Abstract
Alzheimer’s disease (AD) pathogenesis involves an imbalance between free radical formation and destruction. In order to obtain a novel preclinical anti-AD drug candidate, we synthesized a series of novel hydroxyl chalcone analogs which possessed anti-free radical activity, and screened their effects on scavenging 2,2-diphenyl-1-picrylhydrazyl (DPPH) and OH free radicals in vitro. Compound C7, 4,2'-dihydroxy-3,5-dimethoxychalcone was found to have potent activity in these anti-free radical activity tests. Further research revealed that C7 could elevate glutathione peroxidase (GSH-PX) and super oxide dismutase (SOD) levels and lower malonaldehyde (MDA) level in vivo in the Alzheimer’s model. The indication of C7’s effect on AD needs further study.
Highlights
Free radicals have been implicated in the etiology of several human diseases, as well as ageing
Hydroxyl-substituted chalcone analogs could develop into novel anti-Alzheimer’s disease (AD) drug candidates
A growing body of evidence indicates that increased oxidative stress resulting from free radical damage to cellular functions is associated with a number of age-related disorders including atherosclerosis and arthritis
Summary
Free radicals have been implicated in the etiology of several human diseases, as well as ageing. A growing body of evidence suggests that AD pathogenesis involves an imbalance between free radical formation and destruction [4,5,6,7,8]. This concept originally derived from the free radical hypothesis of aging, with age-related accumulation of free radicals resulting in damaged cell components. C1–7shown in Table 1 and screened these potential compounds for anti-free radical activity in vitro for further study. We test the compounds’ effect on SOD, MDA and GSH-PX levels to evaluate the anti-oxidation activity in vivo in a free radical-injury Alzheimer’s model
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.