龚作炯
长期从事传染病学临床医疗、科研及教学工作。
个性化签名
- 姓名:龚作炯
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学术头衔:
博士生导师
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学科领域:
内科学
- 研究兴趣:长期从事传染病学临床医疗、科研及教学工作。
龚作炯,武汉大学人民医院主任医师,教授,博士生导师。1987年获武汉大学医学硕士学位,1998获比利时鲁汶天主教大学医学博士学位。现任武汉大学人民医院感染科主任,担任中华医学会感染病学会全国委员,中国中西医结合传染病学会全国委员,湖北省感染病学会副主任委员,湖北省肝病学会副主任委员,武汉市感染病学会副主任委员,及《中华传染病杂志》、《中西医结合肝病杂志》、《华中医学杂志》《武汉大学学报(医学版)》等杂志编委。
长期从事传染病学临床医疗、科研及教学工作。出国学习前(1993年前),曾参加武汉大学医学院与美国军事医学传染病研究所合作进行的科研项目“病毒唑治疗流行性出血热的临床研究”,在国际上首次证实病毒唑可作为流行性出血热早期抗病毒治疗的药物,并明显降低其死亡率。该课题获原国家教委二等奖。主持完成“流行性出血热出凝血机理研究”,该课题系统地探讨了流行性出血热出凝血发生的病理机理,并首次应用发色底物法建立了流行性出血热出凝血指标的检测方法,对流行性出血热出血的救治具有重要的指导意义。系列论文被当年中国内科年鉴及中华医学杂志英文版转载。在国外求学期间(1993-1998年), 主要从事病毒性肝炎的研究。博士论文:"In vitro infection of hepatitis B virus:direct involvement of human Annexin V and in vitro test system for the evaluation of antiviral drugs"。该书50余万字,由比利时鲁汶天主教大学(Katholieke Universiteit Leuven,KUL)出版社公开出版发行。1998年5月获比利时鲁汶天主教大学医学博士学位,并继续从事博士后研究。近年来在国内、外学术刊物上发表论文150余篇,其中21篇论文被SCI收录(Hepatology, J.Hepatology, J.Viral Hepatitis),32篇论文参加国际学术会议交流。“乙型肝炎病毒受体研究”、“乙型肝炎病毒体外感染模型的建立及抗病毒药物的评价”分别获2002年、2003年湖北省自然科学三等奖。
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成果数
8
【期刊论文】Effects of PPARg agonist pioglitazone on rat hepatic fibrosis
龚作炯, Guang-Jin Yuan, Ming-Liang Zhang, Zuo-Jiong Gong
World J Gastroenterol 2004; 10 (7): 1047-1051,-0001,():
-1年11月30日
AIM: To investigate effects of pioglitazone on rat hepatic fibrosis and to explore its mechanism. METHODS: Rat hepatic fibrosis was induced by carbon tetrachloride (CCl4). Forty Sprague-Dawley rats were divided randomly into 4 groups: control, model, and two treatment (PI, PII) groups. Except for rats in control group, all rats were given subcutaneous injection of 400mL/L CCl4, twice a wk for 8 wk. Rats in PI and PII groups were also treated with pioglitazone of 3mg/kg, daily via gastrogavage beginning on the 1st day and at the end of the 2nd week, administration of CCl4 respectively. Liver functions (ALT, AST), serum fibrotic markers (HA, LN, PCIII) and hepatic hydroxyproline (HP) concentration were determined respectively. Histochemical staining of formalin-fixed liver sections with HE, Masson-Trichrome, and immunohistochemical staining for a-smooth muscle actin (a-SMA) were performed. Modified Knodell and Chevallier semi-quantitative scoring system (SSS) was used to evaluate necroinflammatory activity and fibrosis degree. RESULTS: Compared with model group, pioglitazone significantly reduced the serum levels of ALT, AST , HA, LN and PCIII (P<0.05 or <0.01). The HP concentrations in PI (210.90
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龚作炯, Sandra De Meyer, Zuojiong Gong, Erik Depla, Geert Maertens and Sing Hiem Yap
Journal of Hepatology 1999; 31: 783-790,-0001,():
-1年11月30日
Background/Aims: We have previously demonstrated that human liver Annexin V (hAV), a Ca2+-dependent phospholipid binding protein, binds specifically to small HBsAg (SHBsAg). Because of the propensity of AV to bind phospholipids, we here examine the role of phospholipids, as component of the HBV envelope, in binding to hAV and in HBV infection. Methods: The influence of phospholipids (phosphatidylserine and phosphatidylcholine) on the binding of hAV to SHBsAg or to anti-hAV monoclonals was determined by ELISA. Their influence on HBV infection was investigated using an in vitro HBV infection assay. Results: Two monoclonals, specific against MY were able to block the binding of hAV to SHBsAg and recognized different epitopes of hAV The binding of one of these monoclonals to hAV could be inhibited by phosphatidylserine, but not by phosphatidylcholine. Further experiments revealed that phosphatidylserine could also inhibit the binding of hAV to SHBsAg and could even prevent HBV infection in vitro. Phosphatidylcholine had no effect on the binding of hAV to SHBsAg and could not prevent HBV infection in vitro. However, since phosphatidylserine was not able to abolish the binding of the other blocking monoclonal to hAV, a non-phospholipid component of the HBV envelope must also be involved in hAV binding. Conclusions: These results indicate that phosphatidylserine and a non-phospholipid component of the HBV envelope are involved in hAV binding and in HBV infection.
hAV, HBsAG, HBV infection, Phosphatidylserine.,
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龚作炯, Shi-Ling Song, Zuo-Jiong Gong, Quan-Rong Zhang, uan-Xin Huang
World J Gastroenterol 2005; 11 (15): 2269-2276,-0001,():
-1年11月30日
AIM: The transforming growth factor-beta (TGF-β)/Smad signaling pathway system plays a prominent role in the control of cell growth and extracellular matrix formation in the progression of liver fibrogenesis. Smad proteins can either positively or negatively regulate TGF-β responses. In this study, the therapeutic effects of Chinese traditional compound decoction, JinSanE, and the changes of TGF-β/Smad signaling pathway system in carbon tetrachloride (CCl4)-induced rat experimental liver fibrosis were examined. METHODS: Seventy-two healthy Wistar rats were assigned to groups including normal control group, CCl4 model group, JinSanE treatment group I and JinSanE treatment group II. Each group contained 18 rats. All groups, except the normal control group, received CCl4 subcutaneous injection for 8 wk. Rats in JinSanE groups I and II were orally treated with JinSanE daily at the 1st and 5th wk, respectively, after exposure to CCl4. The expression of TGF-β1 and TGF-β1 type II receptor (TRII) mRNA in the liver was determined by reverse transcription polymerase chain reaction, and the expression of TGF-β1, Smad3 and Smad7 by immunohistochemistry. The liver histopathology was also examined by HE staining and observed under electron microscope. The activities of several serum fibrosis-associated enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST), the levels of serum hyaluronic acid (HA) were assayed. RESULTS: Hepatic fibrosis caused by CCl4 was significantly inhibited in the JinSanE-treated groups. The degrees of necrosis/degeneration and fibrosis scores were significantly lower in the JinSanE-treated groups than in the model control group. The expression of TGF-β1, TRII and Smad3 was significantly higher in the model group than that in the JinSanE-treated groups, and the active/total TGF-β1 ratio in the JinSanE groups was suppressed. Expression of TRII mRNA and Smad3 proteins showed a distribution pattern similar to that of TGF-β1 with a direct correlation in terms of the degree of hepatic fibrosis. The amount of positive staining Smad7 cells was significantly less in the model group than in the JinSanE-treated groups and the normal group. The contents of ALT, AST and HA were significantly lower in the JinSanE-treated groups than those in the model group. CONCLUSION: Traditional Chinese medicine, JinSanE, prevents the progression of hepatic damage and fibrosis through the inhibition of TGF-β1, TRII and Smad3 signal proteins, and increases expression of Smad7 signal protein in vivo.
TGF-β, Liver fibrogenesis
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龚作炯, ZUO JIONG GONG, SANDRA DE MEYER, JOS VAN PELT, KURT HERTOGS, ERIK DEPLA, ANN SOUMILLION, JOHAN FEVERY, AND SING-HIEM YAP
,-0001,():
-1年11月30日
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【期刊论文】培哚普利和缬沙坦对肝纤维化大鼠TGF-β1及其Ⅱ型受体mRNA与Smad3、Smad7表达的影响
龚作炯, 宋仕玲, 黄砚青, 阮鹏, 张志荣
Jiangsu Med J, June 2004, Vol 30, No.6,-0001,():
-1年11月30日
目的 观察培哚普利和缬沙坦抗大鼠肝纤维化的疗效。方法 60只Wistar大鼠随机平均分为4组:正常组、模型组、培哚普利治疗组和缬沙坦治疗组。四氯化碳诱导大鼠肝纤维化模型,治疗组于造模第4周开始分别予以培哚普利和缬沙坦灌胃。RT-PCR检测肝组织转化生长因子-Ⅱ型受体(TGFR Ⅱ mRNA);免疫组化技术检测TGF-β1、Smad3及Smad7在肝内的表达及定位,肝组织HE染色检测病理改变。结果 与模型组大鼠比较,经培哚普利或缬沙坦治疗大鼠肝内TGF-β1与TGFR Ⅱ mRNA、以及Smad3蛋白表达明显降低;而Smad7的表达增加。TGF-β1与Smad3的免疫阳性反应信号主要位于纤维间隔中的细胞浆,Smad7则主要在肝细胞浆表达,上述物质在两种药物组之间表达差异无显著性(P>0.05)。培哚普利或缬沙坦治疗后肝小叶均趋于正常,纤维间隔明显变薄。结论 培哚普利或缬沙坦均能有效地减轻肝纤维化大鼠的肝脏损伤及纤维化程度,其机理可能与直接或间接抑制肝内TGF-β1、与TGFR Ⅱ mRNA及Smad3表达,并促进Smad7表达有关。
血管紧张素Ⅱ抑制剂, 血管紧张素Ⅱ, 受体阻滞剂, 肝纤维化, 转化生长因子-β1 TGFR Ⅱ Smad3 Smad7
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【期刊论文】Epigallocatechin-3-Gallate Ameliorates Alcohol-Induced Liver Injury in Rats
龚作炯, Guangjin Yuan, Zuojiong Gong*, Xiaorong Zhou, Pin Zhang, Xiaomei Sun and Xi Li
Int. J. Mol. Sci. 2006, 7, 204-219,-0001,():
-1年11月30日
Endotoxemia is a common event in alcoholic liver disease. Elevated intestinal permeability is the major factor involved in the mechanism of alcoholic endotoxemia and the pathogenesis of alcoholic liver disease. This study examined the effect of epigallocatechin-3-gallate (EGCG) on alcohol-induced gut leakiness, and explored the related mechanisms involved in its protection against alcohol-induced liver injury in rats. Four groups of female Sprague-Dawley rats were studied. Alcohol and alcohol/EGCG groups rats received fish oil along with alcohol daily via gastrogavage for 6 weeks, and dextrose and dextrose/EGCG groups rats were given fish oil along with isocaloric dextrose instead of alcohol. The dextrose/EGCG and alcohol/EGCG groups received additional treatment of EGCG (100mg.kg-1 body weight) daily intragastrically by gavage. Intestinal permeability was assessed by urinary excretion of lactulose and mannitol (L/M ratio). Liver injury was evaluated histologically and by serum alanine aminotransferase (ALT). Plasma endotoxin and serum tumor necrosis factor-α (TNF-α) levels were assayed; liver malondialdehyde (MDA) contents determined. CD14 and inflammatory factors, such as TNF-α, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) mRNAs in the liver were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR). Rats given fish oil plus alcohol had gut leakiness (L/M ratio was increased), which was associated with both endotoxemia and liver injury. The above responses were accompanied by increased CD14, TNF-α, COX-2 and iNOS mRNA expressions in the liver. EGCG supplementation partly blocked the gut leakiness, reduced endotoxemia and lipid peroxidation, and blunted the elevated expressions of CD14, TNF-α, COX-2 and iNOS, all of which were associated with improved liver injury. These results show that EGCG can block alcohol-induced gut leakiness, reduce endotoxemia, and inhibit inflammatory factors expressions in the liver, thereby ameliorates alcohol-induced liver injury.
epigallocatechin-3-gallate, alcohol-induced liver injury, intestinal permeability, endotoxemia, CD14, cyclooxygenase-2, inducible nitric oxide synthase.,
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龚作炯, Guang-Jin Yuan, Jin-Chun Ma, Zuo-Jiong Gong, Xiao-Mei Sun, Shi-Hua Zheng, Xi Li
World J Gastroenterol 2005; 11 (12): 1825-1828,-0001,():
-1年11月30日
AIM:To investigate effects of ischemic pre-conditioning on the liver endogenous oxidant-antioxidant system during ischemia/reperfusion injury. METHODS: Twenty-four male Sprague-Dawley rats were randomly divided into sham-operated (Sham), ischemia/reperfusion (I/R), ischemic pre-conditioning plus ischemia/reperfusion (IPC) groups. Serum ALT, AST and hyaluronic acid levels were assayed and pathologic alterations observed. Liver malondialdehyde (MDA) contents, endogenous antioxidant enzymes, superoxidase dismutase (SOD), catalase (CAT), gultathionine peroxidase (GSH-Px) activities, neutrophils accumulation marker, myeloperoxidase (MPO) activities were measured respectively. RESULTS: Compared with I/R group, sinusoidal endothelial cells as well as hepatocytes damages, as assessed biochemically and histochemically, were improved significantly in IPC group; neutrophils infiltration was also markedly reduced. In IPC group, liver peroxidation, as measured by MDA contents, was significantly decreased when compared with I/R group; endogenous antioxidant enzymes, SOD, CAT and GSH-Px activities were markedly higher than that in I/R group. CONCLUSION: Ischemic pre-conditioning exerts protective effects on both hepatic sinusoidal endothelial cells and hepatocytes during liver I/R injury. Its mechanisms may involve dimunition of neutrophils infiltration and modulation of the imbalance of endogenous oxidant-antioxidant system in the organism.
Ischemic preconditioning, Ischemia/, reperfusion, Antioxidant enzymes, Sinusoidal endothelial cells, Liver
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龚作炯, Yan-Qing Huang, Lu-Wen Wang, Shao-Nan Yan and Zuo-Jiong Gong
Hepatobiliary Pancreat Dis Int 2004; 3: 543-547,-0001,():
-1年11月30日
BACKGROUND: It has been shown that telomerase activity and hepatitis B virus (HBV) replication are closely associated with cell cycle. This study aimed to further investigate the effects of cell cycle on telomerase activity and on HBV replication. METHODS: Human hepatoma cells transfected with HBV DNA (HepG2 2. 2. 15 cell line) were treated respectively with serum deprivation, all-trans retinoic acid (RA), dimethyl sulfoxide (DMSO), or sodium butyrate. The cell cycle of HepG2 2. 2. 15 cells was analyzed by flow cytometry. The telomerase activities of the cells were detected by TRAP-PCR-ELISA. HBV DNA in culture medium was assayed by a fluorescent quantitative PCR assay and a semiquantitative dot blot hybridization technique. HBsAg and HBeAg in culture media were quantitatively examined by an ELISA assay. RESULTS: Treatments with serum deprivation, RA, DM-SO, or sodium butyrate inhibited the proliferation of HepG2 2. 2. 15 cells and led to cell arrest in the G0/G1 phase of cell cycle. The percentage of the G0/G1 phase in the groups of sodium butyrate, DMSO, RA and serum-free was 85.2%, 71.9%, 68.3% and 65.2%, respectively, but in the control group, 43.1% (P<0.01). The activities of telomerase of the cells were also significantly inhibited by 82.8%, 74.6%, 76.1% and 69.4% respectively. In addition, HBV replication of the HepG2 2. 2. 15 cells remarkably increased as shown by the contents of HBV DNA, HBsAg and HBeAg in the culture media of the cells treated with sodium butyrate, DMSO, RA or serum deprivation (P<0.01). The amounts of HBV DNA in the groups of sodium butyrate, DMSO, RA, serum deprivation and control were 6.7
cell cycle, telomerase, hepatitis B virus, HepG2 2., 2., 15, replication
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