Hesheng Luo

Renmin University of China, Peping, Beijing, China

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Publications (19)45.19 Total impact

  • Xiaojing Quan · Hesheng Luo · Han Fan · Qincai Tang · Wei Chen · Ning Cui · Guang Yu · Hong Xia ·
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    ABSTRACT: Brain-derived neurotrophic factor (BDNF) has prokinetic effects on gut motility and is increased in the colonic mucosa of irritable bowel syndrome. We aimed to investigate the possible involvement of BDNF in stress-induced colonic hypermotility. Male Wistar rats were exposed to daily 1-h water avoidance stress (WAS) or sham WAS for 10 consecutive days. The presence of BDNF and substance P (SP) in the colonic mucosa was determined using enzyme immunoassay kits. Immunohistochemistry and western blotting were performed to assess the expression of BDNF and its receptor, TrkB. The contractions of muscle strips were studied in an organ bath system. Repeated WAS increased the fecal pellet expulsion and spontaneous contractile activities of the colonic muscle strips. Both BDNF and SP in the colonic mucosa were elevated following WAS. Immunohistochemistry revealed the presence of BDNF and TrkB in the mucosa and myenteric plexus. BDNF and TrkB were both up-regulated in colon devoid of mucosa and submucosa from the stressed rats compared with the control. BDNF pretreatment caused an enhancement of the SP-induced contraction of the circular muscle (CM) strips. TrkB antibody significantly inhibited the contraction of the colonic muscle strips and attenuated the excitatory effects of SP on contractions of the CM strips. Repeated WAS increased the contractile activities of the CM strips induced by SP after BDNF pretreatment, and this effect was reversed by TrkB antibody. The colonic hypermotility induced by repeated WAS may be associated with the increased expression of endogenous BDNF and TrkB. BDNF may have potential clinical therapeutic use in modulating gut motility.
    Digestive Diseases and Sciences 05/2015; 60(8). DOI:10.1007/s10620-015-3695-8 · 2.61 Impact Factor
  • Pengbo Wu · Yongxiang Shu · Fang Guo · Hesheng Luo · Guo Zhang · Shiyun Tan ·
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    ABSTRACT: To explore the association between patatin-like phospholipase domain-containing protein 3(PNPLA3) gene rs738409 polymorphism and the susceptibility of non-alcoholic fatty liver disease(NAFLD). Data bases were comprehensively searched to retrace all the related studies on the association between PNPLA3 gene rs738409 polymorphism and susceptibility. Of NAFLD, the pooled OR with 95% CI of the association between PNPLA3 gene rs738409 polymorphism and NAFLD susceptibility were performed using different genetic models. Subgroup analysis based on the source of population and sensitivity analysis was performed to detect the stability of results. 28 original studies with 6 216 patients and 8 218 controls were involved in the final combination of data. Findings from the meta-analyses showed that there were strong associations between PNPLA3 gene rs738409 polymorphism and the susceptibility of NAFLD, under different genetic model comparisons[GG vs. CC:OR = 2.42, 95%CI:1.83-3.21, P < 0.001;CG vs. CC:OR = 1.28, 95%CI:1.15-1.43, P < 0.001;CG+GG vs. CC:OR = 1.31, 95%CI:1.17-1.46, P < 0.001; GG vs. CC+GC:OR = 2.26, 95%CI:1.76-2.90, P < 0.001]. Similar results were found in both Asian and Caucasian populations. Results from the Meta-analysis strongly suggested that there appeared significant association between PNPLA3 gene rs738409 polymorphism and the susceptibility of NAFLD.
    Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi 04/2015; 36(1):78-82.
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    Xiaojing Quan · Hesheng Luo · Yin Liu · Hong Xia · Wei Chen · Qincai Tang ·
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    ABSTRACT: Objective: To examine the hypothesis that hydrogen sulfide (H2S) regulates the colonic motility by modulating both L-type voltage-dependent calcium channels and large conductance Ca2+-activated K+ (BKCa) channels. Methods: Immunohistochemistry was performed on rat colonic samples to investigate the localization of the H2S-producing enzymes cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE). The contractions of proximal colonic smooth muscle were studied in an organ bath system. The whole-cell patch-clamp technique was used to record both L-type calcium currents (ICa,L) and BKCa currents in colonic smooth muscle cells (SMCs) isolated from male Wistar rats. Results: Immunohistochemistry revealed the presence of CBS and CSE in mucosa, smooth muscle cells and myenteric neurons. The H2S donor NaHS inhibited spontaneous contractions of the longitudinal muscle and circular muscle strips in a dose-dependent manner, and the inhibitory effects were not blocked by tetrodotoxin. NaHS inhibited the peak ICa,L in colonic SMCs at a membrane potential of 0 mV. The current-voltage (I-V) relationship of L-type calcium channels was modified by NaHS, and the peak of the I-V curve was shifted to the right. NaHS (200 μΜ) evoked a significant rightward shift of the steady-state activation curve and inhibited the inactivation of L-type calcium channels. Furthermore, NaHS reversibly decreased the peak ICa,L in a dose-dependent manner. Likewise, BKCa channels were significantly inhibited by NaHS, and the addition of NaHS caused a time- and dose-dependent reduction in the BKCa current. Conclusion: The relaxant effect of H2S on colonic muscle strips may be associated with the direct inhibition of H2S on L-type calcium channels. H2S may be involved in the regulation of calcium homeostasis in colonic SMCs of rat colon.
    PLoS ONE 03/2015; 10(3):e0121331. DOI:10.1371/journal.pone.0121331 · 3.23 Impact Factor
  • Yaling Liu · Yu Zhou · Xiao Feng · Pengchun Yang · Jingfang Yang · Ping An · Hesheng Luo ·

    Genes Chromosomes and Cancer 10/2014; 53(10). DOI:10.1002/gcc.22193 · 4.04 Impact Factor
  • Ning Cui · Hesheng Luo ·
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    ABSTRACT: Objective: To explore the correlative factors and clinical characteristics of digestive system injury during the treatment of anticoagulant and (or) antiplatelet-agents. Methods: A total of 1 443 hospitalized patients on anticoagulant and (or) antiplatelet-agents from January 2010 to December 2013 at Renmin Hospital of Wuhan University were analyzed retrospectively. Results: Their length of hospital stay was from 5 to 27 days. Most of them were elderly males (n = 880, 61.0%) with an average age of (62 ± 6) years. 1 138 patients (78.9%) were farmers, workers or someone without a specific occupation. During the treatment of anticoagulant/antiplatelet-agents, statistical difference existed (P = 0.01) between positively and negatively previous digestive disease groups for actively newly occurring digestive system injury (16.0% (41/256) vs 15.9% (189/1 187)). After the dosing of anticoagulant and (or) antiplatelet-agents, 57 (66.3%, 57/86) patients were complicated by hemorrhage of digestive tract, taking 62.9% (61/97) of all positive result patients for Helicobacter pylori test. Comparing preventive PPI group with no PPI group, there was no marked statistical differences (P = 2.67) for digestive system complication (including hemorrhage of digestive tract) while receiving anticoagulant and (or) antiplatelet-agents (13.9% (74/533) vs 17.1% (156/910)). During anticoagulant and/or antiplatelet-agent therapy, 185 patients (12.8%) were complicated by peptic ulcer or peptic ulcer with bleeding, 40 patients (2.8%) had erosive gastritis and 5 (0.3%) developed acute gastric mucosal lesions. And 42 of 76 patients complicated by hemorrhage of digestive tract underwent endoscopic hemostasis while 2 patients were operated. Ninety-seven patients (6.7%) died, including 61 (62.9%, 61/97) from hemorrhage of digestive tract. The remainder became cured, improved and discharged. Moreover, no significant statistical differences existed (P = 2.29) among three combination group (aspirin, clopidogrel, warfarin), two combination group (aspirin, clopidogrel), exclusive aspirin group and exclusive warfarin group in short-term (<27 d) mortality. Conclusions: It is necessary to clearly dictate the details of medication to the patients not highly educated. Elder, male, history of digestive system disease and Helicobacter pylori infection are possibly highly risk correlative factors for digestive system complications during anticoagulant/antiplatelet-agent therapy. The short-term protective effect of routine dose of PPI is inconspicuous. No significant correlation exists between short-term mortality and the dosage (or type) of anticoagulant/antiplatelet-agents.
    Zhonghua yi xue za zhi 05/2014; 94(20):1553-8. DOI:10.3760/cma.j.issn.0376-2491.2014.20.009
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    ABSTRACT: MicroRNA-126 (miR-126) has been reported to be a tumor suppressor that targets CXCR4 in colorectal cancer (CRC) cells. This study investigated whether miR-126 has any prognostic impact in patients with CRC. MiR-126 and CXCR4 mRNA expression in 92 pairs of CRC and adjacent nontumorous tissues was examined using quantitative real-time PCR, and CXCR4 protein expression was assessed by immunohistochemistry (IHC) and Western blotting. The correlation between miR-126 and CXCR4 protein expression and clinicopathological features and overall survival rate was determined. MiR-126 was downregulated in CRC tissues that expressed high levels of CXCR4 mRNA. IHC and Western blotting detected high expression of CXCR4 protein in CRC tissues. An inverse correlation was observed between miR-126 and CXCR4 protein expression in CRC tissues. Moreover, low miR-126 and high CXCR4 protein expression was associated with distant metastasis, clinical TNM stage, and poor survival. Multivariate analysis indicated that miR-126 was an independent prognostic factor for overall survival, suggesting its clinical significance as a prognostic predictor in CRC patients. © 2014 Wiley Periodicals, Inc.
    Genes Chromosomes and Cancer 04/2014; 53(4):358-65. DOI:10.1002/gcc.22146 · 4.04 Impact Factor
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    ABSTRACT: Gemcitabine (GEM) is a first line chemotherapeutic drug for advanced pancreatic cancer. Dendritic cell (DC) vaccine is a promising method of immunotherapy for malignant tumor. Recent research has indicated that gemcitabine can enhance the efficacy of DC vaccine, but precise mechanism is still unknown. Here, we aimed to investigate the effect of GEM on DCs. The results showed that GEM-treated pancreatic cancer cell medium stimulated maturation of DCs. When co-cultured with autologous T lymphocytes, the pulsed DCs promoted the proliferation of T cells, and exhibited specific cytotoxic T lymphocytes (CTLs) antitumor activity. Further research showed that stimulation of DC maturation may be related to the elevated level of Hsp70 induced by GEM. Our study indicates that GEM changes the immunogenicity of tumor cells, and enhances the efficacy of DC based immunotherapy for pancreatic cancer.
    International immunopharmacology 01/2014; 19(1). DOI:10.1016/j.intimp.2013.12.022 · 2.47 Impact Factor
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    ABSTRACT: Recent evidence shows that altered microRNA-126 (miR-126) expression is implicated in the progression of colorectal cancer (CRC). However, the precise roles and mechanisms of miR-126 in CRC remain unclear. The aim of this study was to investigate the roles of miR-126 in CRC cells and to elucidate miR-126-mediated mechanisms in CRC cells. First, miR-126 expression was analyzed using qRT-PCR in 4 human CRC cell lines (SW480, SW620, HT-29 and HCT-116). Furthermore, the biological properties of miR-126 in CRC cells in vitro were examined by applying Cell Counting Kit 8, cell cycle, cell apoptosis and transwell assays. The mechanisms and pathways of miR-126-mediated in CRC cells were detected by using qRT-PCR, western blotting and luciferase reporter assay. We found that miR-126 overexpression inhibited cell proliferation, migration and invasion, and induced cell arrest in the G0/G1 phase of CRC cells, suggesting that miR-126 functions as a tumor suppressor in CRC cells. Furthermore, we identified the CXC chemokine receptor 4 (CXCR4) as a target of miR-126, and showed that it was negatively regulated by miR-126. We demonstrated that miR-126-mediated tumor suppression might be partly dependent on AKT and ERK1/2 signaling pathways. In conclusion, our data revealed that miR-126 functions as a tumor suppressor in CRC cells by regulating CXCR4 expression via the AKT and ERK1/2 signaling pathways and might be a novel target for therapeutic strategies in CRC.
    International Journal of Oncology 11/2013; 44(1). DOI:10.3892/ijo.2013.2168 · 3.03 Impact Factor
  • Chuncui Ye · Shiyun Tan · Lin Jiang · Ming Li · Peng Sun · Lei Shen · Hesheng Luo ·
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    ABSTRACT: The aim of this study was to determine the clinical and endoscopic manifestations, and pathological characteristics of intestinal schistosomiasis in China, in order to raise awareness of intestinal schistosomiasis and prevent misdiagnosis and missed diagnosis. The retrospective analysis of clinical and endoscopic manifestations, and histopathological characteristics, were conducted for 96 patients with intestinal schistosomiasis. Among these patients, 21 lived in areas that were not infected with Schistosoma and 25 (26%) had no history of schistosome infection or contact with infected water. These patients were mainly hospitalized due to symptoms of diarrhea, mucus and bloody purulent stool. Sixteen cases were of the acute enteritis type, and colonoscopy results determined hyperaemic edema and dispersed small mucosal ulcers. The acute infection in patients was pathologically characterized by the deposition of intact ova with a large quantity of eosinocyte infiltration. Forty‑one cases were of the chronic enteritis type which predominantly manifested with yellow nodules and disorder of the vascular surfaces in the intestines. Thirty‑nine cases were diagnosed with mixed type enteritis, which demonstrated acute and chronic histopathological appearances. In addition, six cases of complicated colorectal cancer were observed. Of the 24 misdiagnosed patients, eight were misdiagnosed with ulcerative colitis, five with colorectal cancer, five with colorectal tuberculosis, four with chronic bacillary dysentery and two with irritable bowel syndrome. Intestinal schistosomiasis demonstrated no specific clinical or endoscopic manifestations and it was determined that patients with abdominal pain, diarrhea and mucous stool may be infected with intestinal schistosomiasis. Epidemiological investigations and colonoscopy combined with multi‑block and multi‑site biopsies may improve the diagnosis of intestinal schistosomiasis. In addition, it is necessary for intestinal schistosomiasis to be followed up by colonoscopy, due to its possible correlation with colorectal tumors.
    Molecular Medicine Reports 08/2013; 8(4). DOI:10.3892/mmr.2013.1648 · 1.55 Impact Factor
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    ABSTRACT: To investigate the potential role of hydrogen sulphide (H(2)S) and ATP-sensitive potassium (K(ATP)) channels in chronic stress-induced colonic hypermotility. Male Wistar rats were submitted daily to 1 h of water avoidance stress (WAS) or sham WAS (SWAS) for 10 consecutive days. Organ bath recordings, H(2)S production, immunohistochemistry and western blotting were performed on rat colonic samples to investigate the role of endogenous H(2)S in repeated WAS-induced hypermotility. Organ bath recordings and western blotting were used to detect the role of K(ATP) channels in repeated WAS. Repeated WAS increased the number of fecal pellets per hour and the area under the curve of the spontaneous contractions of colonic strips, and decreased the endogenous production of H(2)S and the expression of H(2)S-producing enzymes in the colon devoid of mucosa and submucosa. Inhibitors of H(2)S-producing enzymes increased the contractile activity of colonic strips in the SWAS rats. NaHS concentration-dependently inhibited the spontaneous contractions of the strips and the NaHS IC(50) for the WAS rats was significantly lower than that for the SWAS rats. The inhibitory effect of NaHS was significantly reduced by glybenclamide. Repeated WAS treatment resulted in up-regulation of Kir6.1 and SUR2B of K(ATP) channels in the colon devoid of mucosa and submucosa. The colonic hypermotility induced by repeated WAS may be associated with the decreased production of endogenous H(2)S. The increased expression of the subunits of K(ATP) channels in colonic smooth muscle cells may be a defensive response to repeated WAS. H(2)S donor may have potential clinical utility in treating chronic stress- induced colonic hypermotility.
    PLoS ONE 02/2013; 8(2):e55853. DOI:10.1371/journal.pone.0055853 · 3.23 Impact Factor
  • Qingshan Pei · Xiaoping Zou · Xiaoqi Zhang · Min Chen · Yi Guo · Hesheng Luo ·
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    ABSTRACT: EUS elastography is a novel technique that can be used for distinguishing benign from malignant lymph nodes and focal pancreatic masses. However, the studies pertaining to EUS elastography for differential diagnosis of solid pancreatic masses have reported widely varied sensitivities and specificities. A meta-analysis of all relevant articles was performed to estimate the overall diagnostic accuracy of EUS elastography for differentiating benign and malignant solid pancreatic masses. The literatures were identified by searching in PubMed and Embase databases. Two reviewers independently extracted the information from the literatures for constructing 2 × 2 table. A random-effect model or a fixed-effect model was used to estimate the sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio. A summary receiver operating characteristic curve (SROC) also was constructed. Meta-regression and subgroup analysis were used to explore the sources of heterogeneity. 13 studies including a total of 1042 patients with solid pancreatic masses were selected for meta-analysis. The pooled sensitivity and specificity of EUS elastography for differentiating benign and malignant solid pancreatic masses were 95% (95% confidence interval [CI], 93%-96%), 69% (95% CI, 63%-75%), respectively. The area under SROC (AUC) was 0.8695. Two significant variables were associated with heterogeneity: color pattern and blinding. As a less invasive modality, EUS elastography is a promising method for differentiating benign and malignant solid pancreatic masses with a high sensitivity, and it can prove to be a valuable supplement to EUS-FNA.
    Pancreatology 09/2012; 12(5):402-8. DOI:10.1016/j.pan.2012.07.013 · 2.84 Impact Factor
  • Ping An · Yihao Tian · Mingkai Chen · Hesheng Luo ·
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    ABSTRACT: Aim: Hepatic stellate cells (HSC) are the major players in hepatic fibrosis. As a most potent mitogen, transforming growth factor-β (TGF-β) strongly activates HSC and increases intracellular Ca2+ concentration. Here, we assessed the potential role of Ca2+/calmodulin-dependent protein kinase II (CaMKII), a main downstream effector of the Ca2+ signal in liver fibrogenesis cascade. Methods: A human immortal HSC cell line, LX-2, and primary rat hepatic stellate cells were used in current study. CaMKII blockage and Akt inhibition were performed by KN-93/CaMKIIα siRNA and LY294002, respectively. HSC proliferation was detected by 5-bromodeoxyuridine incorporation assay. Real-time polymerase chain reaction, western blot and enzyme-linked immunosorbent assay were used to measure mRNA, cellular protein and protein in medium, respectively. Procollagen α1(I) expression was detected by immunocytochemistry. The role of CaMKII on TGF-β/Smad-induced collagen α1(I) expression was determined by (CAGA)12-MLP luciferase activity assay. Results: TGF-β dramatically increased CaMKII mRNA, and total and phosphorylated CaMKII expression. KN-93 and CaMKIIα siRNA suppressed TGF-β-mediated HSC proliferation. CaMKII interruption blocked TGF-β-elicited Akt activation. LY294002 arrested HSC proliferation and collagen α1(I) production but had no effect on CaMKII. Furthermore, CaMKII led to increased p21 and p27 expression. KN-93 and CaMKIIα siRNA inhibited TGF-β-induced and basal collagen α1(I) production but had no effect on the activity of (CAGA)12-MLP luciferase in response to TGF-β stimulation. Conclusion: CaMKII is a pivotal signal in TGF-β-induced fibrogenic cascades by means of stimulating HSC proliferation, and involved in a basal collagen production. Therefore, CaMKII will be a potentially effective target in the development of therapeutic intervention strategies to attenuate hepatic fibrosis.
    Hepatology Research 02/2012; 42(8):806-18. DOI:10.1111/j.1872-034X.2012.00983.x · 2.74 Impact Factor
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    Chengbai Liang · Hesheng Luo · Ying Liu · Jiwang Cao · Hong Xia ·
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    ABSTRACT: To study the relationship between brain-gut peptides, gastrointestinal hormones and altered motility in a rat model of repetitive water avoidance stress (WAS), which mimics the irritable bowel syndrome (IBS). Male Wistar rats were submitted daily to 1-h of water avoidance stress (WAS) or sham WAS (SWAS) for 10 consecutive days. Plasma hormones were determined using Enzyme Immunoassay Kits. Proximal colonic smooth muscle (PCSM) contractions were studied in an organ bath system. PCSM cells were isolated by enzymatic digestion and IKv and IBKca were recorded by the patch-clamp technique. The number of fecal pellets during 1 h of acute restraint stress and the plasma hormones levels of substance P (SP), thyrotropin-releasing hormone (TRH), motilin (MTL), and cholecystokinin (CCK) in WAS rats were significantly increased compared with SWAS rats, whereas vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP) and corticotropin releasing hormone (CRH) in WAS rats were not significantly changed and peptide YY (PYY) in WAS rats was significantly decreased. Likewise, the amplitudes of spontaneous contractions of PCSM in WAS rats were significantly increased comparing with SWAS rats. The plasma of WAS rats (100 µl) decreased the amplitude of spontaneous contractions of controls. The IKv and IBKCa of PCSMs were significantly decreased in WAS rats compared with SWAS rats and the plasma of WAS rats (100 µl) increased the amplitude of IKv and IBKCa in normal rats. These results suggest that WAS leads to changes of plasma hormones levels and to disordered myogenic colonic motility in the short term, but that the colon rapidly establishes a new equilibrium to maintain the normal baseline functioning.
    PLoS ONE 02/2012; 7(2):e31774. DOI:10.1371/journal.pone.0031774 · 3.23 Impact Factor
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    ABSTRACT: Accurate assessment of human epidermal growth factor receptor (HER) 2 is essential for efficient selection of patients who may benefit from therapies targeting this surface receptor (e.g., trastuzumab). Intratumoral heterogeneity of HER2 expression may potentially contribute to inaccurate assessment of HER2 status. To clarify intratumoral heterogeneity of HER2 expression and its potential clinical impact on assessment of HER2 status, we analyzed 148 endoscopic biopsy specimens and 117 excisional tumor specimens collected from 148 patients with primary gastric cancer. Specifically, we assessed HER2 protein overexpression and gene amplification using, respectively, immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH). There were 28 IHC-positive cases and 25 FISH-positive cases among these 148 patients. Heterogeneous HER2 protein expression was demonstrated in 23 of 29 (79.3%) IHC-positive cases, while gene expression heterogeneity was found in 11 of 25 (44.0%) FISH-positive cases. Intratumoral heterogeneity was the main reason of discordant results between IHC and FISH or between endoscopic biopsy and excisional tumor specimens. The clinical significance and impact of intratumoral HER2 expression heterogeneity on treatment outcome in gastric cancer require further studies.
    Cell biochemistry and biophysics 09/2011; 62(1):221-8. DOI:10.1007/s12013-011-9286-1 · 1.68 Impact Factor
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    ABSTRACT: Primo-vessels have been observed in the rat abdominal cavity as floating thread like structures on and not adhering to fascia-wrapped internal organs. To date their presence, locations, and lengths have been irregular and unpredictable, and their identification not regularly repeatable, thus they have remained a nagging enigma in primo-vascular system research for several years. In this work, locations were found where primo-vessels were regularly present and observed repeatedly. These vessels were not floating or freely movable but lay in a regular position in the mesentery in the abdominal cavity of the rat, being observed between the cecum and small intestine and between the colon and mesentery root. The difference between a lymph vessel and a primo-vessel is described in anatomical and histological aspects. In addition, trypan blue was found to enter primo-vessels through the surrounding membranes and filled spaces between fibers comprising the primo-vessels. It is conjectured that the previously observed floating primo-vessels had anomalously and irregularly emerged, for some unknown physiological reasons, from primo-vessels normally located in the fascia-like mesentery.
    12/2010; 3(4):232-40. DOI:10.1016/S2005-2901(10)60042-8
  • SuYu Chen · Hong Shi · Xiaoping Zou · Hesheng Luo ·
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    ABSTRACT: The role of prophylactic ulinastatin in the prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis is debated. A meta-analysis of all published randomized clinical trials was performed to evaluate the efficacy of ulinastatin on post-ERCP pancreatitis. Searches were conducted in multiple databases composed of PubMed, EMBASE, the Cochrane Library, the Science Citation Index Expanded, and the China National Knowledge Infrastructure series full-text database. Primary outcome was post-ERCP pancreatitis, with or without hyperamylasemia. Seven randomized clinical trials fulfilling the inclusion criteria were selected for meta-analysis, 5 comparing ulinastatin with placebo and 2 for ulinastatin versus gabexate. The incidence of post-ERCP pancreatitis was reduced by ulinastatin (odds ratio, 0.53; 95% confidence interval, 0.31-0.89; P = 0.02; test for heterogeneity: I = 0%; P = 0.51), so was the event of hyperamylasemia (odds ratio, 0.42; 95% confidence interval, 0.30-0.59; P < 0.00001; test for heterogeneity: I = 13%; P = 0.33). Subsequent sensitivity and subgroup analyses produced conflicting results. Ulinastatin shows to be of value on preventing post-ERCP pancreatitis and hyperamylasemia for patients in average risk, when given intravenously at a dose of not less than 150,000 U, just before ERCP. More high-quality trials are needed for further confirmation.
    Pancreas 11/2010; 39(8):1231-7. DOI:10.1097/MPA.0b013e3181dc67e7 · 2.96 Impact Factor
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    Min Chen · Xiaoping Zou · Hesheng Luo · Jun Cao · Xiaoqi Zhang · Bin Zhang · Wenjia Liu ·
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    ABSTRACT: Upregulation of proton extrusion is critical for tumor cell survival in an ischemic microenvironment with a lower extracellular pH (pHe). Lower pHe and higher intracellular pH (pHi) benefit cancer cells for invasion and growth. Vacuolar H(+)-ATPases (V-H(+)-ATPases) play a critical role in regulating the transmembrane pH gradient. Proton Pump Inhibitors (PPI), mainly treating acid-related diseases, could inhibit the expression of V-H(+)-ATPases. We have investigated whether PPI decreases the pHi of the human gastric adenocarcinoma cell line, SGC7901, by inhibiting V-H(+)-ATPases so as to enhance the cytotoxicity of anti-tumor drugs. We have assessed the optimal treatment time, pretreatment dosage of PPI and the possible mechanism of action. PPI exceeding 10 microg/ml inhibited protein expression of V-H(+)-ATPases in a dose-dependent manner, decreased the pHi value and reversed the transmembrane pH gradient, whereas PPI at final concentration of 1 microg/ml could not. Changes of the pH gradient were positively correlated with PPI concentration. The inhibitory effects of PPI on V-H(+)-ATPases primarily occurs from 12h to 24h after PPI pretreatment (P<0.05). The pHi value of SGC7901 was lowest 24h after PPI pretreatment (P<0.05). Administration of anti-tumor drugs 24h after PPI pretreatment produced the most cytotoxic effects on SGC7901 (P<0.05) and significantly improved the early and total apoptosis rates (P<0.01). PPI exceeding 20 microg/ml also significantly reduced the ADR-releasing index, thereby enhancing the intracellular ADR concentration (P<0.01). Therefore, PPI could enhance the cytotoxic effects of anti-tumor drugs on the SGC7901 cells.
    Cell Biology International 06/2009; 33(9):1008-19. DOI:10.1016/j.cellbi.2009.05.004 · 1.93 Impact Factor
  • Xiaomin Sun · Baoping Yu · Long Xu · Weiguo Dong · Hesheng Luo ·
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    ABSTRACT: The presence of interstitial cells of Cajal (ICC) has been described throughout the digestive tract. In this study, we investigated whether ICC also exist in the gallbladder wall of CD1 mice. Immunofluorescent confocal microscopy was used to identify the morphology and distribution of ICC in either whole-mount flat preparations or enzyme-dispersed cells from the gallbladder of CD1 mice. Methylene blue staining and transmission electron microscopy were performed to detect the presence of ICC, and reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were used to confirm the expressions of ICC-specific marker c-kit in the gallbladder tissues. The presence of c-kit-positive cells was demonstrated in both the gallbladder wall and the enzyme-dispersed cells. The ICC were distributed throughout the wall of the gallbladder and organized into a network. Under transmission electron microscopy, ICC were characterized by their well-developed perinuclear endoplasmic reticulum, abundant mitochondria, free ribosomes and intermediate filaments, and distinctive caveolae and lack of myosin filaments. The expressions of ICC-specific marker c-kit were also confirmed in the gallbladder tissue. The murine gallbladder wall contains ICC.
    Scandinavian Journal of Gastroenterology 11/2006; 41(10):1218-26. DOI:10.1080/00365520600708800 · 2.36 Impact Factor
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    ABSTRACT: This study was to evaluate the effects of thalidomide on expression of adhesion molecules in liver cirrhosis. The cirrhosis was induced in Wistar rats by intraperitoneal injection of CCl(4), and thalidomide (10 mg/kg/day or 100 mg/kg/day) was given by intragastric administration for 8 weeks. Liver histopathology and immunohistochemistry were significantly improved and the expressions of ICAM-1, VCAM-1, E-selectin, and TNF-alpha mRNA and protein were decreased significantly in rats treated with a high dose of thalidomide. Close positive correlation was observed in the expression of the TNF-alpha mRNA and that of ICAM-1, VCAM-1, and E-selectin mRNA, respectively. These results indicate that thalidomide exerts its effect on the downregulation of adhesion molecules via TNF-alpha signaling pathway to inhibit liver fibrosis.
    Mediators of Inflammation 02/2006; 2006(4):93253. DOI:10.1155/MI/2006/93253 · 3.24 Impact Factor

Publication Stats

200 Citations
45.19 Total Impact Points


  • 2010-2015
    • Renmin University of China
      Peping, Beijing, China
  • 2006-2013
    • Wuhan University
      • Department of Gastroenterology
      Wu-han-shih, Hubei, China