Key result
Brahma Rasayana and Chyavanaprash prevent doxorubicin-induced cardiotoxicity and tissue damage in mice.
Why the study?
The efficacy of Ayurvedic formulations Brahma Rasayana and Chyavanaprash to alleviate doxorubicin-induced acute cardiotoxicity was examined.
Do the ayurvedic formulations Brahma Rasayana and Chyavanaprash prevent doxorubicin-induced acute cardiotoxicity in mice?
Do the ayurvedic formulations Brahma Rasayana and Chyavanaprash prevent doxorubicin-induced acute cardiotoxicity in mice?
The ayurvedic formulations Brahma Rasayana and Chyavanaprash demonstrated protective effects against doxorubicin-induced acute cardiotoxicity in a murine model by preserving antioxidant status and cardiac architecture.
BRM/CHM may attenuate DOX cardiotoxicity in mice; leaves open any clinical cardioprotective role.
AIM OF STUDY: The present work aimed to examine the efficacy of two ayurvedic formulations, Brahma Rasayana (BRM) and Chyavanaprash (CHM) to alleviate doxorubicin (DOX) induced acute cardiotoxicity. MATERIALS AND METHODS: Swiss albino mice were administered with DOX (25 mg/kg, i.p.) and two doses of BRM or CHM (1 and 2 g/kg). Cardiotoxicity was assessed by measuring the levels of various antioxidant parameters in the heart as well as release of marker enzymes in the serum was assayed. Histology of the heart was also performed to check for DOX-induced damages. RESULTS: Administration of either BRM or CHM (1 and 2 g/kg) maintained the antioxidant status in the heart thereby preventing tissue damage as well as the release of marker enzymes. DOX-induced variation of cardiac architecture was also prevented by BRM and CHM administration. CONCLUSION: BRM and CHM administration could prevent DOX-induced acute cardiotoxicity.
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AlSuhailbani et al. (2016) studied Doxorubicin-induced acute cardiotoxicity. Brahma Rasayana (BRM) and Chyavanaprash (CHM) was evaluated on Cardiotoxicity assessed by antioxidant parameters, marker enzymes, and histology. Administration of Brahma Rasayana or Chyavanaprash (1 and 2 g/kg) prevented doxorubicin-induced acute cardiotoxicity and tissue damage in mice.
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