Impact of N-acetylcysteine and etodolac treatment on systolic and diastolic function in a rat model of myocardial steatosis induced by high-fat-diet.

OBJECTIVES: Obesity is a worldwide problem, leading to cardiomyopathy. Oxidative stress and inflammation have been reported to play significant roles in developing obesity cardiomyopathy. N-acetylcysteine is a glutathione prodrug that preserves liver against steatosis via constraining the production of reactive oxygen species. Etodolac is a nonsteroidal anti-inflammatory drug which has been demonstrated to protect liver against fibrosis. The aim of the present study was to evaluate and compare the effects of N-acetylcysteine and etodolac on impaired cardiac functions due to high-fat-diet (HFD) induced myocardial steatosis in rats. MATERIAL AND METHODS: Thirty-two male Sprague-Dawley rats were randomly divided into four groups. Control group was maintained on standard-rat-basic-diet (SD) for 20 weeks, while HFD was given to three study groups for 20 weeks. Then N-acetylcysteine was given to one of the study groups (HFD+NAC), and etodolac to another group (HFD+ETD) as a supplement for 4 weeks while all groups were continued on SD. At the end of the study periods, hearts were examined by Langendorff technique and rat livers were evaluated histologically. RESULTS: HFD and HFD+ETD groups presented with significantly higher steatosis and fibrosis in liver compared to other groups. HFD+NAC preserved diastolic functions. Also HFD+NAC and HFD+ETD groups had significantly better systolic funtions than HFD group. CONCLUSIONS: Obesity is associated with diastolic dysfunction rather than systolic dysfunction. NAC may protect the heart against diastolic dysfunction due to obesity. NAC and etodolac treatment improve systolic function, even in the absence of systolic dysfunction.

The relation of Helicobacter pylori with intestinal metaplasia, gastric atrophy and BCL-2.

BACKGROUND/AIMS: It is assumed that the sequence of events in gastric cancer is as follows: chronic gastritis, atrophy, intestinal metaplasia (IM), dysplasia, and carcinoma. It is also known that Helicobacter pylori (Hp) can be involved in the chain of these chronic phenomena. Therefore, we studied the relation of Hp with chronic inflammation, atrophy, activity level, IM and bcl-2. METHODS: The number of patients included in this study was 52; 35 (67.3%) were female and 17 (32.7%) were male. The average ages of women and men were determined as 44.5 and 41.5 years, respectively. Hp was determined in 53.8% of all cases and chronic inflammation was found in all cases. No dysplasia or gastric cancer was found in our cases. A statistically significant positive correlation was found between the Hp intensity and the degrees of chronic inflammation, atrophy and activity. RESULTS: Bcl-2 was found positive in 7.1% of the patients with Hp, and in 4.1% of the Hp-negative patients. However, bcl-2 was positive in 2 (8.7%) of 23 Hp-positive patients with chronic atrophic gastritis and in 1 (11.1%) of 9 Hp-negative patients with chronic atrophic gastritis. In other words, bcl-2 was found more in Hp-negative chronic atrophic gastritis than in Hp-positive chronic atrophic gastritis. Also, atrophy and IM were present together in 2 bcl-2-positive patients in whom Hp was positive. Bcl-2 was found positive more in IM than atrophy, proportionally. According to these data, although bcl-2 was found positive more often in Hp (+) cases proportionally, it was not statistically significant. Nevertheless, no significant difference was found between bcl-2 positivity and atrophy according to the statistical data. The data regarding the relation between IM and bcl-2 were statistically significant, and a positive correlation was found between them. CONCLUSIONS: We concluded that Hp infections result in chronic gastritis, have a role in the development of atrophy and IM, and that Hp infection has a significant relation with neutrophile activation. The more Hp intensity increases, the greater the degrees of chronic gastritis, activity and atrophy. We also found that Hp, which is known to increase apoptosis, increases the expression of bcl-2, an anti-apoptotic gene, not directly but rather by causing atrophy development. We observed more bcl-2 positivity in IM than in atrophy. Further studies with an extensive series of cases, including patients with dysplasia and gastric cancer, are needed to clarify statistical rates and to support the suggestion that bcl-2 expression increases with the progression to gastric cancer.