Background: Cardamom is a well-known spice in Indian subcontinent, used in culinary and traditional medicine practices since ancient times. The current investigation was untaken to evaluate the potential benefit of cardamom powder supplementation in high carbohydrate high fat (HCHF) diet induced obese rats. Method: Male Wistar rats (28 rats) were divided into four different groups such as Control, Control + cardamom, HCHF, HCHF + cardamom. High carbohydrate and high fat (HCHF) diet was prepared in our laboratory. Oral glucose tolerance test, organs wet weight measurements and oxidative stress parameters analysis as well as liver marker enzymes such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) activities were assayed on the tissues collected from the rats. Plasma lipids profiles were also measured in all groups of animals. Moreover, histological staining was also performed to evaluate inflammatory cells infiltration and fibrosis in liver. Results: The current investigation showed that, HCHF diet feeding in rats developed glucose intolerance and increased peritoneal fat deposition compared to control rats. Cardamom powder supplementation improved the glucose intolerance significantly (p > 0.05) and prevented the abdominal fat deposition in HCHF diet fed rats. HCHF diet feeding in rats also developed dyslipidemia, increased fat deposition and inflammation in liver compared to control rats. Cardamom powder supplementation significantly prevented the rise of lipid parameters (p > 0.05) in HCHF diet fed rats. Histological assessments confirmed that HCHF diet increased the fat deposition and inflammatory cells infiltration in liver which was normalized by cardamom powder supplementation in HCHF diet fed rats. Furthermore, HCHF diet increased lipid peroxidation, decreased antioxidant enzymes activities and increased advanced protein oxidation product level significantly (p > 0.05) both in plasma and liver tissue which were modulated by cardamom powder supplementation in HCHF diet fed rats. HCHF diet feeding in rats also increased the ALT, AST and ALP enzyme activities in plasma which were also normalized by cardamom powder supplementation in HCHF diet fed rats. Moreover, cardamom powder supplementation ameliorated the fibrosis in liver of HCHF diet fed rats. Conclusion: This study suggests that, cardamom powder supplementation can prevent dyslipidemia, oxidative stress and hepatic damage in HCHF diet fed rats.
BackgroundThe objective of the present study aimed to investigate the effect of CoQ10 treatment on isoprenaline (ISO)-induced cardiac remodeling in rats.MethodsRats were divided into three groups namely Control group, ISO treated group and CoQ10 + ISO treated group, each consisting of 6 rats. The cardiac specific CK-MB, AST, ALT activity and other oxidative stress parameters were estimated in heart and kidneys. Additionally histological examination was also performed to visualize the inflammatory cells infiltration and fibrosis in both tissues.ResultsAdministration of ISO resulted in an increase in the heart-to-body weight (HW/BW) ratio and an also increased the serum CK-MB, AST and ALT enzyme activity. Serum levels of lipid peroxidation products, and oxidative stress markers showed significant increase in ISO-treated rats. Histopathological examination of heart tissue revealed focal areas of endocardium degeneration, mononuclear cells infiltration, fibrous tissue deposition, and increased thickness of the myocardium of left ventricle. Similar degeneration was also found in kidneys. Treatment with CoQ10 (100 mg/kg) significantly improved the oxidative stresses in ISO treated rats. Moreover, CoQ10 treatment prevented inflammatory cells infiltration and reduced fibrosis in ISO administered rats.ConclusionIn conclusion, our study provides evidence that CoQ10 may prevent the development of cardiac remodeling, and fibrosis in ISO administered rats.
We evaluated the cardioprotective effect of Aloe vera gel isoprenaline (ISO)-administered myocardial infarction in rats. ISO administration increased lipid peroxidation and oxidative stress in rats, which were ameliorated by A. vera gel supplementation. Our study also revealed that creatine kinase-MB (CK-MB) activities were increased in ISO-administered rats, while the activities of cellular antioxidants, such as superoxide dismutase and catalase, and glutathione concentration were decreased. A. vera gel lowered CK-MB enzyme activities and the glutathione concentration in ISO-administered rats, and increased antioxidant activities. Histopathological examination also revealed increases in thickness of the left ventricle myocardium, increases in mononuclear cell infiltrations, increased degeneration of focal areas of the endocardium, and increased fibrous tissue deposition in the heart of ISO-administered rats; whereas, A. vera prevented infiltration of inflammatory cells and reduced left ventricular fibrosis. In conclusion, we show that A. vera supplementation protects against development of cardiac inflammation, fibrosis, and oxidative stress in ISO-administered rats.
Angiotensin-II is considered as a peptide responsible for the vascular dysfunction and complications in various tissues including liver through inducing free radicle mediated oxidative stress. This study aimed to evaluate the effect of ramipril, an angiotensin-converting enzyme inhibitor (ACE inhibitor), on oxidative stress, inflammation, and fibrosis in the liver of alloxan-induced diabetic rats. In this investigation, rats were divided into four groups (six rats in each group): control, control+ramipril, alloxan, and alloxan+ ramipril. A single dose (90 mg/kg) of alloxan was given intra-peritoneally to induce type two diabetes. After the induction of diabetes, ramipril (10 mg/kg) was administered to each animal for 21 days. An oral glucose tolerance test (OGTT) was performed. All animals were sacrificed at the end of the study. Blood and liver tissues were collected from each animal and stored for further biochemical studies. Liver marker enzymes and oxidative stress parameters were also assayed followed by histological examination in the liver. Alloxan administration in rats showed oral glucose intolerance and increased fasting blood glucose levels. Ramipril (10 mg/kg) treatment in alloxan administered rats improved the OGTT and lowered fasting blood glucose level. This study also revealed the elevation of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) enzymes activities in the alloxan administered rats which were attenuated by ramipril treatment. Oxidative stress parameters such as advanced protein oxidative products (APOP), nitric oxide (NO), and malondialdehyde (MDA) were also increased in alloxan administered rats which were diminished by the treatment of ramipril. Moreover, alloxan administration increased inflammation and fibrosis in the liver, which was further prevented by ramipril treatment. In conclusion, ramipril alleviated oxidative stress and fibrosis in the liver by suppressing oxidative stress. This investigation suggests that ACE inhibitors may be useful for treating diabetic complications and liver injury in alloxan-administered rats.
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