Methanolic extract of coconut (Cocos nucifera L.) haustorium mitigates pro-oxidant-mediated apoptotic cell death via Nrf-2 pathway and lipopolysaccharide-induced cytokine release in cells

Cocos nucifera L is well-known for its edible and medicinal uses; multiple products from the different parts of the plant are being used by various communities in India. A less explored product is the coconut haustorium, the solid endosperm portion, which is highly nutritious. The present study first time evaluated the antioxidant, anti-inflammatory and cytoprotective properties of methanolic extract of Coconut haustorium (CHE). The cytoprotective effect of CHE was evaluated in hydrogen peroxide/malondialdehyde-induced toxicity IEC-6 (normal intestinal cell). Initially the biologically safe concentration of CHE and IC50 value of hydrogen peroxide and malondialdehyde was estimated by MTT assay. Treatment with H2O2 and MDA led to glutathione depletion and reduction in the catalase and glutathione reductase activity; which resulted in the increased oxidative stress and thereby cell death. Pretreatment with the different concentrations (10, 20 and 40 µg/mL) of CHE offered significant and dose-dependent protection against the toxicity induced by hydrogen peroxide and malondialdehyde. It is observed that the CHE pretreatment restored the antioxidant enzyme activities and GSH levels back to normal; the improvement in antioxidant status may be through the upregulation of Nrf2/HO1 pathway as observed in CHE pretreated cells. The anti-inflammatory potential was evaluated in the lipopolysaccharide (LPS-1 µg/mL) induced model in macrophages (Raw 264.7 cells). CHE pretreatment reduced the LPS- induced release of cytokines such as IL-1β, IL-6, and tumor necrosis factor-alpha (TNF-α). The results indicated the antioxidant, anti-inflammatory and cytoprotective effect of less explored haustorium from Coconut.