Caffeic acid protects rat heart mitochondria against isoproterenol-induced oxidative damage

Kumaran, K. Senthil; Prince, P. Stanely Mainzen

doi:10.1007/s12192-010-0187-9

Cited by 71 publications

(32 citation statements)

References 51 publications

(40 reference statements)

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“…Carnitine palmitoyltransferase I; CPTI), decreased adenine nucleotide translocator (ANT) activity, mitochondrial membrane lipid peroxidation. This results in irreversible loss of mitochondrial functions such as mitochondrial respiration, oxidative phosphorylation, and ion transport (Kumaran & Prince, 2010;Valavanidis et al, 2009). Beside this, Dox exhibits high affinity for cardiolipin, an anionic phospholipid in the inner mitochondrial membrane that is required for eukaryotic energy metabolism (Houtkooper & Vaz, 2008).…”

Section: Discussionmentioning

confidence: 99%

Ameliorative effect of naringin against doxorubicin-induced acute cardiac toxicity in rats

Kwatra

Kumar

Jangra

et al. 2015

Pharmaceutical Biology

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Context: Doxorubicin (Dox) is one of the most active chemotherapeutic agents used to treat various types of cancers. Its clinical utility is compromised due to fatal cardiac toxicity characterized by an irreversible cardiomyopathy. Objective: This study evaluates the cardioprotective potential of naringin (NR) against Dox-induced acute cardiac toxicity in rats. Materials and methods: Male Wistar rats were randomly divided into five groups. NR (50 and 100 mg/kg) was administered intraperitoneally (i.p.) daily from 0 to 14 d. Doxorubicin (15 mg/kg, i.p.) was given as a single dose on the 10th day. On the 14th day, all animals were sacrificed and oxidative stress parameters that include malondialdehyde (MDA), glutathione (GSH) level, superoxide dismutase (SOD), catalase (CAT) activities, and all mitochondrial complexes (I-IV) activities were evaluated along with histopathological studies of the heart. Results: Doxorubicin-induced cardiotoxicity was confirmed by increased (p50.05) MDA, decreased (p50.05) GSH levels, SOD, and CAT activities, mitochondrial complexes (I-IV) activities in the heart tissue. NR (100 mg/kg) showed cardioprotection as evident from significant decreased MDA (p50.001) level, raised (p50.001) GSH level, SOD and CAT activities and increased mitochondrial complexes I (p50.01), II (p50.001), III (p50.001), and IV (p50.05) activities. Further, Dox-induced cardiotoxicity was confirmed by histopathological studies. These obtained results indicated the protective role of NR against Dox-induced cardiac toxicity in rats. Conclusion: NR can be used in combination with Dox due to its high cardioprotective effect against Dox-induced cardiomyopathy.

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Section: Discussionmentioning

confidence: 99%

Ameliorative effect of naringin against doxorubicin-induced acute cardiac toxicity in rats

Kwatra

Kumar

Jangra

et al. 2015

Pharmaceutical Biology

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“…Isoprenaline was dissolved in normal saline and injected subcutaneously at a dose of 200 mg/kg body weight once daily for 2-consecutive days (Priscilla and Prince, 2009;Kumaran and Prince, 2010).…”

Section: Induction Of Myocardial Infarctionmentioning

confidence: 99%

Cardioprotective activity of fruit of Garcinia pedunculata on isoprenaline-induced myocardial infarction in rat

Mundugaru

Udaykumar

Sivanesan

et al. 2016

Bangladesh J Pharmacol

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The present study reveals the protective effect of Garcinia pedunculata aqueous fruit extract in isoprenaline-induced myocardial infarction in Wistar rats. Isoprenaline (200 mg/kg) administration subcutaneous once daily for two consecutive days significantly (p<0.01) increased the CK-MB, AST, ALT, ALP activity and CRP (p<0.05) levels. Pretreatment with extract (400 mg/kg) orally for 14 consecutive days significantly ameliorated the effect of isoprenaline by reducing the activity of CK-MB and the levels of ALP, SGPT respectively. No significant changes were seen in the case of SGOT activity and CRP levels. Severe necrotic lesions in the myocardial tissue were observed in isoprenaline-treated group. In extract-treated group, mild degenerative changes of myo-cardial tissues to nearly normal cytoarchitecture were seen. The results indicate the cardioprotective effect of G. pedunculata against isoprenaline- induced myocardial infarction rat model.

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“…The hypoxia occurring during MI impairs energy production by mitochondria [40] . Moreover, pronounced enhancement of lipid peroxidation occurs in the mitochondria during MI.…”

Section: Discussionmentioning

confidence: 99%

Role of Different Doses of Vitamin E in Protection Against Isoproterenol-Induced Myocardial Damage in Adult Male Albino Rat: A Light and Electron Microscopic Study

Aboraya

Ibrahim

Qureshi

2017

Egyptian Journal of Histology

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Introduction: Cardiovascular diseases are one of the most common diseases in the world. It is essential to find an efficient natural protective agent against the myocardial damage. Aim: To determine the protective role of different doses of vitamin E against isoproterenol-induced myocardial damage. Material and Methods: Fifty adult male albino rats were divided into four main groups: Control group (I), vitamin E-treated group (II) equally divided into 2 subgroups; subgroup (IIa) received Vit E (50mg/kg) and subgroup (IIb) received Vit E (100mg/kg) for one month, isoproterenol-treated group (III) received 3ml normal saline orally for one month and isoproterenol (150mg/kg) intraperitoneally (IP) in the last two days of that month. Vitamin E and isoproterenol-treated group (IV) equally divided into two subgroups; Subgroup (IVa) received vitamin E (50mg/kg) orally for one month and isoproterenol (150mg/kg) IP in the last two days of that month and subgroup (IVb) received vitamin E (100mg/kg) orally for one month and isoproterenol (150mg/kg) IP in the last two days of that month. Heart specimens were processed for light and electron microscopic studies. Results: Rats injected by isoproterenol developed structural changes in the myocardium in the form of fragmentation of the myofibrils, vacuolated destroyed mitochondria, dilated SER, intracellular and extracellular edema and interstitial mononuclear cellular infiltration. Animals pretreated with vitamin E at a dose of 50mg/kg before injection of isoproterenol revealed minimal protection as they showed myocardial damage similar to isoproterenol-treated group. While animals pretreated with vitamin E at a dose of 100 mg/kg before injection of isoproterenol showed minimal microscopic alterations of the myocardium with preservation of the normal structure of the cardiac myocytes. Conclusion: Vitamin E at a high dose (100mg/kg) has a protective role on myocardium against isoproterenol-induced myocardial damage.

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Caffeic acid protects rat heart mitochondria against isoproterenol-induced oxidative damage

Cited by 71 publications

References 51 publications

Ameliorative effect of naringin against doxorubicin-induced acute cardiac toxicity in rats

Ameliorative effect of naringin against doxorubicin-induced acute cardiac toxicity in rats

Cardioprotective activity of fruit of <i>Garcinia pedunculata</i> on isoprenaline-induced myocardial infarction in rat

Role of Different Doses of Vitamin E in Protection Against Isoproterenol-Induced Myocardial Damage in Adult Male Albino Rat: A Light and Electron Microscopic Study

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