Cardioprotective effect of fluvastatin on isoproterenol-induced myocardial infarction in rat

Zhou, Ran; Chen, Nansheng; Zheng, Ping; Yang, Lin; Zheng, Jie; Dai, Guidong

doi:10.1016/j.ejphar.2008.02.057

Cited by 154 publications

(94 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Supramaximal doses of isoprenaline induced subendocardial myocardial ischemia, hypoxia, necrosis, and finally fibroblastic hyperplasia with decreased myocardial compliance and inhibition of diastolic and systolic function 22 .…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Cardioprotective Activity of Fulvic Acid Against Isoproterenol Induced Oxidative Damage in Rat Myocardium

Shikalgar¹,

Naikwade²

2018

Int. Res. J. Pharm.

View full text Add to dashboard Cite

The aim of study was to evaluate cardio protective activity of fulvic acid in Isoprenaline induced cardiac toxicity. In current investigation, female/male wistar rats were divided into five groups, normal, control, Fulvic acid 100mg/kg, Fulvic acid 200mg/kg, and Fulvic acid 300 mg/kg. Isoprenaline 85 mg/kg was administered on 29 th and 30 th day during study period to all except normal group. Fulvic acid was administered to respective groups once daily for total 30 days, on the last day of study, the animals were anesthetized to record ECG and BP (by cannulating carotid artery), blood was collected from carotid artery and SGOT, LDH And CK-MB were estimated, Animals were sacrificed to isolate heart and preparation of tissue homogenate. The antioxidant status is analyzed by measuring MDA content, SOD CAT, GSH activity. The tissue sample is also preserved for histological studies. Isoprenaline causes cardiac damage which was manifested by alteration in serum cardiac markers, antioxidant markers, ECG and hemodynamic and histological changes. These alterations were restored due to treatment with fulvic acid 300mg/kg. With data obtained in study it have been concluded that fulvic acid treatment for 4 weeks protect the heart of rat from cardiotoxicity as a result of isoprenaline administration.

show abstract

Section: Discussionmentioning

confidence: 99%

Evaluation of Cardioprotective Activity of Fulvic Acid Against Isoproterenol Induced Oxidative Damage in Rat Myocardium

Shikalgar¹,

Naikwade²

2018

Int. Res. J. Pharm.

View full text Add to dashboard Cite

show abstract

“…The declined enzyme activities secondary to drug and the extract treatments might be ascribed to their ability to maintain membrane integrity thereby restricting the leakage of these enzymes [37,38]. Thus, the enhancement in enzyme activities resulting from extracts supplementation may help in preventing oxidative damage by detoxifying ROS; that in turn, reduce hyperlipidemia.…”

Section: The Hepatic Ameliorative Effect Of I Tricolor and S Tomentosamentioning

confidence: 99%

Statistical Data Analysis Which Result From the Bio-Diagnosis and Bio-Treatment of Injured Rats With the Hyperlipidemia and Hyperglycemia Diseases

Abduallah¹,

Abd‐Alla²,

Ali³

et al. 2016

Asian J Pharm Clin Res

View full text Add to dashboard Cite

Objective: This study in bioinformatics aims to investigate the potential effect of Ipomoea tricolor and Sophora tomentosa on liver function enzymes activity, serum lipid profile, oxidative stress biomarkers, and on blood glucose in high fat diet-induced hypercholesterolemia (HC) and STZ-induced hyperglycemia (HG) in rats.Methods: Blood glucose level, liver function enzymes, alanine aminotransferases and aspartate aminotransferases, alkaline phosphatase, and lactate dehydrogenase (LDH) were determined. Besides, lipid profile including total cholesterol (TC), triacylglycerol (TG), total lipid, and high-density lipoprotein-cholesterol was investigated. Moreover, oxidative stress biomarkers, lipid peroxide, and nitric oxide as well as non-enzymatic antioxidant, glutathione (GSH) were also examined in different therapeutic groups.Results: A significant increase in blood glucose level, liver function enzyme activities, LDH, lipid profile and oxidative stress markers, while significant decrease in LDH-C and GSH level in HC-HG induced rats compared to control one. A marked amelioration in all biochemical parameters under investigation on treatment of HC-HG rats with I. tricolor and S. tomentosa with different fluctuating percentages of improvement. Histopathological examination of liver and pancreas was also performed and declared HC-HG showed congestion in portal vessels and sinusoids with mild centrilobular hepatocyte degeneration, marked hepatocyte ballooning and hydropic degeneration, while HC-HG treated rats with I. tricolor and S. tomentosa showed normal lobular hepatic architecture with mild sinusoidal dilatation and congestion. On the other hand, a histological organization of pancreas of HC-HG rats showing disarrangement changes in pancreatic blood vessels and interlobular duct as well as disordered in acini. The treatment of HC-HG rats with I. tricolor and S. tomentosa showed enhancement in Langerhans cells and restore of most pancreatic tissue in comparison with standard drugs. Conclusion:The statistical results showed that each extract ameliorated high blood glucose level liver injury, HC and oxidative stress indicating relieving of oxidative damage associated with the complexity of HG and HC. These results demonstrated that these two plants extracts may be a candidate intelligent antioxidant, hypolipidemic, hypoglycemic, and hepatoprotective nutraceuticals which need further clinical investigation to be applied effectively to reduce perturbation in HC associated diabetes.

show abstract

“…Other potent hypolipidemic drugs, statins, are being also intensively studied in this respect. By inhibition of the enzyme HMG-CoA reductase statins have been reported to prevent the synthesis of isoprenoid intermediates of cholesterol biosynthesis pathway involved in posttranslational modification of small GTP-binding proteins, such as Ras, Rho, and Rac, which modulate a variety of cellular processes (Takemoto and Liao 2001), e.g., oxidative stress and inflammation (Van Linthout et al 2007;Zhou et al 2008;Adameová et al 2009b), vascular endothelial dysfunction (Takemoto and Liao 2001) and the outcome of myocardial response to I/R (Adameová et al 2006(Adameová et al , 2009a. It is hypothesized that in the myocardium, treatment with statins induces preconditioning-like effects attributed to up-regulation of "survival" pathways, such as PI3K/Akt, ERK1/2 and eNOS (Di Napoli et al 2001;Efthymiou et al 2005;Merla et al 2007).…”

Section: Cardioprotective Effects Of Exogenous Ppar Agonistsmentioning

confidence: 99%

The role of PPAR in myocardial response to ischemia in normal and diseased heart

Ravingerová¹,

Adameová²,

Čarnická³

et al. 2012

gpb

View full text Add to dashboard Cite

Abstract. Peroxisome proliferator-activated receptors (PPAR), ligand-activated transcription factors, belong to the nuclear hormone receptor superfamily regulating expression of genes involved in different aspects of lipid metabolism, inflammation and cardiac energy production. Activation of PPAR-α isoform by its natural ligands, fatty acids (FA) and eicosanoids, promotes mitochondrial FA oxidation as the primary ATP-generating pathway. On the other hand, PPAR-γ regulates lipid anabolism or storage, while, until recently, the function of PPAR-β/δ has been less explored. Under conditions associated with acute or chronic oxygen deprivation, PPAR-α modulates expression of genes that determine substrate switch (FA vs. glucose) aimed at maintenance of basic cardiac function. Although PPAR-α and PPAR-γ synthetic agonists, hypolipidemic and antidiabetic drugs, have been reported to protect the heart against ischemia/ reperfusion injury, it is still a matter of debate whether PPAR activation plays a beneficial or detrimental role in myocardial response to ischemia, in particular, in pathological conditions. This article reviews some findings demonstrating the impact of PPAR activation on cardiac resistance to ischemia in normal and pathologically altered heart. Specifically, it addresses the issue of susceptibility to ischemia in the diabetic myocardium, with particular regards to the role of PPAR. Finally, involvement of PPAR in the mechanisms of lipid-independent cardioprotective effects of some hypolipidemic drugs is also discussed.

show abstract

Cardioprotective effect of fluvastatin on isoproterenol-induced myocardial infarction in rat

Cited by 154 publications

References 34 publications

Evaluation of Cardioprotective Activity of Fulvic Acid Against Isoproterenol Induced Oxidative Damage in Rat Myocardium

Evaluation of Cardioprotective Activity of Fulvic Acid Against Isoproterenol Induced Oxidative Damage in Rat Myocardium

Statistical Data Analysis Which Result From the Bio-Diagnosis and Bio-Treatment of Injured Rats With the Hyperlipidemia and Hyperglycemia Diseases

The role of PPAR in myocardial response to ischemia in normal and diseased heart

Contact Info

Product

Resources

About

Cardioprotective effect of fluvastatin on isoproterenol-induced myocardial infarction in rat

Cited by 154 publications

References 34 publications

Evaluation of Cardioprotective Activity of Fulvic Acid Against Isoproterenol Induced Oxidative Damage in Rat Myocardium

Evaluation of Cardioprotective Activity of Fulvic Acid Against Isoproterenol Induced Oxidative Damage in Rat Myocardium

Statistical Data Analysis Which Result From the Bio-Diagnosis and Bio-Treatment of Injured Rats With the Hyperlipidemia and Hyperglycemia Diseases

The role of PPAR in myocardial response to ischemia in normal and diseased heart

Contact Info

Product

Resources

About

The role of PPAR in myocardial response to ischemia in normal and diseased heart