Adriamycin induced myocardial failure in rats: Protective role of Centella asiatica

Arunachalam, Gnanapragasam; Yogeeta, Surinder Kumar; Subhashini, Rajakannu; Ebenezar, Kesavarao Kumar; Sathish, Venkatachalem; Devaki, Thiruvengadam

doi:10.1007/s11010-006-9245-0

Cited by 37 publications

(21 citation statements)

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“…This dose of EPO was effective in preventing cardiac remodeling after coronary ligation (29). AD group (n ϭ 10) rats were injected with doxorubicin (AD; PHARMACIA Italia; 2.5 mg/kg body wt ip) in six equal doses over the period of 2 wk (16). The EPO-AD group (n ϭ 10) received both EPO (1,000 IU/kg body wt sc) and doxorubicin (2.5 mg/kg body wt ip).…”

Section: In Vivo Studiesmentioning

confidence: 99%

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Erythropoietin protects against doxorubicin-induced heart failure

Ammar

Saba

Ammar

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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The hormone erythropoietin (EPO) has been demonstrated to have cardioprotective properties. The present study investigates the role of EPO to prevent heart failure following cancer treatment with doxorubicin [adriamycin (AD)]. Male Wistar rats (150 Ϯ 10 g) were treated with saline (vehicle control group); with EPO, subcutaneously at 1,000 IU/kg body wt, three times per week for 4 wk (EPO group); with adriamycin, intraperitoneally at 2.5 mg/kg body wt, three times per week for 2 wk (AD group); and with adriamycin and EPO (EPO-AD group). Echocardiographic measurements showed that EPO-AD treatment prevented the AD-induced decline in cardiac function. Each of the hearts was then exposed to ischemia and reperfusion during Langendorff perfusion. The percentage of recovery after ischemia-reperfusion was significantly greater in EPO-AD than the AD-treated group for left ventricular developed pressure, maximal increase in pressure, and rate pressure product. The level of oxidative stress was significantly higher in AD (5 M for 24 h)-exposed isolated cardiomyocytes; EPO (5 U/ml for 48 h) treatment prevented this. EPO treatment also decreased AD-induced cardiomyocyte apoptosis, which was associated with the decrease in the Bax-to-Bcl2 ratio and caspase-3 activation. Immunostaining of myocardial tissue for CD31 showed a significant decrease in the number of capillaries in AD-treated animals. EPO-AD treatment restored the number of capillaries. In conclusion, EPO treatment effectively prevented ADinduced heart failure. The protective effect of EPO was associated with a decreased level of oxidative stress and apoptosis in cardiomyocytes as well as improved myocardial angiogenesis. apoptosis; myocardial infarction; oxidative stress THE ANTINEOPLASTIC DRUG DOXORUBICIN is effective in the treatment of a broad spectrum of malignancies, but its clinical use is limited by adverse side effects: irreversible degenerative cardiomyopathy and congestive heart failure (30, 33). The efficacy of doxorubicin [adriamycin (AD)] as a cytotoxic agent for the treatment of various human tumors prompted a search for treatments to reduce or prevent doxorubicin-induced cardiomyopathy and congestive heart failure (24). So far, however, available treatments to protect the heart from doxorubicin-induced damage have been varied and limited.The cytokine erythropoietin (EPO) is produced by the kidney and is indispensable for the proliferation, survival, and differentiation of erythroid progenitor cells (39). EPO receptors have also been identified in nonhematopoietic tissues, including the heart (34, 38). Recent studies (7,27,31) suggest that EPO also exerts a cardioprotective effect against infarction and ischemia-reperfusion injury. EPO administration before or during ischemia significantly enhanced left ventricular (LV) contractility and the recovery of cardiac function after myocardial ischemia and reperfusion injury. Several studies (8,18) suggested that EPO treatment improved ventricular contractile function in animal models of heart failure and tha...

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Section: In Vivo Studiesmentioning

confidence: 99%

“…The EPO-AD group (n ϭ 10) received both EPO (1,000 IU/kg body wt sc) and doxorubicin (2.5 mg/kg body wt ip). AD was stopped after 2 wk and EPO treatment was continued for 4 wk (16).…”

Section: In Vivo Studiesmentioning

confidence: 99%

Erythropoietin protects against doxorubicin-induced heart failure

Ammar

Saba

Ammar

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…Recent findings suggest that Centella asiatica has cognition-enhancing properties through its ability to protect against oxidative stress [10,11] , reduce the extent of mitochondrial damage [12] and increase axonal regeneration and neurite elongation [13] . Asiatic acid (AA) is a pentacyclic triterpene found in Centella asiatica.…”

Section: Introductionmentioning

confidence: 99%

Asiatic acid, a pentacyclic triterpene in Centella asiatica, attenuates glutamate-induced cognitive deficits in mice and apoptosis in SH-SY5Y cells

et al. 2012

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Aim: To investigate whether asiatic acid (AA), a pentacyclic triterpene in Centella asiatica, exerted neuroprotective effects in vitro and in vivo, and to determine the underlying mechanisms. Methods: human neuroblastoma Sh-SY5Y cells were used for in vitro study. Cell viability was determined with the MTT assay. hoechst 33342 staining and flow cytometry were used to examine the apoptosis. The mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) were measured using fluorescent dye. PGC-1α and Sirt1 levels were examined using Western blotting. Neonatal mice were given monosodium glutamate (2.5 mg/g) subcutaneously at the neck from postnatal day (PD) 7 to 13, and orally administered with AA on PD 14 daily for 30 d. The learning and memory of the mice were evaluated with the Morris water maze test. hE staining was used to analyze the pyramidal layer structure in the CA1 and CA3 regions. Results: Pretreatment of Sh-SY5Y cells with AA (0.1-100 nmol/L) attenuated toxicity induced by 10 mmol/L glutamate in a concentration-dependent manner. AA 10 nmol/L significantly decreased apoptotic cell death and reduced reactive oxygen species (ROS), stabilized the mitochondrial membrane potential (MMP), and promoted the expression of PGC-1α and Sirt1. In the mice models, oral administration of AA (100 mg/kg) significantly attenuated cognitive deficits in the Morris water maze test, and restored lipid peroxidation and glutathione and the activity of SOD in the hippocampus and cortex to the control levels. AA (50 and 100 mg/kg) also attenuated neuronal damage of the pyramidal layer in the CA1 and CA3 regions. Conclusion: AA attenuates glutamate-induced cognitive deficits of mice and protects SH-SY5Y cells against glutamate-induced apoptosis in vitro.

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“…In addition, transmission electron microscopy study confirms the restoration of cellular normalcy and accredits the cytoprotective role of Centella asiatica against adriamycin induced myocardial injury. Results of Gnanapragasam et al suggest that the aqueous extract of Centella asiatica not only possesses antioxidant properties but it may also reduce the extent of mitochondrial damage (Gnanapragasam et al, 2007). Oral administration of Aloe barbadensis gel -aloe vera (100 and 200 mg/kg), to the albino rats during 10 days, produced a significant protection against cardiotoxicity induced by DOX (single dose 7.5 mg/kg i.v.).…”

Section: Natural Productsmentioning

confidence: 98%