To Test The Role Of Withaferin A In Neuroprotection On Sh-Sy5Y Cell Line Challenged By Kainic Acid

Abstract

Withania somnifera (WS) has been used in traditional medicine for a variety of neural disorders. Recently, chronic neurodegenerative conditions have been shown to benefit from treatment with this crude extract. Neurotoxicity induced by Kainic acid causes stroke, head trauma and leads to various neurodegenerative diseases. It is a common pathway for neuronal injury and death. Withaferin A (WA) is the steroidal lactone and phytochemical of medicinal plant WS. These days research on the medicinal plant is the major theme so as to identify the novel, natural and safe phytotherapies has been flourished. WS is a popular ayurvedic plant with an array of medicinal properties including neuroprotection. It also appears to exert a great influence on the cardiopulmonary, endocrine, and central nervous systems. Recently several in-vitro and in-vivo preclinical studies validating the therapeutic value of newly identified phytochemicals have been launched. The use of medicinal plants and its chemical component can be exploited in the treatment of neurodegenerative diseases like Parkinson, Alzheimer's, Epilepsy and so on. Ayurvedic products are the only promising way to treat these diseases with negligible side effects. In the current study the neuroprotective role WA has been studied on SH-SY5Y neuroblastoma cell line challenged by kainic acid. Cell viability and expression of neuronal cell differentiation marker NCAM was investigated on v Kainic acid challenged SH-SY5Y cells with and without the presence of WA. When the cells are challenged via Kainic acid there is a decrease in cell viability due to the phenomenon of excitotoxicity and this was reversed by WA treatment. NCAM is an important cell surface plasticity marker that have role in repair and regeneration. Potential mechanisms underlying the observed neuroprotection were examined. Additionally, morphological changes were monitored following KA treatment. Upon excitotoxicity with Kainic acid NCAM expression increased but the effect is reverse upon pre-treatment with WA. Altogether, the present study suggests that WA is neuroprotective and provides neuroprotection against KA induced excitotoxicity could have therapeutic potential to target factors involved in neurodegenerative diseases.