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Since its discovery in the 1960 s, doxorubicin (DOX) has constantly elicited the broadest spectrum of cancerocidal activity against human cancers. However, cardiotoxicity caused by DOX directly as well as its metabolites is a great source of concern over the continuous use of DOX in chemotherapy. While the exact mechanism of DOX-induced cardiotoxicity is yet to be completely understood, recent studies indicate oxidative stress, inflammation, and several forms of cell death as key pathogenic mechanisms that underpin the etiology of doxorubicin-induced cardiotoxicity (DIC). Notably, these key mechanistic events are believed to be negatively regulated by 3,4-dihydroxybenzoic acid or protocatechuic acid (PCA)—a plant-based phytochemical with proven anti-oxidant, anti-inflammatory, and anti-apoptotic properties. Here, we review the experimental findings detailing the potential ameliorative effects of PCA under exposure to DOX. We also discuss molecular insights into the pathophysiology of DIC, highlighting the potential intervention points where the use of PCA as a veritable chemoprotective agent may ameliorate DOX-induced cardiotoxicities as well as toxicities due to other anticancer drugs like cisplatin. While we acknowledge that controlled oral administration of PCA during chemotherapy may be insufficient to eliminate all toxicities due to DOX treatment, we propose that the ability of PCA to block oxidative stress, attenuate inflammation, and abrogate several forms of cardiomyocyte cell death underlines its great promise in the amelioration of DIC.

Momordica charantia (M. charantia) is known for its antioxidant and antidiabetic properties. The aim of this study is to investigate the renoprotective effects of M. charantia in rats following treatment with highly active antiretroviral therapy (HAART) regimen triplavar. Adult male Sprague-Dawley rats weighing 178.1–220.5 g (n = 36) were divided into six groups (A–F) with each group comprising of six (n = 6) rats. The drugs and extract were administered via oral gavage. The therapeutic dose of triplavar was adjusted using the human therapeutic dose equivalent for the rat model. Animals were euthanized on the tenth week with kidneys removed for examination and blood obtained via cardiac puncture. Levels of oxidative stress enzymes (superoxide dismutase-SOD, catalase-CAT, and reduced glutathione-GSH) were significantly lowered in all groups not receiving M. charantia. The levels of thiobarbituric acid reactive substances (TBARS) were increased resulting in free radical formation via auto-oxidation. Renal parameters showed no albuminuria, normal blood urea nitrogen (BUN), serum creatinine (SCr) and electrolytes in groups treated with M. charantia. HAART treated (Group B) showed severe albuminuria, a significantly (p

As the roll-out of antiretroviral therapy continues to drive downwards morbidity and mortality in people living with HIV/AIDS (PLWHAs), organ toxicities (especially the liver) are frequently becoming a major concern for researchers, scientists and healthcare planners.This study was conducted to investigate the possible protective effect of Hypoxis hemerocallidea (AP) against highly active antiretroviral therapy (HAART)-induced hepatotoxicity. A total of 63 pathogen-free adult male Sprague-Dawley rats were divided into 9 groups and treated according to protocols.While no mortality was reported, animals treated with adjuvant HAART and AP recorded least% body weight gain. Significant derangements in serum lipid profiles were exacerbated by treatment of with AP as LDL (increased p