of hepatic functions in the background of chronic hepatic lesion.The indocyanine green retention and the level of serum albumin are important parameters to indicate hepatic impairment.When the former was over 40% or the latter below 2.8g% the operative danger was high and the mortality was over 50%.In accordance with the classification of hepatic function,the preoperative functional state of liver were classified:grade A,B and C.the mortality of posthepatectomy were respectively 16.7%,3O%,and 72%.The multiple progressive regression equation is employed for calculating the postoperative outcome.The equation predicted the postoperative outcome with 88.9% accuracy.
Objective To investigate the effect of hepatocyte-l ike cells induced by CD34+ cells in vitro on the repair of the injured hepatic tissues of mice in vivo. Methods Mononuclear cells were isolated from umbil ical blood by density gradient centrifugation and enriched CD34+ cells were obtained. The cells were (1 × 105 cells/mL) cultured in serumfreemedium containing stem cell factor (SCF), hepatocyte growth factor (HGF), EGF, oncostatin M (OSM), bFGF (the concentration were 50, 20, 20, 10, 10 ng/mL respectively) in vitro for 10 days. Forty-eight 6-week-old female ICR mice werechosen to prepare l iver injury model by injecting carbon tetrachloride and 2-acetylamionoflu-orene. The mice were randomly divided into two groups (n=24 per group): the experimental group, the cultured cells were injected into the mice through the tail vein; the control group, the equivalent serum-free medium was injected. Six mice from each group were killed at 7, 14, 21, and 28 days after operation to receive HE staining, PCR gel electrophoresis, immunohistochemistry staining, and hepatic function detection. Results HE staining: the morphology of injured hepatic tissues in the control group recovered to normal 28 days after operation, while in the experimental group, it recovered to normal 14 days after operation. PCR gel electrophoresis and immunohistochemistry staining: the cells expressing human serum albumin were detected in the hepatic tissue of the experimental group at each time point after operation; while in the control group, no such cells were detected within 28 days after operation. Hepatic function detection: the activity of alanine aminitransperase in the control group recovered to normal 14 days after operation; the mean activity of aspartate aminotransferase of two groups failed to recover within 28 days. Conclusion The hepatocyte-l ike cells induced by CD34+ cells in vitro can promote the morphological and functional recovery of the injured hepatic tissue in mice. Moreover, it can be transformed into human-derived hepatic cells in l iver-injured mice.
Objective To investigate the protective effect of melatonin on rat liver injury induced by bile duct ligation. Methods Sixty-four rats were randomly divided into four groups：control group （CN group， n=16）， shamoperation group （SO group， n=16）， bile duct ligation group （BDL group， n=16）， and bile duct ligation with melatonin injection （BDL＋MT group， n=16）. The model of obstructive jaundice was done by ligation of the common bile duct. Melatonin was injected daily （0.5 mg/kg） via peritoneal cavity from 1 d before the operation to 7 d following oper-ation. On day 4 and 8 after the ligation， the plasma levels of total bilirubin （TBIL）， alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， gamma glutamyl transferase （GGT）， and alkaline phosphatase （AKP） were measured by routine methods. Malonaldehyde （MDA）， superoxide dismutase （SOD）， glutathione （GSH）， catalase （CAT）， and glutathione peroxidase （GSH-Px） in the liver tissue were determined by spectrophtometry， too. Hepatocytes apoptosis was analyzed by terminal deoxynucleotidyl transferase-mediated deoxynuridine triphosphate nick-end labeling （TUNEL） assay. Results Compared with the CN group and SO group， the levels of TBIL， ALT， AST， GGT， and AKP in the plasma， the content of MDA in the liver tissue， and the apoptosis index （AI） in the hepatocyte markedly increased （P＜0.05， P＜0.01）， the content of GSH and the activities of SOD， CAT， and GSH-Px in the liver tissue markedly decreased（P＜0.01） in the BDL group. Compared with the BDL group， the levels of TBIL， ALT， AST， GGT， and AKP in the plasma， the content of MDA in the liver tissue， and the AI in the hepatocyte markedly decreased （P＜0.01）， the content of GSH and the activities of SOD， CAT， and GSH-Px in the liver tissue markedly increased （P＜0.01） in the BDL＋MT group. In the BDL group， the level of MDA in the liver tissue and the levels of TBIL， ALT， AST， GGT， and AKP were positively correlated （P＜0.01）， the content of GSH and the activities of SOD， CAT， and GSH-Px in the liver tissue and TBIL， ALT， AST， GGT， and AKP were negatively correlated （P＜0.01）. The level of MDA in the liver tissue and AI in the hepatocyte was positively correlated （P＜0.01）. The content of GSH and the activities of SOD， CAT， and GSH-Px in the liver tissue and AI were negatively correlated （P＜0.01）. Conclusions The participation of free radical of oxygen in the pathogenesis and severity of cholestasis produced by the acute obstruction of the extra-hepatic biliary duct is likely. The result of the present study indicates that melatonin exerts a protective effect on cholestatic liver injury in rats with BDL. The mechanism of melatonin’s protection on hepatocyte may be through its antioxidant action and by inhibiting hepatocyte apoptosis.
【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.
目的 探讨肝外伤的早期诊断与治疗效果。方法 回顾性分析采用不同手段治疗的各种肝外伤52例患者的临床资料。结果 男30例，女22例，腹部开放性伤18例(34.6%)，腹部闭合性伤34例(65.4%)，腹腔穿刺阳性率为92.3%(48/52)，超声检查阳性率为88.9%(40/45),CT检查阳性率为100%(50/50)。非手术治愈16例； 手术治疗36例(包括3例因非手术治疗而中转手术)，手术方式包括单纯缝合止血、大网膜填塞+缝合止血、明胶海绵填塞+缝合止血、清创性肝切除、腹腔镜探查+缝合止血。治愈率为96.2%(50/52)，死亡率为3.8%(2/52)。2例死于肝内血管损伤大出血。结论 CT检查进行肝损伤分级和血流动力学状态是决定治疗方式的关键，腹腔镜探查是明确诊断的良好微创方法。
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 the protective effect of hesperdin (HDN) on acetaminophen (APAP)-induced acute liver injury in mice. MethodsForty-eight male BALB/c mice were randomly divided into six groups:normal group, model group, HDN (the doses respectively were 500, 250 and 125 mg/kg) group and bifendate group. The HDN group was separately intragastrically given different doses of hesperidin for ten days. The bifendate group was given bifendate. Acute liver injury was induced by injecting APAP (150 mg/kg) in all mice except those in the normal group. After 16 hours, all mice were sacrificed. Serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured. The contents of glutathione (GSH) and malondialdehyde (MDA) in liver homogenates were determined. Pathological changes in hepatic tissue were observed under an optical microscope. The expression of high mobility group protein B1 (HMGB1) in hepatic tissue was measured by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. ResultsHDN could significantly reduce serum ALT, AST, liver homogenate MDA levels, improve liver tissue GSH activity and the liver injury was lightened. By RT-PCR and immunohistochemistry, it showed that HDN could inhibit the releasing and expression of HMGB1. ConclusionHDN protects mice from acetaminophen-induced liver injury possibly via mechanisms related to inhibition of the expression and releasing of HMGB1.