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ABSTRACT: ETHNOPHARMACOLOGICAL RELEVANCE: Simo Decoction (SMD), a traditional Chinese medicine, included four elements, such as Fructus aurantii, Radix aucklandiae, Semen arecae and Radix linderae. It has been used to improve gastrointestinal dysmotility in clinical practice for a long history in China. However, the explicit mechanisms are unclear. The aim of this study was to investigate the effect of SMD on contractions of antral circular smooth muscle strips of Sprague-Dawley (SD) rats and its underlying mechanism. MATERIALS AND METHODS: The antral circular strips were prepared in the organ bath under baseline or to be incubated with muscarinic receptor antagonist atropine (10(-6)M), muscarinic M3 receptor antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) (0.4×10(-6)M), muscarinic M2 receptor antagonist gallamine (10(-6)M), adrenergic receptor agonist adrenaline (10(-7)M), exogenous nitric oxide (NO) donor l-arginine (10(-4)M), nicotinic receptor antagonist hexamethonium chloride (10(-4)M) and Ca(2+) channel antagonist nifedipine (30nM), and consecutive concentrations of SMD were added to the bath to observe the strip responses. As a control, the responses of strips after administration with the same volume of Krebs solution as SMD were also noted. The strip responses to acetylcholine (10(-7)-10(-3)M) were also noted in organ bath to compare with SMD-induced contraction. RESULTS: SMD dose-dependently evoked hypercontractility of antral circular strips, and the maximal contractile effect of circular smooth muscle induced by SMD was significantly higher than that induced by acetylcholine (10(-3)M). The responses of antral circular strips to SMD were completely antagonized by atropine, 4-DAMP or 4-DAMP+gallamine, but partly inhibited by gallamine and partly suppressed by adrenaline, l-arginine, hexamethonium chloride and nifedipine. CONCLUSIONS: SMD promotes contractions of antral circular strips in rats mainly via activation of muscarinic M3 receptor, but partly via activation of muscarinic M2 receptor, Ca(2+) channel and nicotinic receptor, inhibition of adrenergic receptor and releasing of NO.
Journal of ethnopharmacology 09/2012; · 2.32 Impact Factor
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ABSTRACT: Systemic lupus erythematosus (SLE) is a multiple organ autoimmune disorder, including the liver, but the possible reason in
impairment in the liver is still unclear. Our present study assessed alterations of transcription factor Foxp3+ regulatory T cells (Tregs) and several other immune molecules [programmed cell death 1 and its ligand (PD1 and PD-L1), and
interleukin 10 (IL-10) and transform growth factor β (TGF-β)] in the liver and other major organs of lupus-prone BXSB mice
by flow cytometry, real-time quantitative reverse transcription PCR, and enzyme-linked immunosorbent assay. Results showed
that both frequency and number of Foxp3+ Tregs were dramatically reduced in the thymus, spleen and kidney of the BXSB mice (P<0.05), but those in the liver were kept in nearly normal range, when compared to negative control C57BL/6 mice. In comparison
to control mice, the mRNA levels of Foxp3, PD1 and PD-L1 were significantly decreased in the kidneys of BXSB mice (P<0.05), but there was no significant difference in the livers of the BXSB mice (P>0.05). Protein levels of IL-10 and TGF-β in serum showed no significant difference between BXSB and C57BL/6 mice, but were
significantly increased in the kidneys and livers of BXSB mice as compared with those in C57BL/6 mice (P<0.05). These results suggest that reduced Foxp3+ Tregs are involved in the pathogenesis of SLE in BXSB mice, and relatively higher number of these cells in the livers than
in the other target organs could constitute a protective mechanism against hepatic lesions in lupus-prone mice, which may
provide insights into development of new therapeutic approaches in SLE patients.
Key wordsFoxp3–hepatic lesion–lupus–BXSB mice
Journal of Huazhong University of Science and Technology 04/2012; 31(4):476-481. · 0.38 Impact Factor
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ABSTRACT: PurposeVisceral hypersensitivity is an important pathological mechanism of irritable bowel syndrome. Electroacupuncture (EA) could
relieve chronic visceral hypersensitivity (CVH) in rats. However, little information is available about the mechanism. The
aim of this study was to confirm the effects of EA at acupoint ST-36 (Zusanli) on CVH induced by the chemical colorectal irritation
during postnatal development of rats, and to explore the possible 5-HT3 receptor mechanism.
MethodsRats were randomized into four groups, including the normal control group, CVH group, CVH with EA group, and CVH with sham
EA group. The abdominal electromyogram (EMG) in response to colorectal distension was selected as the index for measurement
of visceral hypersensitivity. 5-HT3 receptors were analyzed through reverse transcription–polymerase chain reaction and western blot.
ResultsEA at ST-36 significantly decreased evoked EMG. The expression of 5-HT3 receptor in the colon was increased in rats with CVH, and decreased after EA treatment.
ConclusionsEA at acupoint ST-36 attenuates CVH in rats and decreases 5-HT3 receptor level in the colon. Decreased 5-HT3 receptor level in the colon may mediate the beneficial effect of EA in rats with CVH.
KeywordsElectroacupuncture–ST-36–Visceral hypersensitivity–Colorectal distension–5-HT3 receptor
International Journal of Colorectal Disease 04/2012; 26(5):569-574. · 2.38 Impact Factor
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ABSTRACT: Postinfectious irritable bowel syndrome (PI-IBS), which results from inflammation has been emphasized a lot recently. Dendritic cells (DCs) may contribute to intestinal mucosal immune activation in the pathogenesis of PI-IBS. This study tested the hypothesis that phenotype and function of intestinal lamina propria DCs (LPDCs) changed in the development of a PI-IBS mouse model.
Mice infected with Trichinella spiralis underwent abdominal withdrawal reflex (AWR) to evaluate visceral sensitivity. LPDCs were isolated and purified by intestine digestion and magnetic label-based technique. Surface markers were analyzed by flow cytometry. Endocytic activity, mixed lymphocyte reaction (MLR) and chemotaxis were studied. Cytokine production of the LPDCs cocultured with CD4(+) T cells was determined.
Intestinal inflammation resolved after 8 weeks infection with sustained visceral hyperalgesia. Surface markers CD86 and MHCII were lower in the acute infection group, but increased in the PI-IBS stage. Enhanced ability of endocytic activity and decreased abilities to attract and stimulate CD4(+) T cell proliferation were in the acute infection group. However, LPDCs in the PI-IBS stage showed weakened endocytic ability with enhanced abilities to attract and stimulate CD4(+) T cell proliferation. Cocultured LPDCs with CD4(+) T cells showed a predominant Th2 response in the acute infection stage, and more important roles of Th1, Th17 responses in the PI-IBS stage.
The hypothesis was supported that the phenotype and function of LPDCs changed in the development of PI-IBS, which induced the maintenance of intestinal mucosal immune activation and might provide a clue for the treatment of the disease.
Journal of Gastroenterology and Hepatology 12/2011; 27(5):935-44. · 2.87 Impact Factor
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ABSTRACT: Human intelectin-1 (ITLN-1) is a novel identified galactose-binding lectin that is expressed in the colonic goblet cells. Since gastric adenocarcinomas can arise through a process of intestinalization, we speculate that ITLN-1 may be aberrantly expressed in gastric cancer. This study was undertaken to examine the ITLN-1 expression in gastric cancer and correlate it with clinical outcomes.
One hundred and ninety-six gastric cancer patients were evaluated for the ITLN-1 expression by immunohistochemistry. The ITLN-1 transcripts were measured by real-time quantitative PCR.
ITLN-1 expression was absent in normal gastric mucosa, whereas areas of intestinal metaplasia revealed ITLN-1 immunoreactivity. One hundred and forty-two gastric cancer patients (72.4%) were positive for ITLN-1 expression. In a subtotal of 20 patients, ITLN-1 transcripts were significantly enhanced in gastric cancer tissues than in normal gastric mucosa (P < 0.001). The expression rate of ITLN-1 was higher in intestinal-type carcinomas than in diffuse-type carcinomas (P = 0.003). ITLN-1 positivity in gastric cancer was positively correlated with tumor differentiation (P = 0.001) and CDX2 expression (P < 0.001), and inversely correlated with depth of invasion (P = 0.007), lymph node metastasis (P = 0.001), distant metastasis (P = 0.014), clinical stage (P = 0.006), Ki-67 expression (P = 0.001), and heparanase expression (P < 0.001), without correlation with age, gender, tumor location, or tumor size. In univariate and multivariate analyses, ITLN-1 was an independent prognostic factor for longer survival of gastric cancer patients (P = 0.001).
The aberrant ITLN-1 expression in gastric cancer is correlated with clinicopathological features and may be a useful prognostic factor for predicting the outcomes of gastric cancer patients.
Journal of Cancer Research and Clinical Oncology 11/2011; 138(1):163-72. · 2.56 Impact Factor
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ABSTRACT: Systemic lupus erythematosus (SLE) is a multiple organ autoimmune disorder, including the liver, but the possible reason in impairment in the liver is still unclear. Our present study assessed alterations of transcription factor Foxp3(+) regulatory T cells (Tregs) and several other immune molecules [programmed cell death 1 and its ligand (PD1 and PD-L1), and interleukin 10 (IL-10) and transform growth factor β (TGF-β)] in the liver and other major organs of lupus-prone BXSB mice by flow cytometry, real-time quantitative reverse transcription PCR, and enzyme-linked immunosorbent assay. Results showed that both frequency and number of Foxp3(+) Tregs were dramatically reduced in the thymus, spleen and kidney of the BXSB mice (P<0.05), but those in the liver were kept in nearly normal range, when compared to negative control C57BL/6 mice. In comparison to control mice, the mRNA levels of Foxp3, PD1 and PD-L1 were significantly decreased in the kidneys of BXSB mice (P<0.05), but there was no significant difference in the livers of the BXSB mice (P>0.05). Protein levels of IL-10 and TGF-β in serum showed no significant difference between BXSB and C57BL/6 mice, but were significantly increased in the kidneys and livers of BXSB mice as compared with those in C57BL/6 mice (P<0.05). These results suggest that reduced Foxp3(+) Tregs are involved in the pathogenesis of SLE in BXSB mice, and relatively higher number of these cells in the livers than in the other target organs could constitute a protective mechanism against hepatic lesions in lupus-prone mice, which may provide insights into development of new therapeutic approaches in SLE patients.
Journal of Huazhong University of Science and Technology 08/2011; 31(4):476-81. · 0.38 Impact Factor
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ABSTRACT: Irritable bowel syndrome (IBS) is a highly prevalent functional disorder with poor understanding on its pathogenesis and pathology. China has huge amount of population and have a lot of literatures on IBS in Chinese publications. The aim of this article was to review the reported investigations on IBS in China and discuss the difference between China and other country.
Literatures pertaining IBS epidemiology, pathogenesis and pathophysiology, which published in the high level journals in china and SCI journals after 1998 were reviewed.
In the general health population, 5-6% meets the Rome II IBS criteria. Intestinal infection, food intolerance, genetic factor and psychological disturbance were responsible for the pathogenesis of IBS. In IBS patients, the impaired reaction to rectal distension, abnormal gastrointestinal motility, impaired autonomic nerve function, weakened colon epithelium connection, altered cerebral nuclei activation were the main pathophysiological findings.
Comparing to the findings from other area, literatures from China provided more evidences on epidemiological data of IBS in China, post-infection IBS, visceral hypertension and gastrointestinal motility abnormalities in IBS. This detailed literature review may help the understanding and promoting the future studies on IBS.
Journal of Gastroenterology and Hepatology 04/2011; 26 Suppl 3:88-93. · 2.87 Impact Factor
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ABSTRACT: Visceral hypersensitivity is one of the most important mechanisms of functional gastrointestinal diseases. Our previous studies have shown that rapid eye movement (REM) sleep deprivation (REMSD) decreases visceral sensitivity in rats, but the mechanisms involved in this effect, have not yet been clarified. In this study, we investigated the role of the CNS and peripheral endocannabinoids in visceral hyposensitivity induced by REMSD. Animals were randomly divided into the cage-yoked (YC), the REMSD group, which suffered from REMSD for 48 h, and the group with the interventions of Rimonabant after REMSD. The visceral sensitivity of all the groups was assessed, and the expressions of cannabinoid receptor (CB1R), fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MGL) in the CNS and gut regions, were detected. We demonstrate that REMSD decreases visceral sensitivity in rats and that the Rimonabant intervention antagonizes this effect. The expression of CB1R in the CNS region was significantly higher in the REMSD compared to the YC group. We did not see similar results in the gut. At the same time, the expressions of FAAH and MGL in the CNS and colon, excluding the iliac terminus, were lower in the REMSD compared to the YC group. Endocannabinoids are involved in the mechanism of visceral hyposensitivity in rats induced by REMSD. Possibly those in the CNS play the main role in this activity.
International Journal of Molecular Medicine 11/2010; 27(1):119-26. · 1.98 Impact Factor
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ABSTRACT: Visceral hypersensitivity is an important pathological mechanism of irritable bowel syndrome. Electroacupuncture (EA) could relieve chronic visceral hypersensitivity (CVH) in rats. However, little information is available about the mechanism. The aim of this study was to confirm the effects of EA at acupoint ST-36 (Zusanli) on CVH induced by the chemical colorectal irritation during postnatal development of rats, and to explore the possible 5-HT(3) receptor mechanism.
Rats were randomized into four groups, including the normal control group, CVH group, CVH with EA group, and CVH with sham EA group. The abdominal electromyogram (EMG) in response to colorectal distension was selected as the index for measurement of visceral hypersensitivity. 5-HT(3) receptors were analyzed through reverse transcription-polymerase chain reaction and western blot.
EA at ST-36 significantly decreased evoked EMG. The expression of 5-HT(3) receptor in the colon was increased in rats with CVH, and decreased after EA treatment.
EA at acupoint ST-36 attenuates CVH in rats and decreases 5-HT(3) receptor level in the colon. Decreased 5-HT(3) receptor level in the colon may mediate the beneficial effect of EA in rats with CVH.
International Journal of Colorectal Disease 11/2010; 26(5):569-74. · 2.38 Impact Factor
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ABSTRACT: Trimebutine maleate, which modulates the calcium and potassium channels, relieves abdominal pain in patients with irritable bowel syndrome. However, its effect on postinfectious irritable bowel syndrome is not clarified. The aim of this study was to investigate the effectiveness of trimebutine maleate on modulating colonic hypercontractility in a mouse model of postinfectious irritable bowel syndrome. Mice infected up to 8 weeks with T. spiralis underwent abdominal withdrawal reflex to colorectal distention to evaluate the visceral sensitivity at different time points. Tissues were examined for histopathology scores. Colonic longitudinal muscle strips were prepared in the organ bath under basal condition or to be stimulated by acetylcholine and potassium chloride, and consecutive concentrations of trimebutine maleate were added to the bath to record the strip responses. Significant inflammation was observed in the intestines of the mice infected 2 weeks, and it resolved in 8 weeks after infection. Visceral hyperalgesia and colonic muscle hypercontractility emerged after infection, and trimebutine maleate could effectively reduce the colonic hyperreactivity. Hypercontractility of the colonic muscle stimulated by acetylcholine and high K(+) could be inhibited by trimebutine maleate in solution with Ca(2+), but not in Ca(2+) free solution. Compared with 8-week postinfectious irritable bowel syndrome group, 2-week acute infected strips were much more sensitive to the stimulators and the drug trimebutine maleate. Trimebutine maleate was effective in reducing the colonic muscle hypercontractility of postinfectious irritable bowel syndrome mice. The findings may provide evidence for trimebutine maleate to treat postinfectious irritable bowel syndrome patients effectively.
European journal of pharmacology 04/2010; 636(1-3):159-65. · 2.59 Impact Factor
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ABSTRACT: Given that previous studies indicated that early growth response 1 (EGR1) exerts pro-tumorigenic effects through regulating heparanase (HPA) transcription, it was hypothesized that EGR1 may correlate with the progression of gastric cancer. One hundred and fifteen patients with gastric cancer were evaluated for the protein and transcript expression of EGR1 and HPA on immunohistochemistry and real-time quantitative polymerase chain reaction (PCR). In normal gastric mucosa, EGR1 protein expression was absent or weak, whereas gastric cancer was positive for EGR1. Seventy gastric cancer patients (60.9%) were positive for cytoplasmic EGR1 expression, and 26 (22.6%) had nuclear expression of EGR1. In the gastric cancer examined, the transcripts of EGR1 were enhanced compared to that of normal gastric mucosa, and positively correlated with EGR1 protein expression. The cytoplasmic or nuclear expression of EGR1 and its transcripts in gastric cancer was positively correlated with tumor infiltration (P < 0.05), lymph node and distant metastasis (P < 0.05), tumor node metastasis (TNM) stages (P < 0.05), but not with age, gender, tumor location and size, histological types or differentiation. Moreover, the protein and transcript expression of EGR1 was correlated with that of HPA in gastric cancer. These results indicate that aberrant expression of EGR1 in gastric cancer is associated with tumor invasion and metastasis, and HPA transcription.
Pathology International 04/2010; 60(4):268-77. · 1.62 Impact Factor
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ABSTRACT: Heparanase facilitates the invasion and metastasis of cancer cells, and is over-expressed in many kinds of malignancies. Our studies indicated that heparanase was frequently expressed in advanced gastric cancers. The aim of this study is to determine whether silencing of heparanase expression can abolish the malignant characteristics of gastric cancer cells.
Three heparanase-specific small interfering RNA (siRNAs) were designed, synthesized, and transfected into cultured gastric cancer cell line SGC-7901. Heparanase expression was measured by RT-PCR, real-time quantitative PCR and Western blot. Cell proliferation was detected by MTT colorimetry and colony formation assay. The in vitro invasion and metastasis of cancer cells were measured by cell adhesion assay, scratch assay and matrigel invasion assay. The angiogenesis capabilities of cancer cells were measured by tube formation of endothelial cells.
Transfection of siRNA against 1496-1514 bp of encoding regions resulted in reduced expression of heparanase, which started at 24 hrs and lasted for 120 hrs post-transfection. The siRNA-mediated silencing of heparanase suppressed the cellular proliferation of SGC-7901 cells. In addition, the in vitro invasion and metastasis of cancer cells were attenuated after knock-down of heparanase. Moreover, transfection of heparanase-specific siRNA attenuated the in vitro angiogenesis of cancer cells in a dose-dependent manner.
These results demonstrated that gene silencing of heparanase can efficiently abolish the proliferation, invasion, metastasis and angiogenesis of human gastric cancer cells in vitro, suggesting that heparanase-specific siRNA is of potential values as a novel therapeutic agent for human gastric cancer.
BMC Cancer 02/2010; 10:33. · 3.01 Impact Factor
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ABSTRACT: The aim of this study was to investigate the therapeutic potential of cutaneous gastric electrical stimulation (CGES) at a tachygastrial frequency for obesity.
Implantable gastric electrical stimulator has been proposed for the treatment of obesity and it has recently been reported that the gastric electrical stimulation at a tachygastrial frequency inhibits gastric motility.
Ten lean and 10 obese healthy volunteers were studied in 3 randomized sessions: no CGES, CGES at the physiologic frequency (3 cycles/min), and CGES at tachygastrial frequency (12 cycles/min). Electrical stimulation was performed using sinusoidal waves. The protocol included the following sequence: 20-minute baseline, 30-minute CGES, 30-minute recording without CGES, 30-minute CGES, ingestion of a 500 kcal liquid meal, and 30-minute CGES. Gastric slow waves were recorded using cutaneous electrogastrography during the periods without CGES. Gastric emptying was assessed by ultrasound. Dyspeptic symptoms were recorded.
(1) The half-time of gastric emptying was longer with CGES at the tachygastrial frequency than CGES at the physiologic frequency in both lean subjects (75.0+/-16.5 min vs. 41.0+/-8.7 min, P<0.01) and obese subjects (64.1+/-13.3 min vs. 32.7+/-5.0 min, P<0.01). (2) Postprandial dyspeptic symptom score (mainly satiety and fullness) was significantly higher with CGES at the tachygastrial frequency than CGES at the physiologic frequency in both lean (3.2+/-1.47 vs. 1.7+/-0.94, P<0.01) and obese (3.9+/-1.89 vs. 1.8+/-1.15, P<0.01) subjects.
CGES at a tachygastrial frequency enhances postprandial fullness and satiety, and delays gastric emptying. Its therapeutic potential for obesity needs to be studied.
Journal of clinical gastroenterology 02/2010; 44(5):335-9. · 2.21 Impact Factor
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ABSTRACT: Transduction with recombinant, replication-defective adenoviral (rAd) vectors encoding a transgene is an efficient method for gene transfer into dendritic cells (DCs). Livin is a member of the inhibitor of apoptosis protein family. Lung cancer and many other tumors express livin at high levels; whereas, normal fully differentiated cells generally do not. Therefore, livin represents a tumor-specific target for cancer vaccine therapy. Self proteins like livin may not stimulate potent antitumor immune responses due to central immunologic tolerance. Small variations in protein sequence that may exist between homologous proteins of different species can break tolerance to the native antigen. To study immunogenicity of a xenogeneic livin protein, we constructed an recombinant adenoviral vectors containing the human livin alpha genes (rAd-hlivin alpha) and vaccinated C57BL/6 mice with mouse bone marrow dendritic cells (BMDCs) transfected with rAd-hlivin alpha gave rise to potent livin-specific cytotoxic T lymphocyte (CTL) capable of lysing Lewis lung carcinoma (LLC) cells. Moreover, vaccination of mice with rAd-hlivin alpha-transduced DCs (rAd-hlivin alpha DCs) induced a potent protective and therapeutic anti-tumor immunity to LLC in a subcutaneous model along with prolonged survival compared to mice vaccinated with control recombinant adenovirus-transduced DCs(rAd-c DCs) or DCs alone. Therefore, xenogeneic differences between human and murine sequences might be exploited to develop immunogenic tumor vaccines.
Lung cancer (Amsterdam, Netherlands) 09/2009; 68(3):338-45. · 3.14 Impact Factor
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ABSTRACT: Trichinella spiralis infection in rodents is a well-known model of intestinal inflammation associated with hypermotility. The aim of the study was to use this experimental model to elucidate if Th17 cells are involved in the development of gastrointestinal hypermotility. Colonic smooth muscle contractility was investigated in response to acetylcholine. The levels of IL-17, IL-23 and TGF-beta1 in colon were measured by Western blotting. Flow cytometric detection of intracellular IFN-gamma/IL-4/IL-17 cytokine production was used to analyze the proportions of CD4+ T cells subsets in colon. Our results showed that colonic muscle contractility was increased 2 weeks post infection (PI) and stayed high 12 weeks PI when no discernible inflammation was present in the gut. The proportion of Th17 cells and the expression of IL-17 were up-regulated in colon 2 weeks PI and returned to normal 8 weeks PI. The content of IL-17 was correlated with the colonic smooth muscle hypercontracility 2 weeks PI. Meanwhile, TGF-beta1 was increased 2 weeks PI, while IL-23 was normal. Our results suggest that Th17 cells affect the colonic muscle contractility in mice infected with Trichinella spiralis at intestine stage but not at muscle stage and the effect of Th17 cells on muscle contractility might be induced by TGF-beta1. Other cytokines might be involved in the hypercontracility of colonic smooth muscle at muscle stage.
Journal of Huazhong University of Science and Technology 09/2009; 29(4):481-5. · 0.38 Impact Factor
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ABSTRACT: Although irritable bowel syndrome (IBS) is a common disorder in the West, information on the prevalence of IBS in university students is relatively scant, especially in Asia. The aims of the present study were to investigate the prevalence and pattern of symptoms of IBS and its relationship with psychological stress status in Chinese university students.
Basic demographic data and IBS symptoms were sought using the Rome II criteria and a validated bowel symptom questionnaire. Another questionnaire used related to psychosomatic symptoms of depression and anxiety.
In total, 491 of the 530 students in the trial met the selected criteria, which included 241 men. The participants were medical college students (313/491) and non-medical college students (178/491). The apparent prevalence of IBS was 15.7%, with a prevalence of 14.5% in men and 16.8% in women. The most common symptom was abdominal pain associated with change in the consistency of stool (36.9%), followed by altered stool frequency (16.3%), and abdominal pain relieved by defecation (12.4%), predominantly in women. The self-reported psychological and psychosomatic symptoms of anxiety (P < 0.001) and depression (P < 0.001) were encountered more frequently in participants with IBS. The depression (P = 0.03) and anxiety measures (P = 0.02) significantly predicted IBS status.
The prevalence of IBS in Chinese university students is often compared with university students in developed countries and the general Chinese population. Depression and anxiety could potentially induce IBS. Medical education should be considered when aiming to reduce stress of university students who are susceptible to IBS.
Journal of Gastroenterology and Hepatology 09/2009; 24(12):1885-90. · 2.87 Impact Factor
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ABSTRACT: Modulatory drugs of gastrointestinal (GI) motility are a possibility for use to relieve the main clinical presentation of sphincter of Oddi (SO) dysfunctions which are not easily distinguished from those occurring in high prevalence functional GI disorders. The aim of this study was to investigate the effects of GI motility modulators including pinaverium, domperidone, trimebutine, and tegaserod on the contractile activity of SO stimulated by carbachol in the rabbit.
The contraction responses precontracted by carbachol (0.1 microM) of in vitro rabbit SO rings were evaluated before and after the addition of a series concentration (10(-13) to 10(-3)M) of pinaverium, domperidone, trimebutine, and tegaserod.
Pinaverium induced a concentration-dependent relaxation of isolated SO rings (10(-13) vs. 10(-7) vs. 10(-3)M = 16.6 +/- 4.8 vs. 47.1 +/- 5.5 vs. 81.2 +/- 6.2%, p < 0.001 by ANOVA) precontracted with carbachol (0.1 microM). Tegaserod did not significantly effect (10(-13) vs. 10(-7) vs. 10(-3)M = 2.3 +/- 2.2 vs. 6.7+/- 2.1 vs. 10.1 +/- 2.3%, p > 0.05 by ANOVA) SO motility, but domperidone seemed to stimulate SO contractions (10(-12) vs. 10(-7) vs. 10(-3)M = -2.2 +/- 1.5 vs. -13.9 +/- 2.0 vs. -21.0 +/- 2.7%, p < 0.05 by ANOVA). At low doses (10(-13) to 10(-7)M), trimebutine stimulated SO contraction (-8.7 +/- 1.4 vs. -9.3 +/- 2.0%); however, high doses (10(-6) to 10(-3)M) of trimebutine inhibited SO motility (-5.9 +/- 1.7 vs. 14.5 +/- 2.0%, p < 0.05 by ANOVA).
Pinaverium totally inhibits contractions induced by carbachol and tegaserod has no effect on carbachol-induced contractions. Domperidone stimulates contractions induced by carbachol. Trimebutine could either stimulate or inhibit SO contractions depending on its dosage.
Pancreatology 08/2009; 9(5):615-20. · 1.99 Impact Factor
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ABSTRACT: The formation of goblet cells characterizes the intestinal metaplasia of Barrett's esophagus (BE). Hematoxylin-eosin (HE) staining may fail to show intestinal metaplasia in BE, and PAS-Alcian Blue may present difficulties of interpretation due to its more heterogeneous staining. Recent evidence indicates that expression of resistin-like molecule beta (RELMbeta), a goblet cell-specific protein, is uniquely restricted to intestinal epithelium. However, it still remains largely unknown whether RELMbeta can be served as a biomarker for metaplastic epithelium of BE. In this study, 104 biopsy specimens of the distal esophagus from 88 suspected BE patients were collected, including 56 suspected intestinal metaplasia, 26 gastric type mucosa, and 22 squamous epithelium. We evaluated the RELMbeta expression in these biopsy specimens, and compared with those of CDX-2 immunostaining and PAS-Alcian Blue staining (pH 2.5). Of the suspected intestinal metaplasia specimens, 46 presented intestinal-type goblet cells and were immunostaining positive for RELMbeta and CDX-2, the remaining ten possessed only goblet cell mimickers and were not reactive with RELMbeta and CDX-2. Of the gastric-type mucosa specimens, none reacted with either RELMbeta or CDX-2. Moreover, the squamous epithelium was not reactive with RELMbeta and CDX-2. Acid mucin was present in goblet cells in all cases of BE and columnar cells in ten gastric specimens. In addition, the reactivity of RELMbeta was enhanced in six BE specimens with dysplasia. These results provide evidence that RELMbeta protein may be a novel biomarker to distinguish the intestinal-type goblet cells and goblet cell mimickers, and useful in the correct diagnosis of BE.
Digestive Diseases and Sciences 03/2009; 55(1):32-9. · 2.12 Impact Factor
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ABSTRACT: To investigate the influence of beta-Elemene on expression of ANG II and RhoA/ROCK signaling in Hepatic Stellate Cells.
In vitro, HSC-T6 cell line was cultured for 24 hours and treated with several concentration of beta-elemene (5.0, 5.0, 2.5 mg x L(-1)) and Y-27632 (30 micromol x L(-1)) for 4, 12 and 24 h. Secretion of ANG II in the supernatant was detected by Radioimmunoassay. The mRNA expression of AGT, RhoA, ROCK-1 and ROCK-2 for 4 h, 12 h, 24 h was detected by RT-PCR respectively.
On the time point of 4h, the secretion of ANG II in supernatant by 10 mg x L(-1) beta-elemene was 50.970 +/- 8.081 pmol x L(-1), vs the control group (74.500 +/- 10.999) pmol x L(-1), P < 0.05; 5.0 mg x L(-1) and 2.5 mg x L(-) beta-elemene had no inhibitory effect on the secretion of ANG II, P > 0.05. On the time point of 12h, the secretion of ANG II in supernatant by 10 mg x L(-1), 5 mg x L(-1) beta-elemene was 83.727 +/- 6.850 pmol x L(-1), 91.090 +/- 3.226 pmol x L(-1), respectively, lower than the control (104.367 +/- 5.030 pmol x L(-1)), P < 0.01, P < 0.05. On the time point of 24h, compared with the control (116.620 +/- 7.110) pmol x L(-1)), the secretion ofANGII in supernatant by 2.5 mg x L(-1) and 5 mg x L(-1) beta-elemene was (104.133 +/- 3.296) pmol x L(-1), (100.957 +/- 2.581) pmol x L(-1), respectively, P < 0.05, P < 0.01; but the effect of 10 mg x L(-1) beta-elemene was not obviouse, P > 0.05. Compared with control group, the mRNA expression of AGT by different concentration of beta-elemene were significantly inhibited on different time point (4, 12, 24 h), F value was 30.33, 28.04, 107.19, respectively, P = 0.000. On the time point of 4h, 12 h and 24 h, the RhoAmRNA expression could be inhibited by 2.5, 5.0, 10 mg x L(-1) beta-elemene, (P = 0.000), and there existed no dose dependence. On the time point of 4 h and 24 h, ROCK-1 and ROCK-2mRNA could be inhibited by 2.5, 5.0 and 10 mg x L(-1) beta-elemene, P < 0.01, but on the time point of 12 h, there was no inhibitory effect.
Beta-elemene can inhibit the expression of AGTmRNA in HSC and the secretion of ANGII in supernatant. In addition, beta-elemene can inhibit the mRNA expression of RhoA, ROCK-1, ROCK-2mRNA to further regulate the biological effect of ANG II and delay the progress of hepatic fibrosis.
Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica 03/2009; 34(4):458-63.
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ABSTRACT: This study aims to investigate the influence of β-elemene on the secretion of angiotensin II (ANG II) and the expression of
angiotensin receptor type 1 (AT1R) in hepatic stellate cells (HSCs). In vitro, HSC-T6 were cultured for 24 hours and then treated with different doses of β-elemene (2.5, 5 and 10 mg/L). A control group
was also set up. The secretion of ANG II in the supernatant was detected by radioimmunoassay. The mRNA expression of AT1R
at 4, 12 and 24 h after treatment was detected by reverse transcription-polymerase chain reaction (RT-PCR), respectively.
The protein expression of AT1R was detected by western blot. At the 4th h, the ANG II secretion in the supernatant was significantly
inhibited by 10 mg/L β-elemene compared with the control group (P<0.05), while 5.0 mg/L and 2.5 mg/L β-elemene had no inhibitory effect on the secretion of ANG II (P>0.05). At the time point of the 12th h, the secretion of ANG II in the supernatant treated with 10 mg/L and 5.0 mg/L β-elemene
was significantly lower than the control (P<0.01, P<0.05). Following the treatment with 5.0 mg/L and 2.5 mg/L β-elemene for 24 h, significant inhibition of ANG II secretion
was observed (P<0.05), but 10 mg/L β-elemene had no such effect. β-elemene significantly reduced the amount of AT1R mRNA in HSCs after the
treatment for 4, 12, and 24 h in a dose-dependent manner. The expression of AT1R protein also decreased after the treatment
with β-elemene for 24 h. β-elemene can inhibit the secretion of ANG II and the gene and protein expression of AT1R, which
may be the mechanism by which β-elemene prevents the progress of hepatic fibrosis.
Frontiers of Medicine in China 02/2009; 3(1):36-40.
