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K Chattopadhyay

K Chattopadhyay

Jadavpur University, India

Title: Potential efficacy of nano-curcumin against nicotine toxicated mammalian proteins

Biography

Biography: K Chattopadhyay

Abstract

Curcumin is a well-known anti-inflammatory and antioxidant agent that significantly reduces the nicotine-induced toxicity both at cellular and genetic levels. However, the poor aqueous solubility of curcumin makes it less bio-available that hinders the more possible remediation of curcumin against nicotinic abuse in the target cells. An attempt was made to synthesize nano-curcumin (20-50 nm) that would be more soluble in water with enhanced bioavailability. The prepared nanoparticles of curcumin (Cur-NPs) were characterized by ultraviolet-visible (UV-Vis) spectroscopy, field emission scanning electron microscopy (FESEM), X-ray diffraction (XRD) and Zetasizer techniques. Investigations were performed on the structural modifications of nicotine-triggered two important mammalian proteins (α-lactalbumin: α-LA and Cytochrome-c: Cyt-c) via the interaction of concentration dependent curcumin nanoparticles. It was observed that nicotine significantly affected the structural conformation and optical properties of α-LA and Cyt-c proteins by modifying their structural integrity. Cur-NPs significantly regained the structural integrity of those nicotine-treated proteins as reveled by the results from UV-Visible absorption, intrinsic fluorescence emission and circular dichroism (CD) studies. The isothermal titration calorimetric (ITC) investigation demonstrated that Cur-NPs prevented the nicotine molecules for binding in the active site of those proteins. This was due to the greater binding affinity of curcumin towards α-lactalbumin (-4.87 KCal/mol) and Cytochrome c (-7.64 KCal/mol) proteins in comparisons to nicotine (-4.24 KCal/mol; ~ -5.26 Kcal /mol respectively) as observed in molecular docking studies. This study clearly demonstrated that curcumin in its nano particulate form acted as an efficient ameliorative against nicotine-induced toxicity at cellular levels.