Resveratrol Alleviates Hepatic Fibrosis in Associated with Decreased Endoplasmic Reticulum Stress-Mediated Apoptosis and Inflammation.

Hepatic fibrosis (HF) is the typical response to chronic liver disease and is characterized by deposition of abundant extracellular matrix. The aim of the present study was to investigate the protective effect of resveratrol (RSV) in a CCl4-induced rat model of HF. We demonstrate that the administration of RSV effectively improves liver function and ameliorates liver fibrosis by reducing collagen deposition and reversing the expression of COL1A1 and PPAR-γ. Treatment efficacy of RSV could be attributed to reversed epithelial-mesenchymal transition progress with upregulated expression of E-cadherin and downregulated N-cadherin, vimentin, and α-SMA. Moreover, RSV significantly decreased the levels of endoplasmic reticulum stress (ERS)-related proteins CHOP; Bip; cleaved caspase-3, caspase-7, and caspase-12; Bax; and Bak while promotes the expression of anti-apoptosis protein Bcl2. The important role of ERS in HF was confirmed by using 4-PBA, an ERS inhibitor, which markedly ameliorated CCl4-induced HF. Further, mechanistic studies demonstrated that RSV significantly decreased CCl4-induced transforming growth factor-ß synthesis and inflammatory factor (tumor necrosis factor-α and interleukin-6) expression and reduced the inflammation of hepatic stellate cells by inhibiting the NF-κB pathway in vivo and in vitro. In conclusion, the results suggested that RSV ameliorated HF in associated with decreased ERS-induced apoptosis and inflammation in rats.

Baicalin attenuates liver hypoxia/reoxygenation injury by inducing autophagy.

The aim of the present study was to explore the effect of baicalin on liver hypoxia/reoxygenation (H/R) injury and the possible mechanism involved. A cellular H/R model was established and cells were treated with 50, 100 and 200 µmol/l baicalin. Following reoxygenation for 6 h, cell viability, lactate dehydrogenase (LDH), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), caspase 3 and cleaved caspase 3 were assessed. Furthermore, levels of endoplasmic reticulum stress markers binding of immunoglobulin protein (BIP) and CCAAT/enhancer-binding protein homologous protein (CHOP) and autophagy markers microtubule-associated proteins 1A/1B light chain 3B (LC3) and beclin 1 were measured. To confirm the involvement of autophagy in baicalin-mediated attenuation of H/R injury, the autophagy inhibitor 3-methyladenine (3-MA) was administered. The results revealed that baicalin administration increased cell viability and decreased LDH levels, most notably at a dosage of 100 µmol/l. Baicalin pretreatment also downregulated the expression of caspase 3, cleaved caspase 3 and Bax, while upregulating the expression of Bcl-2. Furthermore, BIP and CHOP were decreased while LC3 and beclin-1 were significantly increased by baicalin pretreatment. Inhibiting autophagy using 3-MA, resulted in a significant decrease in LC3-II, beclin-1 and LDH, as well as increase in the expression of BIP, CHOP, caspase 3, cleaved caspase 3 and Bax. Bcl-2 and cell viability were also decreased. In conclusion, the results of the present study indicate that baicalin exerts a protective effect on liver H/R injury and this may be achieved via the induction of autophagy.

Emodin alleviates CCl4­induced liver fibrosis by suppressing epithelial­mesenchymal transition and transforming growth factor­ß1 in rats.

Liver fibrosis is a chronic disease that exhibits a complicated pathophysiology. It is characterized by the deposition of the extracellular matrix. Emodin, an active constituent isolated from rhubarb, has antibacterial, immunosuppressive and anti­inflammatory effects. In the present study, the mechanism through which emodin alleviates liver fibrosis in rats was investigated. A rat model of liver fibrosis was generated by administering CCl4 via subcutaneous injection twice a week for 12 weeks. Emodin or sodium carboxymethylcellulose (CMC), as the vehicle, were intragastrically administered daily. After 12 weeks, the liver function index was examined by blood analysis, histopathological scores of fibrosis was determined by hematoxylin and eosin staining and level of collagen deposition was examined by Masson staining. In addition, protein and RNA samples were collected for further analysis. The results of the present study revealed that emodin significantly reduced the liver function index and level of collagen deposition in a dose­dependent manner. Furthermore, emodin reduced the expression of transforming growth factor­ß1 (TGF­ß1) and the phosphorylation levels of mothers against decapentaplegic homolog 2/3, and inhibited the CCl4­induced downregulation of E­cadherin and upregulation of the mesenchymal markers, fibronectin and vimentin. The expression levels of TGF­ß1, Snail family transcriptional repressor (Snail) 2, Snail, twist­related protein 1 and zinc finger E­box­binding homeobox (ZEB)1 and 2 mRNA were significantly decreased in emodin­treated groups compared with the untreated control. Collectively, the results of the present study suggested that emodin may exert antifibrotic effects via the suppression of TGF­ß1 signaling and epithelial­mesenchymal transition.

miR-153 enhances the therapeutic effect of gemcitabine by targeting Snail in pancreatic cancer.

Pancreatic cancer (PC) is one of the most lethal cancers, with an overall 5 years survival rate of <5%. The clinical benefit of gemcitabine based chemotherapeutic strategy on PC was limited by its high drug resistance rate. Snail, one of the master regulators of epithelial-mesenchymal transition, has been implicated in the progression of various cancers. However, whether it is also linked to the development of chemosensitivity to gemcitabine in PC is unknown, and the regulatory pathways controlling Snail also need to be explored. Cell apoptosis analysis was performed using flow cytometry assay. Quantitative real-time PCR was used to investigate the level of microRNA and the mRNA expression of its target, Snail. Snail expression was measured by immunoblotting and immunohistochemistry. A xenografted tumor model was used to test the in vivo effects of miR-153 on chemosensitivity to gemcitabine. The results of this study demonstrated the decrease of miR-153 expression in PC tumor tissue, which is correlated with a poor prognosis. miR-153 mimic transfection enhanced gemcitabine sensitivity in gemcitabine-resistant PC cells, while downregulation of miR-153 decreased gemcitabine sensitivity. In addition, miR-153 was found to target the 3'-UTR of Snail mRNA. Furthermore, we found that the increase of apoptosis in gemcitabine-resistant PC cells resulted from miR-153 mimic transfection was reversed by overexpression of Snail. miR-153 reverses the resistance of PC cells to gemcitabine by directly targeting Snail, and it may be a potential novel therapeutic target for overcoming gemcitabine resistance in human PC.

PP4R1 accelerates cell growth and proliferation in HepG2 hepatocellular carcinoma.

Hepatocellular carcinoma (HCC), as the fifth most common cancer worldwide, has become the third leading cause of cancer-related deaths. It is reported that protein phosphatase 4 (PP4) is an essential protein for nucleation, growth, and stabilization of microtubules in centrosomes/spindle bodies during cell division. Besides, previous studies have identified protein phosphatase 4 regulatory subunit 1 (PP4R1) as a constitutive interaction partner of PP4 catalytic subunit PP4C. The PP4C-PP4R1 PP4 complex plays a role in dephosphorylation, regulation of histone acetylation, and NF-κB activation. However, little is known about the pathological functions of PP4R1 in human cancers. Thus, in order to investigate how PP4R1 functions in human HCC, two common hepatocarcinogenesis HCC cell lines HepG2 and SMMC-7721 were employed, transduced with recombinant lentivirus expressing PP4R1 short hairpin RNA. Compared with the controls, the cells treated with Lv-shPP4R1 showed a significant decrease in cell proliferation and colony formation. The results of flow cytometry showed that the knockdown of PP4R1 caused HepG2 cells arrest at G2/M phase in the cell cycle. Furthermore, the transduction of Lv-shPP4R1 into HepG2 cells led to the inactivation of two major mitogen-activated protein kinase signaling cascades: p38 and c-Jun N-terminal kinase (JNK), indicating that PP4R1 could promote cell proliferation, which might be regulated by p38 and c-Jun N-terminal kinase pathways. In a word, this study highlights the crucial role of PP4R1 in promoting HCC cell growth, which might elucidate the pathological mechanism of HCC.

Butyrate protects rats from hepatic ischemia/reperfusion injury.

BACKGROUND: Hepatic ischemia/reperfusion (HI/R) injury is a common pathologic process caused by many clinical settings, such as liver resection, liver transplantation, hypovolemic shock and trauma. The use of butyrate, which acts as a four-carbon fatty acid, normally produced by bacterial fermentation of fiber in mammalian intestines, provides anti-oxidant and anti-apoptotic effects. METHODS: Male Sprague-Dawley (SD) rats model of HI/R were subjected to a partial (70%) hepatic ischemia for 45 minutes (min) after pretreatment with either saline or butyrate, followed reperfusion. 30 rats were randomly allocated to three main experimental groups (n = 10 each): (1) The sham-operated group underwent laparotomy without hepatic ischemia. (2) Butyrate was injected into the tail vein in the butyrate group 30 min before HI/R. (3) The control group underwent the same procedure as the butyrate group but with administration of physiological saline. Rats from each group were randomly euthanized to collect blood and liver samples. RESULTS: Butyrate treatment markedly improved hepatic function and histology, as indicated by reduced transaminase levels and ameliorated tissue pathologic changes. SD rats that received butyrate displayed reduced HI/R injury compared with controls. Use of butyrate reduced the histologic injury and significantly decreased serum Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. In addition, butyrate decreased myeloperoxidase (MPO) activity and malondialdehyde (MDA) tissue contents. Apoptotic cells in I/R rats were also significantly reduced after butyrate treatment. Furthermore, butyrate also decreased the mean number of apoptotic cells (positively stained for TUNEL) and increased the mean number of proliferating cells (positively stained for Ki-67). The expression levels of TNF-α and IL-6 were attenuated after butyrate treatment. CONCLUSIONS: Our results suggest that butyrate attenuated I/R-induced liver injury through upregulation of intracellular anti-oxidant stress and anti-apoptotic signaling pathways.

Protective effects of butyrate on intestinal ischemia-reperfusion injury in rats.

BACKGROUND: Butyrate is normally fermented from undigested fiber by intestinal microflora. The goal of the present study was to determine the effects of butyrate and its underlying mechanisms on intestinal injury in a rat model of ischemia and reperfusion (I/R). METHODS: Male Sprague-Dawley rats were subjected to warm ischemia for 45 min by clamping the superior mesenteric artery after treatment with butyrate, followed by 6 and 72 h of reperfusion. Pathologic histology analysis, enzyme-linked immunosorbent assay, immunofluorescence, and Western blot were performed. RESULTS: Butyrate preconditioning markedly improved intestinal injury. The inflammatory factor levels and leukocyte infiltration were attenuated by butyrate. Butyrate also maintained the intestinal barrier structures, increased the expression of tight junction proteins, and decreased endotoxin translocation. CONCLUSIONS: We conclude that butyrate administration attenuates intestinal I/R injury, which is associated with preservation of intestinal tight junction barrier function and suppression of inflammatory cell infiltration in the intestinal mucosa. This suggests butyrate as a potential strategy to prevent intestinal I/R injury.

Cytoprotective role of heme oxygenase-1 in liver ischemia reperfusion injury.

Ischemia/reperfusion (I/R) injury is the main cause of graft dysfunction and failure in vascular occlusion both during liver surgery and during liver transplantation. The pathophysiology of hepatic ischemia-reperfusion includes a number of mechanisms including oxidant stress that contribute to various degrees to the overall organ damage. Heme oxygenases (HO) are essential enzymes which degrade heme into biliverdin-IXalpha, free divalent iron, and carbon monoxide (CO). Due to its anti-inflammatory, anti-apoptotic and, as recently described, anti-viral properties. The inducible HO isoform HO-1 is an important molecule which could find its way into therapy of acute and chronic liver injuries including acute liver failure, alcoholic or viral hepatitis, chronic inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma are life threatening diseases and as a consequence might result in the necessity of liver transplantation. Liver transplantation is limited by ischemia/reperfusion (I/R) injury, which is characterized by hypoxia and nutrient deficiency resulting in oxidative stress, apoptosis and immune activation. Induction of HO-1 and application predominantly of CO have been shown to interfere with liver I/R injury and to improve recipient and graft survival. HO-1 and its reaction products of heme degradation has been linked to cytoprotection, and as an inducible form of HO, serves a vital metabolic function as the rate-limiting step in the heme degradation pathway, and affords protection in models of liver I/R injury. HO-1 system is an important player in liver I/R injury condition, and may offer new targets for the management of this condition. This review aims to summarize cytoprotective role of heme oxygenase-1 (HO-1) and its products within the liver.

Butyrate protects rat liver against total hepatic ischemia reperfusion injury with bowel congestion.

Hepatic ischemia/reperfusion (I/R) injury is an unavoidable consequence of major liver surgery, especially in liver transplantation with bowel congestion, during which endotoxemia is often evident. The inflammatory response aggravated by endotoxin after I/R contributes to liver dysfunction and failure. The purpose of the present study was to investigate the protective effect of butyrate, a naturally occurring four-carbon fatty acid in the body and a dietary component of foods such as cheese and butter, on hepatic injury complicated by enterogenous endotoxin, as well as to examine the underlying mechanisms involved. SD rats were subjected to a total hepatic ischemia for 30 min after pretreatment with either vehicle or butyrate, followed by 6 h and 24 h of reperfusion. Butyrate preconditioning markedly improved hepatic function and histology, as indicated by reduced transaminase levels and ameliorated tissue pathological changes. The inflammatory factors levels, macrophages activation, TLR4 expression, and neutrophil infiltration in live were attenuated by butyrate. Butyrate also maintained the intestinal barrier structures, reversed the aberrant expression of ZO-1, and decreased the endotoxin translocation. We conclude that butyrate inhibition of endotoxin translocation, macrophages activation, inflammatory factors production, and neutrophil infiltration is involved in the alleviation of total hepatic I/R liver injury in rats. This suggests that butyrate should potentially be utilized in liver transplantation.

Butyrate protects liver against ischemia reperfusion injury by inhibiting nuclear factor kappa B activation in Kupffer cells.

BACKGROUND: The inflammatory response after hepatic ischemia reperfusion (I/R) contributes to liver dysfunction and failure after transplantation. Butyrate is a four-carbon fatty acid, normally produced by bacterial fermentation of fiber in mammalian intestines, with anti-inflammatory activities. The purpose of the present study was to investigate the protective effect of butyrate preconditioning, if any, against hepatic I/R injury in rats and the underlying mechanisms involved. METHODS: Male Sprague-Dawley rats were subjected to a partial (70%) hepatic ischemia for 60 min after pretreatment with either vehicle or butyrate, followed by 3, 6, and 24 h of reperfusion. Hepatic injury was evaluated by biochemical and histopathologic examinations. Neutrophil infiltration was measured by myeloperoxidase (MPO) activity. The expression of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) was measured by enzyme-linked immunosorbent assay (Elisa) and Real-time reverse-transcriptase polymerase chain reaction (RT-PCR). The expression of nuclear factor kappa B (NF-κB) p65 was determined by immunohistochemistry and Western blot analysis. RESULTS: Butyrate treatment markedly improved hepatic function and histology, as indicated by reduced transaminase levels and ameliorated tissue pathologic changes. The expression of tumor necrosis factor-alpha, interleukin-6, and myeloperoxidase activity was attenuated by butyrate. Butyrate also reduced I/R-induced nuclear translocation of NF-κB p65 in Kupffer cells. CONCLUSION: Our results suggest that butyrate alleviates I/R-induced liver injury, possibly by suppressing inflammatory factors production and preventing NF-κB activation in Kupffer cells.

SOD mimetic improves the function, growth, and survival of small-size liver grafts after transplantation in rats.

BACKGROUND: Small-for-size syndrome (SFSS) may occur when graft volume is less than 45% of the standard liver volume, and it manifests as retarded growth and failure of the grafts and more mortality. However, its pathogenesis is poorly understood, and few effective interventions have been attempted. AIMS: The present study aimed to delineate the critical role of oxidant stress in SFSS and protective effects of a superoxide dismutase mimetic, Mn(III)tetrakis(4-benzoic acid)porphyrin chloride (MnTBAP), on graft function, growth, and survival in the recipient rats. METHODS: Small size graft liver transplantation (SSGLT) was performed to determine the survival, graft injury, and growth. MnTBAP was administered in SSGLT recipients (SSGLT+MnTBAP). RESULTS: Serum alanine aminotransferase levels were sustained higher in SSGLT recipients, which were correlated with an increased apoptotic cell count and hepatocellular necrosis in liver sections. Malondialdehyde content, gene expression of tumor necrosis factor α and interleukin 1ß, and DNA binding activity of nuclear factor-κB in the grafts were increased significantly in SSGLT recipients compared with sham-operated controls. Both phosphorylated p38 mitogen-activated protein kinase and nuclear c-Jun were increased in SSGLT. All these changes were strikingly reversed by the administration of MnTBAP, with an increase in serum superoxide dismutase activity. Moreover, in situ bromodeoxyuridine incorporation demonstrated that graft regeneration was much more profound in the SSGLT+MnTBAP group than in the SSGLT group. Finally, the survival of recipients with MnTBAP treatments was significantly improved. CONCLUSIONS: Enhanced oxidant stress with activation of the p38/c-Jun/nuclear factor-κB signaling pathway contributes to SFSS-associated graft failure, retarded graft growth, and poor survival. MnTBAP effectively reversed the pathologic changes in SFSS-associated graft failure.

[Living donor liver transplantation treatment of Wilson's disease complicated with neuropathy].

OBJECTIVE: To investigate living donor liver transplantation for Wilson disease with neurologic features. METHODS: From Jan 2001 to Mar 2003, fifteen cases of living donor liver transplantation were performed for Wilson Disease (WD), five of those were complicated with neurologic features. A retrospective analysis was given for cooper metabolism and neurologic features. RESULTS: All operation were living related liver transplantation and donors were mothers. Four left lobes with hepatic middle vein and one right lobe without hepatic middle vein were harvested from donors, and graft volume to recipient body weight ratio was 0.79 approximately 1.08. One patient occurred hepatic artery thrombosis and performed retransplantation later, the other recipients recovered satisfactorily. All patients showed Extrapyramidal sign and three patients companying with language handicap and dyskinesia alleviated postoperation follow-up between 2 and 16 months. All recipients are alive and remain well, and none have developed signs of recurrent WD. CONCLUSION: Living donor liver transplantation is effective treatment for WD complicated with nervous system symptom, ceruloplasmin is normal and Kayser-Fleischer ring and nervous system symptom are to various extents.

[Some principal surgical techniques for living donor liver transplantation].

OBJECTIVE: To investigate some principal surgical techniques of living donor liver transplantation (LDLT). METHODS: Eleven patients of LDLT have been performed at our department from January 2001 to March 2002. The left lobe (segments II, III, IV, including the middle hepatic veins) was transplanted in 8 patients, the left lateral lobe (segments II, III) in one and the right lobe (segments V, VI, VII, VIII, not including the middle hepatic veins) in 2. The plane of liver resection was determined on the basis of donor liver volumetry using CT scan and the anatomic analysis of vascular structure of the hepatic vein, portal vein and hepatic artery using intraoperative ultrasound. The hepatic parenchyma was transected using ultrasound aspirator without blood vessel clamping or graft manipulation. The isolated graft was perfused in situ through the portal vein branch. The liver graft was transplanted into the recipients who underwent total hepatectomy with preservation of the inferior vena cava. The hepatic vein reconstruction was performed in end to end fashion or end to side to the vena cava after venoplasty. Arterial anastomoses were performed using microsurgical technique. Biliary reconstruction was made by using duct-to-duct anastomosis and placement of a T tube. RESULTS: All the 11 donors are uneventfully discharged after operation. In the 11 recipients, an 8-year-old girl needed retransplantation because of hepatic artery thrombosis, one case died of serious chronic rejection on the postoperative day 72. Ten recipients recovered and were discharged from hospital, whose liver function and cuprum oxidase had returned to normal. CONCLUSIONS: The procedure of LDLT is relatively safe for the donor. Reconstruction of vessels is a key step in the procedure. Comprehending anatomical variation of vessels pre- and intra-operatively and correct surgical management might reduce the incidence of complications.

[Multimodal approach to clinical liver transplantation].

OBJECTIVE: To sum up the clinical experience of liver transplantation. METHOD: A retrospective study was made in 11 patients receiving living donor liver transplantation (LDLT)/and 14 patients having orthotopic liver transplantation (OLT), including one time operation of reduced size liver retransplantation and one time operation of cadaveric liver retransplantation. RESULTS: The voluntary donors were a sister and 10 mothers of recipients. The location of graft included 3 patients of segment II, III, part of IV (not including intermediate hepatic veins), 6 patients of segment II, III, IV (including intermediate hepatic veins), and 2 patients of V, VI, VII, VIII (not including intermediate hepatic veins). The weight range of graft was 270 - 620 g. Twenty-four recipients achieved a long-term survival and retained normal liver function during the follow-up. Only 1 patient died from serious rejection on the 72nd day postoperatively. Ten patients with hepatitis B cirrhosis were treated with lamivudine and anti-HBVIg, and HBV-DNA in serum was negative during the follow-up for 4 approximately 21 months. Copperoxidase, ceruloplasmin and main indexes of liver function became normal in all patients with Wilson's Disease. Postoperative complications included abdominal hemorrhage (2 patients), acute respiratory distress syndrome (5), acute rejection (4), and acute renal function failure (2). CONCLUSIONS: The wise solution to improve the result of liver transplantation and optimize liver resources is the "multimodal approach", by which all kinds of techniques for liver transplantation including CLT, LDLT and RSLT should well developed.

Ultrasonic aspiration hepatectomy for 136 patients with hepatocellular carcinoma.

AIM: To study the operative injury, post-operative complications, the hospitalization time, the post-operative survival rate of ultrasonic aspiration hepatectomy with a domestic new type of ultrasonic surgical device in comparison with that of conventional techniques of hepatectomy. METHODS: A total 136 patients with hepatocellular carcinoma (HCC, including 12 patients in 1991 and 124 consecutive patients from July 1995 to December 2000) underwent ultrasonic aspiration in liver resection (group T) and 179 HCC patients received conventional hepatectomy during the corresponding period (group C). The results of the two groups were compared statistically. RESULTS: There was no significant difference in the mean operation time between group T (152+/-11 min) and C (144+/-11 min). No operation or hospital death occurred in both groups. In group T, the mean volumes of bleeding (463+/-15 ml) and blood transfusion (381+/-12 ml) were markedly less than those in group C (557+/-20 ml, and 507+/-18 ml, respectively, P<0.05). The mean hospitalization time of group T (8.9+/-0.6 d) was markedly shorter than that of group C (11.7d+/-0.6 d) (P<0.05). The incidence of complications in group T was markedly lower than in group C, post-operative jaundice occurred in 4/136 and 31/179, respectively (P<0.05), liver failure in 0/136 and 2/179, cholorrhea in 0/136 and 6/179, hydrothorax in 21/136 and 39/179 (P<0.05), ascices in 9/136 and 54/179, respectively (P<0.05 ). There was no significant difference in the 1-year survival rate between the two groups (P>0.05), while the 3-year survival rate of group T (64.2 % ) increased markedly as compared with that of group C (55.7 %) (P<0.01). CONCLUSION: The ultrasonic aspiration hepatectomy with a domestic new type of ultrasonic surgical device could evidently reduce the operative injury and post-operative complications, shorten the hospitalization time and prolong the survivals of HCC patients.

[A clinical report of 12 case-times of living related liver transplantation].

OBJECTIVE: To evaluate and summarize the clinical application of living related liver transplantation (LRLT). METHODS: A retrospective analysis was made in altogether 12 LRLT operations of living related liver transplantation performed in our department. The indication and timing, surgical complications, and nonsurgical issues including infection, rejection, advantages of LRLT in our series were reviewed. RESULT: All the 11 donors are uneventfully after operation; the first receptor was dead, and 10 receptors with Wilson's disease achieve long-term survival. The postoperative survival time till now is 58 w, 51 w, 48 w, 38 w, 37 w, 36 w, 22 w, 18 w, 10 w and 7 w, respectively. No rejection was detected in the recipients with Wilson's disease, whose liver function and cuprum oxidase level had returned to normal. In this 10 cases, 6 of them has returned or gone to school, 2 of them were discharged from hospital, 2 of them has been recovered smoothly in the hospital due to short time postoperatively. The primary complications after operation including blood vessel, biliary tract, lung and the infection of microbe or virus, were mainly involved in our series. CONCLUSION: The process of operation was complicated; the operation technology was exigent and difficult with respect to the safety of the donors and receptors. LRLT has capacious clinical application for there are many unsurpassable advantages, such as plentiful resource and fine quality of graft liver, lower cost of LRLT.

[Application of microsurgical technique to hepatic artery reconstruction in liver transplantation].

OBJECTIVE: To explore the value of the microsurgical technique in the reconstruction of hepatic artery. METHODS: From September 2000 to June 2001, we performed liver transplantation for 11 patients including living related liver transplantation (4) and 7 orthotopic liver transplantation (7). Arterial reconstruction was performed under an operating microscope. RESULTS: No patients developed hepatic arterial thrombosis and serious complication, nor death for multiple organ failure. CONCLUSION: Microsurgical technique in reconstruction of the hepatic artery can improve surgical outcome, not only in orthotopic liver transplantation but also in living related liver transplantation.