Boswellia serrata and Salvia miltiorrhiza extracts reduce DMN-induced hepatic fibrosis in mice by TGF-beta1 downregulation.

BACKGROUND: Hepatic fibrosis is characterised by a progressive accumulation of fibrillar extracellular matrix (ECM) proteins, including collagen that occurs in chronic liver diseases. Transforming growth factor-beta1 (TGF-beta)/Smad3 signalling plays a major role in tissue fibrogenesis acting as a potent stimulus of ECM accumulation. AIM: To evaluate the effects of a combined therapy with anti-inflammatory Boswellia and anti-fibrotic Salvia extracts on the course of chronic hepatitis-associated fibrosis induced by dimethylnitrosamine (DMN) in mice, as well as on the hepatic expression of TGF-beta1 and Smad proteins. METHODS: Chronic hepatitis-associated fibrosis was induced in mice by intraperitoneal DMN administration. Mice were assigned to 5 groups: controls; DMN without any treatment; DMN treated orally with Boswellia extracts (50 mg/kg/day); DMN treated orally with Salvia extracts (150 mg/ kg/day); DMN treated orally with both Boswellia (50 mg/kg/day) and Salvia extracts (150 mg/kg/ day). The liver was excised for macroscopic examination and histological, morphometric and immunohistochemical (IHC) analyses. For IHC, alpha-smooth muscle actin (alpha-SMA), collagen types I-III, TGF-beta1, connective tissue growth factor (CTGF), Smad3, Smad7, CD3, PCNA and TUNEL antibodies were used. RESULTS: The combined oral administration of Boswellia and Salvia extracts improved the course and macroscopic findings of DMN-induced chronic hepatitis-associated fibrosis. The histological severity of the hepatic fibrosis showed a marked improvement following treatment and was associated with a reduction in the hepatic expression of alpha-SMA, collagen I-III, CTGF, TGF-beta1, Smad3, and Smad7. CONCLUSIONS: These data demonstrate that co-treatment of Boswellia plus Salvia extracts is effective in preventing hepatic fibrosis in DMN-induced chronic hepatitis. The anti-fibrotic properties are mainly related to Salvia extracts and appear to be mediated by the inhibition of the TGF-beta1/Smad3 pathway.

Early acid perception in NERD.

Heartburn is the hallmark of gastroesophageal reflux disease. The hypothesis tested in this study is that the time of onset of this symptom may play a role in the development of mucosal lesions. During endoscopy of 61 patients complaining of heartburn and nine control subjects, gastric fluid was aspirated using a catheter introduced through the operative channel, and blindly instilled onto the esophageal mucosa before withdrawing the endoscope. Saline was used as control. Evocated symptoms and endoscopic lesions were recorded. Thirty-seven patients did not present esophageal lesions (nonerosive reflux disease [NERD]); 24 presented esophagitis (ERD). Instillation of gastric fluid on the esophageal mucosa elicited heartburn in 46% of patients with NERD, 8.3% with ERD, and 11.1% of controls. Symptoms lasted throughout the procedure but were no longer present when the gastroscope was withdrawn. The NERD value was significantly higher than that of ERD (P= 0.02) and controls (P= 0.02), while no difference was found between ERD and controls. Saline did not induce symptoms either in controls or patients. NERD patients show an early response to gastric fluid instillation much more frequently than ERD and controls. It is hypothesized that the early onset of symptoms in NERD patients may be a possibility to avoid the progress of mucosal lesions by claiming an earlier medical care.

Increased prevalence of Helicobacter pylori in patients with diabetes mellitus.

BACKGROUND: Whilst upper gastrointestinal disturbances are frequently observed in patients with diabetes mellitus, little is known about the prevalence of Helicobacter pylori infection and peptic disease in these patients. AIM: To evaluate prevalence of Helicobacter pylori infection and peptic disease lesions in diabetics with dyspeptic symptoms. PATIENTS AND METHODS: Study population comprises 74 consecutive diabetes mellitus patients with dyspepsia and 117 consecutive non diabetic dyspeptic patients. Upon enrolment, each patient completed an interview screening questionnaire to obtain information concerning presence and severity of dyspepsia. All patients underwent upper gastrointestinal endoscopy with biopsy specimens being collected from gastric antrum and body Helicobacter pylori was evaluated in each patient by rapid urease test and histology (Giemsa). Gastritis was classified according to the Sydney System. Statistical analysis was performed by chi-square, Fisher exact or t test and logistic regression analysis. A p value <0.05 was considered significant. RESULTS: Prevalence of Helicobacter pylori infection was found to be significantly higher in diabetics than in controls. The prevalence rate of endoscopic lesions was comparable in the two groups, but the association between endoscopic lesions and Helicobacter pylori infection was significantly higher in diabetics. Overall, the presence of chronic gastritis, both non atrophic and atrophic, as well as intestinal metaplasia were comparable in the two groups of patients, whilst the association between chronic gastritis and Helicobacter pylori infection or gastritis activity were significantly higher in diabetics. In neither group, was any correlation found between severity of dyspepsia and presence of endoscopic lesions, chronic gastritis or Helicobacter pylori infection. CONCLUSIONS: These data show a higher prevalence of Helicobacter pylori infection in diabetes mellitus patients with dyspepsia. Helicobacter pylori infection was significantly associated both with the presence of endoscopic lesions and chronic gastritis in diabetic patients, but not in the controls.