CARDIOPROTECTIVE EFFECT OF MORIN AGAINST OXIDATIVE STRESS AND APOPTOTIC DAMAGE IN EXPERIMENTAL MODEL OF ISOPROTERENOL INDUCED MYOCARDIAL NECROSIS IN RATS

PURPOSE: To study the expression of heme-oxygenase-1 (HO-1), an enzyme induced by oxidative stress, in specimens obtained from an experimental model in rats that evaluated the role of gastric and duodenal reflux in esophageal carcinogenesis. METHODS: Esophageal specimens embedded in paraffin obtained from different experimental groups of rats were used for immunohistochemistry analysis of HO-1 expression. The rats had been divided into the following groups and were killed after 22 weeks: (1) cardioplasty to induce acid reflux; (2) esophagoduodenal anastomosis to induce duodenal reflux; (3) no treatment; (4) cardioplasty + diethylnitrosamine (DEN); (5) esophagoduodenal anastomosis + DEN; and (6) DEN. The study sample comprised 3 specimens from each group with the most severe histopathological lesions found on each study branch. RESULTS: The expression of HO-1 was seen only in rat specimens submitted to esophagoduodenal anastomosis (Groups 2 and 5), and the analysis of mean fluorescence intensity revealed a significant increase of HO-1 expression (4.8 and 4.6 fold, respectively) when compared with the control group (Group 3) (p<0.05). The main target for HO-1 induction was the inflammatory cells inside the tumor or in subepithelial areas. Rats exposed to gastric reflux had no HO-1 expression. CONCLUSION: Reflux esophagitis induced by reflux of duodenal contents, which provoked considerable oxidative stress, may play an important role in esophageal carcinogenesis. Acid reflux did not induce oxidative stress in this experimental model.

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Dietary krill oil (Euphausia superba) alleviates oxidative stress and DNA damages bio-markers in an experimental model of cafeteria diet-induced insulin resistance in rats

International Journal of Biosciences (IJB) ◽

10.12692/ijb/10.5.199-206 ◽

2017 ◽

Vol 10 (5) ◽

pp. 199-206

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Experimental Model ◽

Euphausia Superba ◽

Cafeteria Diet ◽

Krill Oil ◽

Dna Damages

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Cardioprotective Potential of Polyphenolic Rich Green Combination in Catecholamine Induced Myocardial Necrosis in Rabbits

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2015/734903 ◽

2015 ◽

Vol 2015 ◽

pp. 1-9 ◽

Cited By ~ 2

Author(s):

Fatiqa Zafar ◽

Nazish Jahan ◽

Khalil-Ur-Rahman ◽

Ahrar Khan ◽

Waseem Akram

Keyword(s):

Oxidative Stress ◽

Antioxidant Enzymes ◽

Histopathological Examination ◽

Cardiac Injury ◽

Myocardial Necrosis ◽

Myocardial Cell ◽

Marker Enzymes ◽

Cardiac Marker ◽

Synthetic Drugs ◽

Plant Mixture

The present study was designed to develop safer, effective, and viable cardioprotective herbal combination to control oxidative stress related cardiac ailments as new alternatives to synthetic drugs. The synergetic cardioprotective potential of herbal combination of four plantsT. arjuna(T.A.),P. nigrum(P.N),C. grandiflorus(C), andC. oxyacantha(Cr) was assessed through curative and preventive mode of treatment. In preventive mode of treatment, the cardiac injury was induced with synthetic catecholamine (salbutamol) to pretreated rabbits with the proposed herbal combination for three weeks. In curative mode of treatment, cardiotoxicity/oxidative stress was induced in rabbits with salbutamol prior to treating them with plant mixture. Cardiac marker enzymes, lipids profile, and antioxidant enzymes as biomarker of cardiotoxicity were determined in experimental animals. Rabbits administrated with mere salbutamol showed a significant increase in cardiac marker enzymes and lipid profile and decrease in antioxidant enzymes as compared to normal control indicating cardiotoxicity and myocardial cell necrosis. However, pre- and postadministration of plant mixture appreciably restored the levels of all biomarkers. Histopathological examination confirmed that the said combination was safer cardioprotective product.

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Role of Cox-2 in Vascular Inflammation: An Experimental Model of Metabolic Syndrome

Mediators of Inflammation ◽

10.1155/2013/513251 ◽

2013 ◽

Vol 2013 ◽

pp. 1-10 ◽

Cited By ~ 13

Author(s):

Nicolás F. Renna ◽

Emiliano R. Diez ◽

Carina Lembo ◽

Roberto M. Miatello

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Drinking Water ◽

Experimental Model ◽

Vascular Remodeling ◽

Vascular Inflammation ◽

Left Ventricular ◽

Wky Rats ◽

Cox 2

The objective of this work was to demonstrate the role of COX-2 enzyme at the vascular in experimental model of metabolic syndrome. SHR male WKY rats were employed; they were distributed in 8 groups (n=8each): control (W); W + L: WKY rats receiving 20 mg/kg of lumiracoxib by intraesophageal administration; SHR; SHR + L: SHR + 20 mg/kg of lumiracoxib by intraesophageal administration; Fructose-Fed Rats (FFR): WKY rats receiving 10% (w/v) fructose solution in drinking water during all 12 weeks; FFR + L: FFR + 20 mg/kg of lumiracoxib by intraesophageal administration; Fructose-Fed Hypertensive Rats (FFHR): SHR receiving 10% (w/v) fructose solution in drinking water during all 12 weeks; and FFHR + L: FFHR + 20 mg/kg of lumiracoxib by intraesophageal administration. Metabolic variables, blood pressure, morphometric variables, and oxidative stress variables were evaluated; also MMP-2 and MMP-9 (collagenases), VCAM-1, and NF-κB by Westernblot or IFI were evaluated. FFHR presented all variables of metabolic syndrome; there was also an increase in oxidative stress variables; vascular remodeling and left ventricular hypertrophy were evidenced along with a significant increase in the expression of the mentioned proinflammatory molecules and increased activity and expression of collagenase. Lumiracoxib was able to reverse vascular remodeling changes and inflammation, demonstrating the involvement of COX-2 in the pathophysiology of vascular remodeling in this experimental model.

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