Role of the Wnt signaling pathway in the development and progression of liver fibrosis / 临床肝胆病杂志

Liver fibrosis has a complex pathogenesis and involves various intracellular and extracellular signal transduction pathways, but its specific pathogenesis remains unclear. Recent studies have confirmed that the activation of hepatic stellate cells due to abnormal activation of the Wnt signaling pathway is an important cause of liver fibrosis, and targeted inhibition of the Wnt signaling pathway can prevent the activation and proliferation of hepatic stellate cells and thus achieve an antifibrogenic effect. This article reviews the role of the Wnt signaling pathway in the development and progression of liver fibrosis and the latest research advances in the antifibrogenic effect of the interference of the Wnt signaling pathway, in order to provide new ideas for anti-hepatic fibrosis and the delay of early-stage cirrhosis.

Role of Wnt signaling pathway in progression of liver cirrhosis / 临床肝胆病杂志

In the past, liver cirrhosis was thought to be irreversible. However, theoretically, the process of liver cirrhosis could be slowed down by inhibiting extracellular matrix (ECM) production and by promoting its degradation. Wnt signaling pathway has been involved in many physiological and pathological processes and some studies have confirmed that abnormal activation of Wnt signaling pathway could cause activation of hepatic stellate cells, and then further induce ECM formation and prompt cirrhosis progression. We believe that new clinical therapeutic direction would emerge after in-depth exploration of the mechanism of Wnt signaling pathway involved in liver cirrhosis progression.

Hepatectomy for hepatic metastasis in 32 gastric cancer patients / 中华普通外科杂志

Objective To evaluate hepatectomy for liver metastasis in patients of gastric carcinoma.Methods Clinical data of 32 gastric cancer cases undergoing hepatectomy for hepatic metastatic tumor were reviewed retrospectively from 2006 to 2012.16 cases underwent radical gastrectomy and synchronous hepatectomy for liver metastasis,the remaining 16 cases underwent radical resection of gastric cancer and liver resection heterochronously.The relationship between prognosis and clinicopathology was analyzed.Results The overall survival rates were 84％,50％ and 37％ in 1 year,3 years and 5 years.The median survival time was 32 months.Gastric cancer invasion depth,intravascular tumor thrombi,lymphatic metastasis and intraoperative blood transfusion was related to poor prognosis by single factor analysis,while gastric serosal invasion,tumor thrombus and liver metastasis tumor ＞ 5 cm related to poor prognosis by multiple factors analysis.Conclusions Gastric cancer patients with liver metastasis who underwent hepatic resection can achieve good prognosis if hepatic metastatic tumor ＜ 5cm or the primary gastric cancer does not invade the serosa and without tumor thrombus.

Alpinetin down-regulating Bcl-2 promotes apoptosis of human hepatic cancer Hep3B cells / 中华普通外科杂志

Objective To study the effects of alpinetin on apoptosis of Hep3B cells and explore the related mechanism.Methods Hep3B cells were cultured in vitro,treated with alpinetin; RT-PCR and Western blot was used to detect the mRNA and protein levels of Bcl-2; MTT assay was used to detect the cellular growth inhibitory rate; Annexin V-FITC/PI double staining was used to detect the apoptosis rate of cells; Mitochondrial membrane potential was analyzed by flow cytometry; Western blot was used to detect protein expression of Caspase-3,9 and Cytochrome C ; the experiment was carried out in four groups:control group,high dosage of alpinetin group,middle dosage of alpinetin group and low dosage of alpinetin group.Results The expression of Bcl-2 in Hep3B cells were decreased by alpinetin.After treated with different dosages of alpinetin (40,80,120 μmol/L),the apoptotic inhibitory rate detected by MTT were 6.38％ ± 1.32％,21.58％ ± 1.97％ and 43.18％ ± 3.89％,significantly higher than those in control group (tlowdose =13.01,tmiddle dose =15.12,thighdose =14.79,average P ＜ 0.01) ; the expression of mitochondrial membrane potential green fluorescence protein (GFP) were 18.93％ ± 2.3％,31.11％ ± 2.67％ and46.06％ ± 2.95％,significantly higher than those in control group (tlow dose =16.70,tmiddle dose =31.38,thigh dose =48.15,average P ＜ 0.01).Western blot analysis showed that the expression of Caspase-3,9 andCytochrome C in cytoplasm significantly was higher than those in control group(Caspase-3:llow dose =11.94,tmiddle dose =10.18,thigh dose =18.82,average P ＜0.01; Caspase-9:tlow dose =15.11,tmiddle dose =20.41,thish dose =21.25,average P ＜0.01; Cytochrome C:tlow dose =15.11,tmiddle dose =28.47,thigh dose =16.01,average P ＜ 0.01).while that Cytochrome C in mitochondria significantly lower than those in control group (tlow dose =16.70,tmiddle dose =12.00,thighdose =27.61,average P ＜ 0.01).Conclusions Alpinetin promotes apoptosis of human hepatic cancer cells Hep3B by down-regulating Bcl-2,probably through mitochondrial pathway.

Pathogenesis of sepsis induced jaundice / 国际外科学杂志

Jaundice is frequent clinic symptoms with high incidence especially among the critical patients. The sepsis complicated with jaundice has drawn more and more consideration. However, the pathogenesis about sepsis complicated with jaundice is not confirmed and it is sometimes identified incorrectly as cholestatic jaundice. This article summarises the pathogenesis and elucidate the management about sepsis complicated with jaundice.