Abstract
The cardioprotective effect of ethanol extract of Callistemon lanceolatus leaves (100 and 200 mg/kg) against doxorubicin-induced cardiomyopathy was studied. Rats were pretreated with the extract for 7 days and simultaneous treatment with doxorubicin along with the extracts for the next 14 days. After 24 hours of last dose of doxorubicin, ECG, invasive blood pressure, serum markers (creatine kinase-MB, lactate dehydrogenase, serum transaminases), tissue antioxidant markers (catalase, superoxide dismutase) and extent of lipid peroxidation (malondialdehyde) were studied. The elevated ST segment, decreased blood pressure, increased level of serum enzymes and decreased level of tissue antioxidant markers were observed in doxorubicin treatment (p<0.01). While 200 mg/kg extract significantly reduced the elevated levels of the serum enzymes and restores the ECG and blood pressure to normal, also significantly increased the tissue antioxidant levels, while decreased the malondialdehyde level (p<0.01) when compared with the control. The histopathological study confirmed the cardioprotection.
Highlights
Doxorubicin-induced myocardial injury has been believed to be mediated through different mechanisms
Oxygen free radical formation by doxorubicin (Chopra et al, 1995; Van Acker et al, 1996) enhances the susceptibility of cardiac tissue to lipid peroxidation leading to a progressive dose–related irreversible loss of myofibrils, dilation of the sarcoplasmic reticulum, cytoplasmic vacuolization, swelling of mitochondria, increased number of lysosomes, myocyte necrosis (Minotti et al, 2004), inhibition of nucleic acid as well as protein synthesis (Monti et al, 1995), release of vasoactive amines (Bristo et al, 1980), change in adrenergic function (Singal et al, 1998), decreased activity of Na+K+ATPase (Geetha and Devi, 1992), alteration in sarcoplasmic calcium transport and imbalance of myocardial electrolytes in response to the doxorubicin (Siveski-Iliskovic et al, 1994)
Lethargic and enlargement of abdomen and liver when compared with the normal. These observations were markedly reduced in the group treated with ethanol extract of C. lanceolatus leaves (200 mg/kg), when compared with the doxorubicin control group
Summary
Doxorubicin-induced myocardial injury has been believed to be mediated through different mechanisms. A common denominator to most of the proposed mechanisms is the formation of an iron-anthracycline complex that generates free radicals, which in turn, causes severe damage to the plasma membrane, and interferes with the cytoskeletal structure (Billingham et al, 1977). Oxygen free radical formation by doxorubicin (Chopra et al, 1995; Van Acker et al, 1996) enhances the susceptibility of cardiac tissue to lipid peroxidation leading to a progressive dose–related irreversible loss of myofibrils, dilation of the sarcoplasmic reticulum, cytoplasmic vacuolization, swelling of mitochondria, increased number of lysosomes, myocyte necrosis (Minotti et al, 2004), inhibition of nucleic acid as well as protein synthesis (Monti et al, 1995), release of vasoactive amines (Bristo et al, 1980), change in adrenergic function (Singal et al, 1998), decreased activity of Na+K+ATPase (Geetha and Devi, 1992), alteration in sarcoplasmic calcium transport and imbalance of myocardial electrolytes in response to the doxorubicin (Siveski-Iliskovic et al, 1994). Semiquinone is a charged moiety that readily donates an electron to an oxygen molecule, resulting in generation of an oxygen free radical or superoxide ion/hydroxyl radicals.
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