The effect of shikonin on Aβ25-35 induced cell cytotoxicity and oxidative injury in PCc12 cell line

Alzheimer's Disease (AD) is a chronic neurodegenerative disorder characterized by progressive loss of memory. Shikonin has been shown to have many positive effects such as anti-oxidant, anti-inflammatory, antithrombotic, antimicrobial, anticancer and wound healing properties. In this study, using the AD model induced with Aβ25-35 in the PC12 cell line, we aimed to investigate the potential protective effect of Shikonin against Aβ toxicity and its resulting oxidative damage. The effects of Aβ25-35 and shikonin on PC12 cell viability was determined by MTT [3-(4,5-dimethyl-2-thiazolyl)-2,5 diphenyl-2H-tetrazolium bromide] assay. To examine the effects of Aβ25-35 and Shikonin oxidative stress, we analyzed the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and lipid peroxidation product, malondialdehyde (MDA) using Enzyme Linked Immunosorbent Assay (ELISA) method. Nitric oxide (NO•) was colorimetrically analyzed by Griess method. On addition of 20μM shikonin, reduced cell viablility noted with 5µM Aβ25-35 was significantly increased. increased levels of NO• and MDA by Aβ25-35 decreased by the addition of shikonin, increased SOD and GSH-Px enzyme activities reduced Aβ by the addition of shikonin. Similarly, CAT enzyme activity decreased with Aβ25-35 by the addition of shikonin. Results obtained from this study reveal the positive effects of shikonin on neurotoxicity and oxidative damage in Aβ25-35-induced AD model created in vitro in the PC12 cells We therefore are of the opinion that shikonin may be a potential agent in preventing the cytotoxicity and oxidative damage induced by Aβ.