Aim To study the mechanism of protective effects of Danbiqing granule (DBQ) on experimental acute bacterial cholangitis in rabbits. Methods The acute bacterial cholangitis was induced by injecting 1 mL of 1×10...Aim To study the mechanism of protective effects of Danbiqing granule (DBQ) on experimental acute bacterial cholangitis in rabbits. Methods The acute bacterial cholangitis was induced by injecting 1 mL of 1×10 8 cfu·mL -1 Escherchia coli suspension into common bile duit. The serum nitrous oxide (NO) levels were measured using nitric acid reductase kit. Phospholipase A 2 (PLA 2) activity was assayed by a method of acid titration (microassay). Serum tumor necrcsis factor α(TNF α), inferleukin 6 (IL 6) and plasma thromboxane B 2 (TXB 2), 6 keto platelet growth factor 1 (PGF 1α ) were determined by radioimmunoassay. Results Compared with control group, serum NO, PLA 2, TNF α, IL 6 and plasma TXB 2 levels increased significantly in model group ( P <0.01) while those of DBQ groups decreased significantly( P <0 01). Conclusion DBQ dramatically inhibits the overproduction of pro inflammatory factor PLA 2 and inflammatory cytokine. Hence, the mechanism of DBQ underlying anti inflammatory and protective effect against acute bacterial cholangitis in rabbits has been revealed.展开更多
AIM: To explore the relationship between small intestinalmotility and small intestinal bacteria overgrowth(SIBO) in Nonalcoholic steatohepatitis (NASH), andto investigate the effect of SIBO on the pathogenesisof NASH ...AIM: To explore the relationship between small intestinalmotility and small intestinal bacteria overgrowth(SIBO) in Nonalcoholic steatohepatitis (NASH), andto investigate the effect of SIBO on the pathogenesisof NASH in rats. The effect of cidomycin in alleviatingseverity of NASH is also studied. METHODS: Forty eight rats were randomly dividedinto NASH group (n = 16), cidomycin group (n = 16)and control group (n = 16). Then each group weresubdivided into small intestinal motility group (n = 8),bacteria group (n = 8) respectively. A semi-solid coloredmarker was used for monitoring small intestinal transit.The proximal small intestine was harvested under sterilecondition and processed for quantitation for aerobes(E. coli) and anaerobes (Lactobacilli). Liver pathologicscore was calculated to qualify the severity of hepatitis.Serum ALT, AST levels were detected to evaluate theseverity of hepatitis. RESULTS: Small intestinal transit was inhibited inNASH group (P < 0.01). Rats treated with cidomycinhad higher small intestine transit rate than rats in NASHgroup (P < 0.01). High fat diet resulted in quantitativealterations in the aerobes (E. coli ) but not in theanoerobics (Lactobacill). There was an increase in thenumber of E. coli in the proximal small intestinal florain NASH group than in control group (1.70 ± 0.12 log10(CFU/g) vs 1.28 ± 0.07 log10 (CFU/g), P < 0.01). TNF-αconcentration was significantly higher in NASH groupthan in control group (1.13 ± 0.15 mmol/L vs 0.57 ±0.09 mmol/L, P < 0.01). TNF-α concentration was lowerin cidomycin group than in NASH group (0.63 ± 0.09mmol/L vs 1.13 ± 0.15 mmol/L, P < 0.01). Treatmentwith cidomycin showed its effect by significantly loweringserum ALT, AST and TNF-α levels of NASH rats. CONCLUSION: SIBO may decrease small intestinalmovement in NASH rats. SIBO may be an importantpathogenesis of Nash. And treatment with cidomycin by mouth can alleviate the severity of NASH.展开更多
The gut flora plays an important role in the pathogenesis of the complications of cirrhosis. Hepatic encephalopathy (HE) represents a broad continuum of neuropsychological dysfunction in patients with acute or chronic...The gut flora plays an important role in the pathogenesis of the complications of cirrhosis. Hepatic encephalopathy (HE) represents a broad continuum of neuropsychological dysfunction in patients with acute or chronic liver disease and/or porto-systemic shunting of blood flow and it manifests with progressive deterioration of the superior neurological functions. The pathophysiology of this disease is complex, as it involves overproduction and reduced metabolism of various neurotoxins, particularly ammonia. Management of HE is diversified and requires several steps: elimination of precipitating factors, removal of toxins, proper nutritional support, modulation of resident fecal flora and downregulation of systemic and gut-derived inflammation. This review will provide an overview of gut barrier function and the influence of gut-derived factors on HE, focusing on the role of gut microbiota in the pathogenesis of HE and the recent literature findings on its therapeutic manipulation.展开更多
基金SupportedbyTianjinNinth Five YearProject,No .983 113 411
文摘Aim To study the mechanism of protective effects of Danbiqing granule (DBQ) on experimental acute bacterial cholangitis in rabbits. Methods The acute bacterial cholangitis was induced by injecting 1 mL of 1×10 8 cfu·mL -1 Escherchia coli suspension into common bile duit. The serum nitrous oxide (NO) levels were measured using nitric acid reductase kit. Phospholipase A 2 (PLA 2) activity was assayed by a method of acid titration (microassay). Serum tumor necrcsis factor α(TNF α), inferleukin 6 (IL 6) and plasma thromboxane B 2 (TXB 2), 6 keto platelet growth factor 1 (PGF 1α ) were determined by radioimmunoassay. Results Compared with control group, serum NO, PLA 2, TNF α, IL 6 and plasma TXB 2 levels increased significantly in model group ( P <0.01) while those of DBQ groups decreased significantly( P <0 01). Conclusion DBQ dramatically inhibits the overproduction of pro inflammatory factor PLA 2 and inflammatory cytokine. Hence, the mechanism of DBQ underlying anti inflammatory and protective effect against acute bacterial cholangitis in rabbits has been revealed.
文摘AIM: To explore the relationship between small intestinalmotility and small intestinal bacteria overgrowth(SIBO) in Nonalcoholic steatohepatitis (NASH), andto investigate the effect of SIBO on the pathogenesisof NASH in rats. The effect of cidomycin in alleviatingseverity of NASH is also studied. METHODS: Forty eight rats were randomly dividedinto NASH group (n = 16), cidomycin group (n = 16)and control group (n = 16). Then each group weresubdivided into small intestinal motility group (n = 8),bacteria group (n = 8) respectively. A semi-solid coloredmarker was used for monitoring small intestinal transit.The proximal small intestine was harvested under sterilecondition and processed for quantitation for aerobes(E. coli) and anaerobes (Lactobacilli). Liver pathologicscore was calculated to qualify the severity of hepatitis.Serum ALT, AST levels were detected to evaluate theseverity of hepatitis. RESULTS: Small intestinal transit was inhibited inNASH group (P < 0.01). Rats treated with cidomycinhad higher small intestine transit rate than rats in NASHgroup (P < 0.01). High fat diet resulted in quantitativealterations in the aerobes (E. coli ) but not in theanoerobics (Lactobacill). There was an increase in thenumber of E. coli in the proximal small intestinal florain NASH group than in control group (1.70 ± 0.12 log10(CFU/g) vs 1.28 ± 0.07 log10 (CFU/g), P < 0.01). TNF-αconcentration was significantly higher in NASH groupthan in control group (1.13 ± 0.15 mmol/L vs 0.57 ±0.09 mmol/L, P < 0.01). TNF-α concentration was lowerin cidomycin group than in NASH group (0.63 ± 0.09mmol/L vs 1.13 ± 0.15 mmol/L, P < 0.01). Treatmentwith cidomycin showed its effect by significantly loweringserum ALT, AST and TNF-α levels of NASH rats. CONCLUSION: SIBO may decrease small intestinalmovement in NASH rats. SIBO may be an importantpathogenesis of Nash. And treatment with cidomycin by mouth can alleviate the severity of NASH.
文摘The gut flora plays an important role in the pathogenesis of the complications of cirrhosis. Hepatic encephalopathy (HE) represents a broad continuum of neuropsychological dysfunction in patients with acute or chronic liver disease and/or porto-systemic shunting of blood flow and it manifests with progressive deterioration of the superior neurological functions. The pathophysiology of this disease is complex, as it involves overproduction and reduced metabolism of various neurotoxins, particularly ammonia. Management of HE is diversified and requires several steps: elimination of precipitating factors, removal of toxins, proper nutritional support, modulation of resident fecal flora and downregulation of systemic and gut-derived inflammation. This review will provide an overview of gut barrier function and the influence of gut-derived factors on HE, focusing on the role of gut microbiota in the pathogenesis of HE and the recent literature findings on its therapeutic manipulation.
