Abstract
The present study investigated 3,3 & PRIME;-dimethoxy-4,4 & PRIME;-dihydroxy-stilbene triazole (DMDHSB) in vitro for alleviation of beta-amyloid mediated damage to the PC12 neuronal cells. Exposure of PC12 cells to DMDHSB significantly (P < 0.05) reversed beta-amyloid induced loss of viability of PC12 cells in dose-dependent manner. Moreover, DMDHSB exposure significantly (P < 0.05) inhibited over production of PGE2 activated by beta-amyloid in PC12 cells. The beta-amyloid promoted higher levels of COX-2 and NO were also down-regulated in PC12 cells on exposure to DMDHSB. The exposure to DMDHSB led to a significant (P < 0.05) inhibition of beta-amyloid promoted higher expression of iNOS. The beta-amyloid promoted higher release of iNOS was effectively alleviated by DMDHSB exposure in PC12 cells. In DMDHSB exposed PC12 cells, the beta-amyloid promoted elevation of NF-kappa B nuclear translocation was effectively prevented compared to the control. It was observed from the docking studies that one-pose of DMDHSB interacted with COX-2 protein at binding affinity of -9.6 kcal/mol at 0-rmsd. Thus, beta-amyloid promoted loss of PC12 cell viability is prevented on DMDHSB exposure through targeting inflammatory response. Therefore, DMDHSB may be developed as therapeutic candidate for investigation in detail against Alzheimer's disease.