Background: Lung cancer is one of the most common malignancies with the highest incidence and mortality rate worldwide. Multidrug Resistance (MDR) continues to pose a major challenge for the clinicians and pharmacologists to effectively treat this disease. A new approach using natural substances with moderate or low cytotoxic properties become a promising hope for reversing multidrug resistance due to pgp- overexpression.
View Article and Find Full Text PDFBackground: Pancreatic cancer is one of the most aggressive and lethal cancers, with poor prognosis and high resistance to current chemotherapeutic agents. Therefore, new therapeutic strategies and targets are underscored. Propolis has been reported to exhibit a broad spectrum of biological activities including anticancer activity.
View Article and Find Full Text PDFDoxorubicin (DOX) is a potent anticancer drug; its use has been limited by its hepatotoxicity, which is due to free radicals generation. Propolis, a honeybee product very rich in flavonoids and therapeutic possibilities, has gained popularity as a food and alternative medicine. The present study treats DOX pro-oxidant effect on hepatic cells and mitochondrial functions.
View Article and Find Full Text PDFThis paper reports an investigation of the ability of propolis extract (a resinous substance collected by honeybees from various plant sources) to restore the collapse of mitochondrial membrane potential induced by ferulenol, a sesquiterpene prenylated coumarin derivative isolated from the plant Ferula vesceritensis . We show that ferulenol was able to induce the permeability transition pore (PTP) opening. This effect is caused by the interaction of the compound with the mitochondrial respiratory chain, more particularly by the fall of membrane potential and the inhibition of complex II.
View Article and Find Full Text PDFTo assess the oxidative stress and mitochondrial dysfunction associated with disease, toxic process and aging, in vivo and in vitro preventive effect of propolis extract against mitochondrial oxidative stress induced by two anticancer drugs (doxorubicin and vinblastin) have been investigated in female wistar rat using liver and heart mitochondria. The results show that doxorubicin and vinblastin altered mitochondrial functions as observed by a decrease in respiratory control value, an activation of swelling and overproduction of superoxide anion. Myocardial tissue from doxorubicin treated rats showed a marked increase in malondialdehyde production, a depletion of reduced glutathione contents and an inhibition of catalase and superoxide dismutase activities.
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