Open Access
Synergistic Therapeutic Effect of L-Carnitine Nanoparticles and Moringa Oleifera Against Doxorubicin Induced Cardiac Toxicity in Male Rats: Biochemical and Histological Study
Publication year - 2022
Publication title -
biointerface research in applied chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.216
H-Index - 11
ISSN - 2069-5837
DOI - 10.33263/briac132.142
Subject(s) - cardiotoxicity , doxorubicin , pharmacology , moringa , toxicity , cardioprotection , medicine , saline , anthracycline , oxidative stress , carnitine , chemistry , chemotherapy , traditional medicine , endocrinology , ischemia , cancer , breast cancer
Doxorubicin (DOX) is a powerful chemotherapeutic agent. However, dose-dependent cardiotoxicity may limit its clinical applicability. This study was directed to explore the possible therapeutic effects of L-Carnitine Nanoparticles (LCNPs) and Moringa Oleifera extract (MO) against doxorubicin-induced cardiac toxicity in male rats. Fifty rats were allocated into two main groups: the first served as a normal control group (con.) (n=10). The remaining 40 rats were given doxorubicin at a cumulative dose of 20 mg/kg b. wt. to induce cardiotoxicity. The Dox-treated rats were subdivided into 4 groups (n = 10/group) to be orally administered with 1) 0.9% normal saline; 2) MO at 400 mg /kg, b. wt./day; 3) LCNPs at 50 mg/kg b. wt./ day for four weeks; 4) MO+LCNPs group as previously indicated doses. The results demonstrated that DOX treatment raised MDA, NO, HO-1, and NF-kB levels while decreasing TAC activity. In addition to increased serum cardiac levels of CRP, CK, LDH, ALT, and Troponin-1 and Endothelin-1. LCNPs or MO treatment alleviated these changes. Whereas co-administration of LCNPs and MO reversed all these parameters. DOX treatment caused severe histopathological alterations in the cardiac tissues, corrected by LCNPs and MO treatment. In conclusion, these data imply that treating with LCNPs and MO in combination provides greater cardioprotection against DOX-induced cardiotoxicity in rats via repressing oxidative stress and boosting antioxidant status.