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。
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.
ObjectiveTo explore the protective effects of abdominal paracentesis drainage (APD) on pancreatitis-associated liver injury in the early phase of severe acute pancreatitis (SAP). MethodsOne hundred and fourteen consecutive patients with SAP, admitted to the General Hospital of Western Theater Command from January 2015 to January 2021, were included in this retrospective study. The patients were divided into the APD group (n=61) and the non-APD group (n=53) based on whether they underwent APD treatment within 72 h of admission. The variables including baseline data, liverfunction tests, inflammation indexes, severity scores and other variables of the two groups were statistically analyzed. ResultsThe hospital mortality in the APD group was lower than that in the non-APD group (8.2% vs. 22.6%, P=0.031). These severity scores (including APACHE Ⅱ score, Ranson score and modified Marshall score) and inflammation indexes (including C-reactive protein, interleukin-6, interleukin-1 and tumor necrosis factor-α) in the APD group were all lower than those in the non-APD group (P＜0.05). In terms of liver function related indexes, the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyl transpeptidase (GGT), total bilirubin (TBIL), and direct bilirubin (DBIL) after treatment in both two groups were significantly lower than those before treatment (P＜0.05). The levels of ALT, AST, TBIL and DBIL after treatment in the APD group were lower than those in the non-APD group (P＜0.05), and the levels of prealbumin and albumin after treatment in the APD group were higher than those in the non-APD group (P＜0.05), but there were no significant differences in the levels of alkaline phosphatase, GGT and 5′ -nucleotidase after treatment in the two group (P＞0.05). ConclusionFor SAP patients with ascitic fluid, application of APD can attenuate liver injury and improve liver function in the early stage of SAP.
Objective To evaluate the association between N-acetyltransferase 2 (NAT2) gene polymorphisms and the risk of antituberculosis drug-induced liver injury (ATDILI). Methods We searched the PubMed, Embase, Wanfang, China National Knowledge Internet and VIP databases to find case-control studies, with the last updated search being performed on June 2017. Odds ratio (OR) with 95% confidence interval (CI) was calculated to evaluate the strength of association. Results A total of 29 studies, involving 1 382 cases and 5 967 controls were included. The results of the Meta-analysis indicated that NAT2 slow acetylators were associated with increased risk of ATDILI compared with fast and intermediate acetylators [OR=3.08, 95%CI (2.44, 3.88), P<0.000 01]. Similar results were also found in subgroup analysis when stratified by ethnicity, isoniazid dosage and diagnostic criteria of ATDILI. Conclusion Individuals with NAT2 slow acetylators may have increased risk of ATDILI.
ObjectiveTo summarize the protective effect of peroxisome proliferator-activated receptor-beta (PPAR-β) in sepsis-induced liver injury and the mechanism, and to provide new ideas for the prevention and treatment of sepsis-induced liver injury.MethodRelevant literatures about protective effect of PPAR-β in sepsis-induced liver injury were collected and reviewed.ResultsPPAR-β played an important role in cell survival, anti-inflammatory, and anti-oxidation. It acted on a variety of pathophysiological processes, could reduce the activation of inflammatory factors, reduce the production of oxygen free radicals, and inhibit the expression of apoptotic proteins, as well as played an important role in anti-inflammatory, anti-oxidative, and anti-apoptotic.ConclusionPPAR-β can inhibit the activation of NF-κB, reduce the release of inflammatory factors, reduce apoptosis, and reduce liver injury by antioxidation, thereby reducing the mortality of sepsis-induced liver injury.
ObjectiveTo understand the latest development in lineage tracing techniques and their applications in the study of liver regeneration mechanisms. MethodA review of domestic and international literature on the application of lineage tracing techniques in liver regeneration was conducted. ResultsA variety of more reliable and advanced lineage tracing techniques had been developed, such as single-cell RNA sequencing, DNA barcode technology, etc., providing powerful tools for a deeper understanding of the mechanisms of liver regeneration. The marked progress had been made in identifying the origins of liver regeneration cells, identifying liver regeneration areas, and studying the mechanisms of liver regeneration after injury. The lineage tracing techniques help to understand the position and function of different types of liver cells within the liver structure, revealing the regenerative potential and contribution of different subpopulations of liver cells. Moreover, these techniques had supported the phenomenon of transdifferentiation between the hepatocytes and the bile duct cells under chronic liver injury conditions, aiding in understanding the specific roles of key signaling pathways in liver regeneration, such as Wnt/β-catenin, Hippo/YAP, and Notch signaling pathways.ConclusionsAlthough lineage tracing techniques have made marked progress in liver regeneration research, liver regeneration is a complex and important physiological process, and the technique still has limitations, such as challenges in marker specificity, longer research cycles and higher costs, potential limitations in translating from animal models to human clinical applications, inability to solve all questions about liver regeneration mechanisms, and ethical and legal issues. Therefore, more in-depth and comprehensive research is still needed to reveal more details of liver regeneration mechanism.
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.
Objective To investigate the protective effect of 4-phenylbutyric acid (PBA) on liver injury induced by severe acute pancreatitis (SAP) in rats and its possible mechanism. Methods Twenty-four SPF adult male Sprague Dawley rats were randomly divided into three groups: shame operation group (SO group,n=8), SAP group (n=8), and PBA group (n=8). SAP model was induced by retrograde injection of 5% sodium taurocholate (1 mL/kg) in biliopancreatic duct in SAP group and PBA group. PBA solution (50 mg/kg) was administeredvia intraperitoneal injection for 3 days prior to establishing models in PBA group. Rats were injected equivalent saline solution instead of PBA solution in SAP group and SO group. All rats were sacrificed at 12 h after modeling. Blood samples were collected by inferior vena cava puncture, and serum levels of amylase (AMY), alanine aminotransferase (ALT), and aspartate transaminase (AST) were measured using a fully automatic chemistry analyzer. The head of pancreas and right lobe of hepatic tissues were harvested and pathological examination was observed under the light microscope. Expressions of glucose-regulated protein 78 (GRP78), CCAAT/enhancer binding protein homologous protein (CHOP) and Caspase-3 in hepatic tissues were evaluated by immunohistochemistry assay. Results Compared with SO group, the serum levels of AMY, ALT and AST were significantly increased in SAP group (P＜0.05). The serum levels of ALT and AST in PBA group were significantly lower than those in SAP group (P＜0.05). There was no difference of the serum levels of AMY between in PBA group and SAP group (P＞0.05). Compared with SO group, the damages of the pancreas and liver tissues and the expressions of GRP78, CHOP and Caspase-3 in hepatic tissues were significantly increased in SAP group (P＜0.05). And the above indices in PBA group were significantly decreased when compared with SAP group. Conclusions PBA can alleviate severe acute pancreatitis-induced liver injury, and the mechanism may be associated with inhibition of endoplasmic reticulum stress (ERS) and reduction of hepatocyte apoptosis.
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 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.