ABSTRACT
The objective of this study was to investigate the effect of astaxanthin on isoproterenol (ISO)-induced myocardial infarction and cardiac hypertrophy in rats. To evaluate the effect of astaxanthin on ISO-induced cardiac dysfunction, 18 aged Long Evans male rats were evenly divided into three groups. Group I (Control group) was given only the laboratory-ground food and normal water. Group II (ISO group) was administered ISO at a dose of 50 mg/kg subcutaneously (SC) twice a week for two weeks. Group III (Astaxanthin + ISO group) was treated with astaxanthin (25 mg/kg) orally every day and ISO 50 mg/kg SC twice a week for two weeks. ISO administration in rats increased the heart and left ventricular wet weights and increased inflammatory cell infiltration and fibrosis. Moreover, ISO administration increased the lipid peroxidation and decreased antioxidant enzyme activities in heart tissues. Astaxanthin treatment prevented the increased wet weight of heart and decreased inflammatory cell infiltration and fibrosis. The protective effect of astaxanthin was associated with reduction of free radicals by improving antioxidant enzyme function, as well as normalization and/or suppression of elevated oxidative stress markers, such as malondialdehyde (MDA), nitric oxide (NO), and advanced protein oxidation product (APOP) in ISO-administered rats. Furthermore, astaxanthin decreased the elevated activities of aspartate transaminase (AST), alanine transaminase (ALT), and creatinin kinase muscle/brain (CK-MB) in ISO-administered rats. In conclusion, astaxanthin may protect cardiac tissues in ISO-administered rats through suppression of oxidative stress and enhancement of antioxidant enzyme functions.
Subject(s)
Antioxidants/pharmacology , Cardiomegaly/drug therapy , Myocardial Infarction/drug therapy , Oxidative Stress/drug effects , Animals , Cardiomegaly/chemically induced , Heart/drug effects , Isoproterenol , Kidney/drug effects , Lipid Peroxidation/drug effects , Male , Myocardial Infarction/chemically induced , Myocardium/metabolism , Rats , Rats, Long-Evans , Xanthophylls/pharmacologyABSTRACT
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.
Subject(s)
Antioxidants/pharmacology , Dyslipidemias/diet therapy , Elettaria/chemistry , Liver Cirrhosis/prevention & control , Obesity/diet therapy , Plant Extracts/pharmacology , Abdominal Fat/drug effects , Abdominal Fat/metabolism , Abdominal Fat/pathology , Alanine Transaminase/metabolism , Alkaline Phosphatase/metabolism , Animals , Aspartate Aminotransferases/metabolism , Diet, High-Fat/adverse effects , Dietary Carbohydrates/adverse effects , Disease Models, Animal , Dyslipidemias/etiology , Dyslipidemias/metabolism , Dyslipidemias/physiopathology , Glucose/metabolism , Glucose Intolerance , Glucose Tolerance Test , Glycation End Products, Advanced/blood , Lipid Peroxidation/drug effects , Liver Cirrhosis/etiology , Liver Cirrhosis/metabolism , Liver Cirrhosis/physiopathology , Male , Obesity/etiology , Obesity/metabolism , Obesity/physiopathology , Oxidative Stress , Powders , Rats , Rats, WistarABSTRACT
BACKGROUND: Astaxanthin is of carotenoids group which possess strong antioxidant properties. The present study was conducted to evaluate the hepatoprotective effects of astaxanthin in carbon tetrachloride (CCl4)-treated rats. MATERIALS AND METHODS: Female Long-Evans rats were administered with CCl4 orally (1 ml/kg) twice a week for 2 weeks and were treated with astaxanthin (10 mg/kg) every day for 2 weeks. Blood plasma samples were isolated from each group and were analyzed for alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase activities. Oxidative stress parameters such as malondialdehyde (MDA), nitric oxide (NO), and advanced protein oxidation product (APOP) were measured. Several enzyme functions such as myeloperoxidase (MPO), superoxide dismutase (SOD), and catalase (CAT) activities in the plasma and liver tissues were also analyzed. Moreover, inflammation and tissue fibrosis were also confirmed by histological staining of liver tissues. RESULTS: This investigation revealed that CCl4 administration in rats increased plasma AST, ALT, and ALP activities which were normalized by astaxanthin treatment. Moreover, CCl4 administration increased as MDA, NO, and APOP level both in plasma and tissues compared to control rats. Astaxanthin also exhibited a significant reduction of those parameters in CCl4-administered rats. Astaxanthin treatment also restored the CAT and SOD activities and lowered MPO activity in CCl4-administered rats. Histological assessment also revealed that the astaxanthin prevented the inflammatory cells infiltration, decreased free iron deposition, and fibrosis in liver of CCl4-administered rats. CONCLUSION: These results suggest that astaxanthin protects liver damage induced by CCl4 by inhibiting lipid peroxidation and stimulating the cellular antioxidant system. SUMMARY: Carbon tetrachloride (CCl4) administration increased oxidative stress-mediated hepatic damage and inflammation in ratsAstaxanthin, a potent antioxidant, prevents oxidative stress and inflammatory cells infiltration in CCl4-administered ratsAstaxanthin also ameliorated the progression of hepatic fibrosis in CCl4-administered rats. Abbreviations Used: APOP: Advanced protein oxidation product; AST: Aspartate aminotransferase; ALT: Alanine aminotransferase; ALP: Alkaline phosphatase; CAT: Catalase; CCl4: Carbon tetrachloride; CVD: Cardiovascular disease; HSCs: Hepatic stellate cells; H2O2: Hydrogen peroxide; MDA: Malondialdehyde; MMP2: Matrix metalloproteinase2; MPO: Myeloperoxidase; NF-κB: Nuclear factor kappa B; NO: Nitric oxide; Nrf2: Nuclear factor erythroid 2-related factor 2; ·ONOO-: Peroxynitrate; ROS: Reactive oxygen species; SOD: superoxide dismutase; TCA: Trichloroacetic acid; TBA: Thiobarbituric acid; TGF-1: Transforming growth factor 1, TGF-ß: Transforming growth factor-ß; TIMP1: Tissue inhibitor of metalloproteinase 1; TNF-α: Tumor necrosis factor-alpha;·CCl3: Trichloromethyl free radical; CCl3O2-: Trichloroperoxyl radical.
ABSTRACT
BACKGROUND: Caryota urens is a member of the Arecaceae family and a common plant in the Southeast Asian region. This plant has been reported as an anti-microbial agent in recent years. Thus, we aimed to find out the MIC (minimum inhibitory concentration) against different pathogenic microorganism. METHODS: The leaves of C. urens were extracted and fractioned using different reagents (chloroform, n-hexane and carbon tetrachloride). Disc diffusion method was implemented for the assessment of in vitro anti-microbial potency (500 and 250 µg/disc). RESULT: The entire fraction showed good effect (with the zone of inhibition 19-25 mm) against both gram positive (Bacillus subtilis, Bacillus megaterium, Bacillus cereus, Sarina lutea) and gram negative (Vibrio mimicus, Shigella boydii, Escherichia coli, Pseudomonas aeruginosa) bacterial pathogens and fungal strains (Aspergillus niger, Saccharomyces cerevisiae). The plants also possess effective free radical scavenging potency with an IC50 of 130.32 µg/mL. CONCLUSION: This finding reflects a link between the presence of anti-oxidative material and a substantial anti-microbial activity, and substantiates all previous claims against C. urens.