No abstract

No abstract

No abstract

Flavonoids have more potent therapeutic efficacy for the treatment of epileptic disorders. Certain flavonoids possess significant synergistic effects and can be taken with particular antiepileptic drugs (AEDs) to reduce the possibility of drug resistance. The combination of herbal and traditional medicines may not only prevent adverse effects but also increase the drug effects in overall comprehensive efficacy. The present study reviewed the potential efficacy of active constituents of selected flavonoids. Furthermore, in recent years, various researches have been attentive to specific flavonoids for their neuroprotective potential in in-vitro and in-vivo models. We have selected some specific flavonoids that have already proven therapeutic potential in animal epileptic models. Certain flavonoids possess significant synergistic effects and can be taken with particular AEDs to reduce the possibility of drug resistance. Some flavonoids are shown to exhibit their neuroprotective effects in Parkinson's disease, Alzheimer's disease, and ischemic stroke, which are the most common examples of neurological disorders. The major outcomes of flavonoids on progressive neurological disorders may be correlated to the regulation of gamma-aminobutyric acid (GABA) receptors. It has been reported that the neuroprotective actions of naringenin in experimental strokes are mediated by a reduction in NF-B-induced neuroinflammation. These discoveries appear to suggest that some flavonoids are more effective than conventional antiepileptic medicines, which have fewer side effects and can be used for the cure of epileptic seizures. Recently, in many research studies, it has been found that plant-derived flavonoids provide synergistic pharmacological action in experimental models of severe epilepsy. Keywords: Flavonoid, Therapeutic efficacy, Traditional medicine, Neuroprotective effect, Alternative therapy.

Anticancer drug resistance is a perilous glitch to accomplish alleviation of disease in patients with cancer. The setback of drug resistance in chemotherapy is a weighty snag of present time. Hassle of carcinoma has ability to develop resistance that arises due to certain alterations in drug targets. In the course of anticancer administrations, development of targeted therapies anticipates a new arena to subdue the drug resistance. Exalted levels of certain glutathione transferase isozymes have been identified with malign transformations as well as with anticancer drug resistance. Glutathione-S-transferases are a large group of phase-II detoxification enzymes which catalyse the conjugation of reduced glutathione to a broad range of exogenous as well as endogenous compounds. The enzymes of this family are divided into two distinct subgroups namely: cytosolic enzymes and membrane bound microsomal enzymes. Human cytosolic glutathione-S-transferases are extremely polymorphic in nature and exist in many forms such as mu, pi, alpha, theta, omega and zeta. Among these enzymes, mu and pi classes take part in regulation of mitogen-activated protein kinase pathway in directing cellular responses with apoptosis signal-regulating kinase and c-Jun Nterminal kinase 1 protein interactions. In normal condition, these two protein are mainly activated in response to cellular stress. The implications of glutathione S-transferase in development of anticancer drug resistance have been observed in two distinct ways. The first way is through direct detoxification mechanism while the second way deals with the action of glutathione S-transferase (mu and pi forms) as inhibitor to mitogen-activated protein kinase pathway.