Salvaging Complex Lower Extremity Injury with Laparoscopically Harvested Omental Flaps.

Background: Traumatic injuries to the lower extremities are frequently accompanied by extensive soft tissue loss, combined with vascular damage or exposure of bony tissues, making it difficult to reconstruct; consequently, patients are commonly at risk of amputation. Due to its superior anatomical and biochemical properties, the omental flap has been used to reconstruct soft tissue defects for decades. However, few studies have reported the omental flap's effectiveness in treating severe and complex lower extremity deformities. We attempted to use a laparoscopically harvested omental flap in conjunction with a second-stage skin graft to reduce infections during limb preservation, increase flap survival probability, and restore the aesthetic and functional integrity of the affected extremity. Methods: Seventeen patients with severe lower extremity wounds underwent omental flap transplantation and were followed up for 6 to 12 months to check for surgical complications, evaluate cosmetic results, and ensure proper limb function. Results: There were no complications, such as intestinal adhesion, intestinal volvulus, and peritonitis, with any of the omental grafts. The affected extremities were well-functioning and aesthetically pleasing. Conclusion: Laparoscopically harvested omental flap transplantation with skin grafting is an alternative reconstruction technique for severe lower extremity injuries with massive soft tissue loss and exposed bones and tendons.

[Application of bilateral facial perforator artery flap in repairing large area defect in middle and lower part of nose].

Objective: To investigate the feasibility and effectiveness of bilateral facial perforator artery flap in repairing large area defect in middle and lower part of nose. Methods: The clinical data of 18 patients with large area defect in middle and lower part of nose repaired by bilateral facial perforator artery flap between January 2019 and December 2022 were retrospectively analyzed. Among them, there were 13 males and 5 females, the age ranged from 43 to 81 years, with an average of 63 years. There were 3 cases of nasal trauma, 4 cases of basal cell carcinoma, 8 cases of squamous cell carcinoma, 1 case of lymphoma, and 2 cases of large area solar keratosis. The size of the defect ranged from 3.0 cm×3.0 cm to 4.5 cm×4.0 cm; the size of unilateral flap ranged from 3.0 cm×1.3 cm to 3.5 cm×2.0 cm, and the size of bilateral flaps ranged from 3.3 cm×2.6 cm to 4.5 cm×4.0 cm. Results: One patient developed skin flap necrosis after operation, and a frontal skin flap was used to repair the wound; 1 case gradually improved after removing some sutures due to venous congestion in the skin flap, and the wound healing was delayed after dressing change; the remaining 16 cases of bilateral facial perforator artery flaps survived well and all wounds healed by first intention, without any "cat ear" malformation. All 18 patients had first intention healing in the donor area, leaving linear scars without obvious scar hyperplasia, and no facial organ displacement. All patients were followed up 3-12 months, with an average of 6 months. Due to the appropriate thickness of the flap, none of the 18 patients underwent secondary flap thinning surgery. All flaps had good blood circulation, similar texture and color to surrounding tissues, symmetrical bilateral nasolabial sulcus, and high patient satisfaction. Conclusion: The bilateral facial perforator artery flaps for repairing large area defect in middle and lower part of nose can achieve good appearance and function, and the operation is relatively simple, with high patient satisfaction.

Relationship between antibiotic resistance and the cagA and vacA genotypes among Helicobacter pylori strain isolates from patients in Xi'an.

The issue of drug resistance of Helicobacter pylori is becoming increasingly serious. To analyze the correlation between the cagA and vacA genotypes of H. pylori strains and their resistance to metronidazole, levofloxacin, and clarithromycin in patients in Xi'an, we studied 117 H. pylori strains isolated from patients in Xi'an. Antibiotic susceptibility testing of H. pylori was performed. The cagA and vacA genotypes were investigated using PCR. Among 117 strains of H. pylori, the rate of detection of cagA was 91.45% (107/117), among which the detection rate of East Asian-type cagA was 85.05% (91/107) and that of Western-type cagA was 14.95% (16/107). There were only two genotypes of vacA: s1m1 and s1m2. The detection rate of vacAs1m1 was 47.01% (55/117) and that of vacAs1m2 was 52.99% (62/117). The dominant strains in Xi'an were cagA + vacAs1m2 strains. The metronidazole resistance rate of vacAs1m2 H. pylori strains was significantly higher than that of vacAs1m1 H. pylori strains (91.94% vs. 69.09%, P = 0.002). The levofloxacin resistance rate of Western-type cagA strains was significantly higher than that of East Asian-type cagA strains (56.25% vs. 20.88%, P = 0.004). The metronidazole resistance rate of cagA + vacAs1m2 H. pylori strains was significantly higher than that of cagA + vacAs1m1 H. pylori strains (91.23% vs. 66.00%, P = 0.001). Our results showed that Western-type cagA strains were more likely to develop levofloxacin resistance than East Asian-type cagA strains. VacAs1m2 strains were more prone to metronidazole resistance than vacAs1m1 strains.

MicroRNA-383 inhibits proliferation, migration, and invasion in hepatocellular carcinoma cells by targeting PHF8.

BACKGROUND: To study the effect of microRNA-383 (miR-383) on cell proliferation, migration, and invasion of hepatocellular carcinoma (HCC) cells, and explore its mechanism. METHODS: The expressions of miR-383 and plant homology domain that refers to protein 8 (PHF8) were detected in tissues and cells by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot respectively. The miR-383 group (transfected miR-383 mimics), miR-con group (transfected miR-con), si-con group (transfected si-con), si-PHF8 group (transfected si-PHF8), miR-383 + ctrl group (cotransfected miR-383 mimics and pcDNA-3.1), miR-383 + PHF8 group (cotransfected miR-383 mimics and pcDNA-3.1-PHF8) were transfected into HepG2 cells by liposome method. Cell proliferation, migration and invasion were measured by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) or trans-well assays respectively. The luciferase activity of each group was detected by dual luciferase reporter gene assay. RESULTS: Compared with normal adjacent tissues, the expression of miR-383 was significantly down-regulated and the expression of PHF8 was significantly up-regulated (p < .05). Compared with normal hepatocellular cell LO2, the expression of miR-383 was significantly reduced (p < .05) in HCC cells. Moreover, overexpression of miR-383 or silencing of PHF8 significantly inhibited the proliferation, migration, and invasion of HCC cells. In addition, PHF8 was targeted by miR-383 and its restoration rescued the inhibitory effect of miR-383 on cell proliferation, migration, and invasion of HCC cells. CONCLUSION: miR-383 could inhibit the proliferation, migration, and invasion of HCC cells by targeting PHF8, which will provide a basis for miR-383 targeted therapy for HCC.

Correlations between the serum bilirubin level and ulcerative colitis: a case-control study.

OBJECTIVE: To analyze whether the bilirubin level is a protective factor in ulcerative colitis (UC) and the predictive value of the bilirubin level. PATIENTS AND METHODS: We compared the bilirubin levels of 100 UC patients and 140 healthy controls as well as those of the subgroups of patients with different UC severities and then analyzed the correlation between the bilirubin level and UC and the correlations among the erythrocyte sedimentation rate (ESR), high sensitivity C-reactive protein (hs-CRP) level, UC severity, and bilirubin level. The predictive value of the bilirubin level for UC was determined by constructing a receiver operating characteristic (ROC) curve. RESULTS: The mean levels of the total bilirubin (TBIL) and indirect bilirubin (IBIL) in the UC were lower in comparison with the mean TBIL and IBIL levels in the control group, and the TBIL and IBIL levels were significantly higher in the mild activity subgroup than in the moderate and severe activity subgroups (P<0.05). TBIL (P<0.001, 95% confidence interval: 0.794-0.918) and especially IBIL (P<0.001, 95% confidence interval: 0.646-0.809) were independent protective factors for UC. There were also significant differences in the serum ESR and hs-CRP levels between the patients with different UC severities (ESR=χ: 23.975; hs-CRP=χ: 26.626, P<0.001), and there was a positive correlation between these two parameters (ESR=r: 0.472; hs-CRP=r: 0.495, P<0.001). However, the TBIL and IBIL levels were correlated negatively with the ESR (rtotal=-0.429, rindirect=-0.461, P<0.001) and hs-CRP (rtotal=-0.289, rindirect=-0.25, P<0.05) levels. The ROC curve showed that the threshold values of TBIL and IBIL were 8.87 and 6.735 µmol/l, the areas under the maximum ROC curve were 0.664 and 0.716, the sensitivities were 0.450 and 0.61, and the specificities were 0.800 and 0.786, respectively. CONCLUSION: TBIL and especially IBIL may be independent protective factors for UC because of their antioxidant and anti-inflammatory effects. A low level of IBIL has a moderate predictive value for UC, and an IBIL level less than 6.735 µmol/l can be used as a defining index for predicting UC.

Portulacaoleraceal extract alleviates trinitrobenzene sulfonic acid-induced colitis in rats.

Portulacaoleraceal (POL) has been widely used as an edible plant and a folk medicine in many countries, due to its several health benefits. This study examined the effects of POL on trinitrobenzene sulfonic acid (TNBS)-induced colitis via enema administration. Sixty male Sprague-Dawley rats were randomly divided into five groups: untreated, TNBS, TNBS + POL 10 g/kg, TNBS + POL 5 g/kg and TNBS + POL 2.5 g/kg groups. Rats were subjected to enema treatment once a day for 10 consecutive days with POL extract or distilled water after induction of TNBS. The changes of body weight, histological parameters, myeloperoxidase (MPO), superoxide dismutase (SOD), nitric oxide synthase activity (NOS), malondialdehyde (MDA) and nitric oxide (NO) levels in colon tissues were investigated. After POL extract treatment, body weights of rats significantly increased, macroscopic and microscopic damage scores reduced, MPO and NOS activity, as well as MDA and NO level significantly decreased, while SOD activity increased in a dose-dependent manner in the TNBS + POL groups compared with the TNBS group. Our results demonstrated that POL enema treatment attenuated pathologic changes of TNBS-induced colitis in rats through restoring colonic damage and reducing inflammatory response in the intestine. Thus, POL enema might be considered as a potential effective treatment for ulcerative colitis patients.

Endoscopic ultrasonography for preoperative staging of esophageal carcinoma.

OBJECTIVE: To evaluate the diagnostic value of endoscopic ultrasonography (EUS) in preoperative staging of esophageal carcinoma (EC). MATERIAL AND METHODS: A total of 86 surgical patients with EC who were confirmed by endoscopy and biopsy underwent preoperative TN staging with EUS examination. The EUS findings were compared with surgical pathologic results. RESULTS: The accuracy of EUS in T and N staging of EC was 82.6% and 84.9%, respectively. While determining whether EC invades the muscularis propria or outer membrane, EUS had the favorable sensitivity, specificity, positive predictive value and negative predictive value. The short-axis diameter of lymph nodes of 5mm had high sensitivity and negative predictive value to determine malignance with low specificity and positive predictive value. The short-axis diameter of 10mm presented the satisfactory sensitivity, specificity, positive predictive value and negative predictive value. CONCLUSION: EUS can accurately determine the TN staging of EC and provide a reliable basis for the treatment of EC.

Chlorogenic acid protects against liver fibrosis in vivo and in vitro through inhibition of oxidative stress.

Liver fibrosis is a scaring process related to chronic liver injury of all causes and as yet no truly effective treatment is available. Chlorogenic acid (CGA) is a phenolic compound and exerts anti-inflammatory and anti-oxidant activities. Our former studies suggested that CGA could prevent CCl4-induced liver fibrosis through inhibition of inflammatory signaling pathway in rats. However, whether the anti-oxidant activity is involved in the anti-fibrotic effect of CGA on liver fibrosis is not yet fully understood. This study examined whether CGA may prevent CCl4-induced liver fibrosis by improving anti-oxidant capacity via activation of Nrf2 pathway and suppressing the PDGF-induced profibrotic action via inhibition of NOX/ROS/MAPK pathway. The studies in vivo showed that the liver fibrosis degree, hydroxyproline content and expression of α-SMA, Collagen Ⅰ, Collagen Ⅲ and TIMP-1 were increased in CCl4-injected rats and which were alleviated markedly by CGA. Furthermore, CGA significantly decreased CYP2E1 expression and increased the expression of nuclear Nrf2 and Nrf2-regulated anti-oxidant genes (HO-1, GCLC and NQO1). CGA decreased MDA level and increased GSH, SOD and CAT levels in liver tissues. In vitro studies PDGF could induce NOX subunits (p47phox and gp91phox) expression, ROS production, p38 and ERK1/2 phosphorylation, HSCs proliferation and profibrotic genes expression in HSCs, all of which were reduced by CGA treatment. In conclusion, the results suggest that CGA protects against CCl4-induced liver fibrosis, at least in part, through the suppression of oxidative stress in liver and hepatic stellate cells.

[Camostat mesilate, a protease inhibitor, inhibits visceral sensitivity and spinal c-fos expression in rats with acute restraint stress].

OBJECTIVE: To observe the effect of gut protease activity on visceral hypersensitivity in rats with acute restraint stress. METHODS: Sprague-Dawley rats were given 30, 100 or 300 mg/kg camostat mesilate (CM), a protease inhibitor, or saline intragastrically 30 min before acute restraint stress induced by wrapping the fore shoulders, upper forelimbs and thoracic trunk for 2 h. Visceral perception of the rats was quantified as the visceral motor response with an electromyography, and the rectal mucosa and feces protease activity and spinal c-fos expression were measured. RESULTS: CM dose-dependently reduced visceral sensitization elicited by rectal distension, but these doses did not completely inhibit stress-induced visceral sensitization. In normal rats, c-fos expression was found mainly in the superal spinal cord dorsal horn, and after the administration the CM, c-fos-positive cells decreased significantly in all dose groups (P<0.05). In 30 mg/kg CM group, fecal and rectal mucosal protease activity significantly decreased as compared with that in the stress group (P<0.05), and as CM dose increased to 100 and 300 mg/kg, the protease activity decreased even further (P<0.01). CONCLUSION: The gut protease is involved in acute stress-induced visceral hypersensitivity, and CM can lower the visceral sensitivity and spinal c-fos expression in rats.

Expression of G protein-coupled estrogen receptor in irritable bowel syndrome and its clinical significance.

OBJECTIVES: Estrogen is suggested to participate in pathogenesis of irritable bowel syndrome (IBS), but expression of G protein-coupled estrogen receptor (GPER) in the colon of IBS patients has never been investigated. The aim of this study was to investigate the expression of GPER and classical estrogen receptors in the colon of IBS patients and healthy controls. METHODS: Colonic biopsies were obtained by endoscopy from patients with IBS (n=46) and healthy subjects (n=13). Expression of GPER, estrogen receptor α (ERα) and estrogen receptor ß (ERß) in mast cells were measured by double-labelling immunofluorescence. Quantification of mRNA expression was performed for GPER, ERα and ERß by real-time polymerase chain reaction. RESULTS: Differential distribution of GPER, ERα and ERß were detected in human colonic mucosa. The expression of GPER in the cytoplasm of mast cells and GPER-positive cells was significantly higher in diarrhea-predominant IBS (D-IBS) patients than that in constipation-predominant IBS (C-IBS, P<0.001) patients and healthy subjects (P=0.005). ERα and ERß were not detected in majority of mast cells in colonic mucosa and no difference of immunostaining results for ERα and ERß was found among these three groups. A positive correlation (r=0.451, P=0.011) between GPER-positive cell counts and abdominal pain severity was observed in D-IBS group. Relative mRNA expression of GPER in D-IBS was also higher than that in C-IBS (P=0.018) and healthy subjects (P=0.011). CONCLUSIONS: The present study, for the first time, demonstrated the expression of GPER in human colonic mucosa and its correlation with abdominal pain severity.

[Effect of high glucose on toll-like receptor 4 expression and LPS-induced proinflammatory cytokine production in hepatic stellate cells in vitro].

OBJECTIVE: To investigate the effect of high glucose on the expressions of toll-like receptor 4 (TLR4) and proinflammatory cytokine production induced by lipopolysaccharide (LPS) in hepatic stellate cells in vitro. METHODS: Hepatic stellate cell line T6 was cultured in vitro and stimulated by high glucose. The mRNA and protein expression of TLR4 were detected by RT-PCR and Western blotting, respectively. After a 24-h pretreatment with high or low glucose, the cells were stimulated with LPS for 2 h, and Western blotting was used to detect the nuclear translocation of nuclear factor-κB (NF-κB); at 24 h of LPS exposure, the cells were examined for MCP-1 and IL-6 mRNA and protein expression levels with RT-PCR and ELISA, respectively. RESULTS: High glucose significantly increased the mRNA and protein expressions of TLR4 (P<0.01) in a time- and dose-dependent manner. High glucose promoted NF-κB nuclear translocation and significantly enhanced the expression and secretion of both MCP-1 and IL-6 (P<0.01). Pretreatment with high glucose significantly promoted LPS-induced NF-κB nuclear translocation (P<0.01) and the mRNA expression and secretion of MCP-1 and IL-6. CONCLUSIONS: High glucose can increase TLR4 mRNA and protein expressions in hepatic stellate cells and promote LPS-induced NF-κB activation and production of proinflammatory cytokines.

Chlorogenic acid reduces liver inflammation and fibrosis through inhibition of toll-like receptor 4 signaling pathway.

Chlorogenic acid (CGA) is a type of polyphenol with anti-inflammatory, antioxidant activities. Our previous studies showed CGA could efficiently inhibit carbon tetrachloride (CCl(4))-induced liver fibrosis in rats. However, the specific underlying mechanism remains unclear. The aim of this study is to investigate the effects of CGA on liver inflammation and fibrosis induced by CCl(4) and whether they are related to inhibition of toll-like receptor 4 (TLR4) signaling pathway. Male Sprague-Dawley (SD) rats were administrated CCl(4) together with or without CGA for 8 weeks. Histopathological and biochemical analyses were carried out. The mRNA and protein expression levels of proinflammatory and profibrotic mediators were detected by RT-PCR and Western blot, respectively. The levels of serum proinflammatory cytokines were detected by ELISA. CGA significantly attenuated CCl(4)-induced liver damage and symptoms of liver fibrosis, accompanied by reduced serum transaminase levels, collagen I and α-smooth muscle actin (α-SMA) expression. As compared with the CCl(4)-treated group, the expression levels of TLR4, myeloid differentiation factor 88 (MyD88), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were reduced in the treatment group of CCl(4) and CGA, whereas bone morphogenetic protein and activin membrane-bound inhibitor (Bambi) expression was increased. CGA also suppressed CCl(4) induced nuclear factor-κB (NF-κB) activation. Moreover, the hepatic mRNA expression and serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1ß (IL-1ß) were significantly increased in CCl(4)-treated rats and attenuated by co-treatment with CGA. Our data indicate that CGA can efficiently inhibit CCl(4)-induced liver fibrosis in rats and the protective effect may be due to the inhibition of TLR4/MyD88/NF-κB signaling pathway.

The expression of protease-activated receptor 2 and 4 in the colon of irritable bowel syndrome patients.

BACKGROUND: Irritable bowel syndrome (IBS) pathophysiology has not been fully understood. Abnormalities of serine proteases have been identified in IBS patients. In addition, protease-activated receptors (PAR) activation interferes with several components of the pathogenesis of IBS, so, evaluating the PAR expression in IBS patients may contribute to understanding the pathogenesis of the disease. AIMS: This study aimed to investigate whether the expression of PAR4 and PAR2 in the colon was changed in IBS patients and was associated with IBS. METHODS: Colon mucosal biopsies of 34 IBS patients (16 constipation- and 18 diarrhea-predominant) and 18 control subjects were collected. Gene transcripts of PAR2, PAR4, tryptase, and trypsin were quantified using real-time polymerase chain reaction (PCR) and the expression of PAR2 and PAR4 receptors was also measured by immunohistology and image analysis. RESULTS: In IBS patients, the mRNA expression of tryptase and trypsin normalized against ß-actin gene was higher compared to control subjects (P < 0.001). No difference was observed in the PAR2 mRNA level or protein level between control subjects on the one hand and IBS patients or subgroups on the other. In IBS or IBS subgroups patients, the expression of PAR4 in the mRNA level or protein level was lower than the control subjects. CONCLUSIONS: This study, for the first time, indicated the PAR4 expression in IBS patients. Decreased PAR4 expression may help us to understand the pathogenesis of IBS.

A protease inhibitor against acute stress-induced visceral hypersensitivity and paracellular permeability in rats.

In the present study, we investigated the effects of camostat mesilate (CM), a synthetic protease inhibitor, on visceral sensitivity and paracellular permeability induced by the acute restraint stress. We also explored the possible mechanisms underlying these effects. The acute restraint stress was induced by wrapping the fore shoulders, upper forelimbs and thoracic trunk of Sprague-Dawley rats for 2h. Either CM (30, 100 and 300mg/kg) or saline was intragastrically administrated to the rats 30min before the acute restraint stress. Visceral perception was quantified as visceral motor response with an electromyography in a subset of rats. Paracellular permeability was determined in another subset of rats. We found that the visceral sensitivity and paracellular permeability were significantly reduced in the CM-treated rats. Moreover, the fecal protease activity was decreased in the CM-treated rats. The ZO-1 protein expression was markedly reduced by the stress treatment, but this decrease was suppressed by CM administration. Our data indicated that CM could efficiently inhibit visceral sensitivity and paracellular permeability induced by the acute restraint stress in rats. Therefore, CM might be an effective drug for the treatment of irritable bowel syndrome.

Neferine inhibits cultured hepatic stellate cell activation and facilitates apoptosis: A possible molecular mechanism.

Neferine is a major alkaloid component of "Lian Zi Xin", embryos of the seeds of Nelumbo nucifera Gaertner, Nymphaeaceae. Previous studies have shown that neferine has an inhibitory effect on pulmonary fibrosis through its anti-inflammatory and anti-oxidative activities and inhibition of cytokines and NF-κB. However, it is unknown whether neferine also has an inhibitory effect on liver fibrosis through inhibition of TGF-ß1 and collagen I and facilitation of apoptosis of hepatic stellate cells. This study examined the effects of neferine on cultured hepatic stellate (HSC-T6) cells and explored its possible action mechanisms by means of MTT assay, enzyme-linked immunosorbent assay, flow-cytometric annexin V-PI assay and Hoechst 33258 staining, as well as real-time PCR and western blotting. The results showed that neferine administration (2, 4, 6, 8 and 10µmol/l) significantly decreased the TGF-ß1 and collagen I produced in HSC-T6 cells, and increased the HSC-T6 cell apoptosis in a dose-dependent manner. Neferine treatment for 48h at concentrations of 6 and 10µmol/l significantly increased Bax and caspase 3 mRNAs and proteins, and reduced Bcl2 and alpha-smooth muscle actin (α-SMA) mRNAs and proteins. Our data indicate that neferine efficiently inhibits cultured HSC-T6 cell activation and induces apoptosis by increasing Bax and caspase 3 expression via the mitochondrial pathway.

Protective effect of a coffee preparation (Nescafe pure) against carbon tetrachloride-induced liver fibrosis in rats.

BACKGROUND & AIMS: We examined the effects of a coffee preparation on liver fibrosis induced by carbon tetrachloride (CCl(4)) and explored the possible mechanisms. METHODS: Rats were divided randomly into four groups: control, CCl(4), and two coffee preparation groups. Except for the control group, liver fibrosis was induced in male Sprague-Dawley (SD) rats by subcutaneous injection with 40% CCl(4) twice a week for 8 weeks. At the same time, a coffee preparation (300 mg/kg and 150 mg/kg) was administered to the two coffee preparation groups intragastrically once daily. RESULTS: Upon pathological examination, a coffee preparation treatment significantly reduced liver damage and symptoms of liver fibrosis. The mRNA expression of collagen I, collagen III, bcl-2, vascular endothelial growth factor (VEGF) and transforming growth factor-beta1 (TGF-beta1) were markedly increased by CCl(4) treatment but suppressed by a coffee preparation treatment. Whereas compared with the CCl(4) group, the mRNA expression of Bax was increased in the coffee preparation group. The protein expression of Bax and bcl-2 were confirmed by western blot. Intragastric administration of a coffee preparation reduced the protein expression of alpha-smooth muscle actin (alpha-SMA) and the glucose-regulated proteins (GRP) 78 and 94 in rats increased by CCl(4). CONCLUSIONS: Our data indicate that a coffee preparation can efficiently inhibit CCl(4)-induced liver fibrosis in rats. The coffee preparation may therefore be a potential functional food for preventing liver fibrosis.

Chlorogenic acid against carbon tetrachloride-induced liver fibrosis in rats.

This study examined the effects of chlorogenic acid (CGA) on liver fibrosis induced by carbon tetrachloride (CCl(4)) and explored the possible mechanisms of action. Liver fibrosis was induced in male Sprague-Dawley (SD) rats by the injection of 40% CCl(4) subcutaneously twice a week for eight weeks. At the same time, CGA (60 and 30mg/kg) was administered intragastrically once daily to a subset of rats. Upon pathological examination, the CGA-treated rats showed significantly reduced liver damage and symptoms of liver fibrosis. The expression of collagen I and collagen III mRNA was increased markedly by the CCl(4) treatment but this increase was suppressed by CGA. As compared with the CGA-treated group, the expression of bcl-2, vascular endothelial growth factor (VEGF), and transforming growth factor (TGF-beta1) mRNA was increased in CCl(4) group, whereas Bax mRNA expression decreased. The expression of Bax and bcl-2 protein was confirmed by western blotting. Intragastric administration of CGA reduced the protein expression of alpha-smooth muscle actin (alpha-SMA) and glucose-regulated proteins 78 and 94 (GRP78 and GRP94) in rats injured by treatment with CCl(4). Our data indicate that CGA can efficiently inhibit CCl(4)-induced liver fibrosis in rats. Therefore, CGA could be an effective drug for preventing liver fibrosis.

[Small intestine motility and gastrointestinal hormone levels in irritable bowel syndrome].

OBJECTIVE: To investigate the relationship between interdigestive migrating motor complex (MMC) and plasma gastrointestinal hormones in patients with diarrhea or constipation-predominant irritable bowel syndrome (IBS) to elucidate the pathophysiology of IBS. METHODS: A small intestine manometry was used to record the MMC cycles for at least 4-6 h in 19 IBS patients and 10 healthy volunteers. The plasma gastrointestinal hormone levels were examined according to altered MMC phases. RESULTS: Compared with the healthy controls, IBS-D patients exhibited shortened duration of the small intestinal MMC cycle, prolonged phase III duration with greater amplitude, as well as faster propagation velocity, whereas the contrary alterations were found in IBS-C patients. The peak plasma motilin level occurred in phase III of the MMC cycle. The plasma somatostatin level was higher in IBS groups than in the healthy controls, but comparable between the diarrhea and constipation groups. Plasma 5-hydroxytryptamine showed periodical fluctuations with the phases of MMC cycles, reaching the peak level in phase II. IBS-D patients had higher 5-hydroxytryptamine levels than IBS-C patients and the healthy controls. CONCLUSIONS: Plasma hormone levels are correlated with the MMC cycles, and the hormone level changes and small intestine motility disorder may play important roles in IBS pathophysiology.