잠시만 기다려 주세요. 로딩중입니다.

Protective Role of Corilagin on Aβ25?35-Induced Neurotoxicity: Suppression of NF-κB Signaling Pathway

Journal of Medicinal Food 2016년 19권 10호 p.901 ~ 911
윤금주, 이선아, 정우식, Ho Chi-Tang, 전미라,
소속 상세정보
윤금주 ( Youn Kum-Ju ) - Dong-A University Department of Food Science and Nutrition
이선아 ( Lee Seon-Ah ) - Dong-A University Department of Food Science and Nutrition
정우식 ( Jeong Woo-Sik ) - Inje University College of Biomedical Science and Engineering Department of Food and Life Sciences
 ( Ho Chi-Tang ) - Rutgers University Department of Food Science
전미라 ( Jun Mi-Ra ) - Dong-A University Department of Food Science and Nutrition

Abstract


Aggregation and deposition of beta-amyloid peptides (Aβ), a pathological hallmark of Alzheimer's disease, has been recognized as a potent activator of neuroinflammation and neuronal dysfunction. In this study, the underlying molecular mechanisms responsible for the neuroprotective effects of corilagin against Aβ25?35-triggered neurotoxicity and inflammatory responses were investigated in PC12 cells. Pretreatment with corilagin effectively protected PC12 cells against Aβ25?35-induced damage and apoptosis. Aβ25?35 induced damage in PC12 cells as revealed by increased production of reactive oxygen species, caspase-3 activity, and cell cycle arrest was attenuated by corilagin pretreatment. Corilagin not only significantly suppressed the production of neurotoxic inflammatory mediators such as tumor necrosis factor-α, nitric oxide, and prostaglandin E2 but also downregulated cyclooxygenase-2 and inducible nitric oxide synthase expression in PC12 cells. It also exerted a beneficial effect by suppressing the degradation of inhibitor of κB (IκB)-α and subsequent activation of transcription factor nuclear factor κB (NF-κB), mostly through inhibition of extracellular signal-regulated kinase activity in comparison to c-Jun N-terminal kinase and p38 MAP kinase (p38) mitogen-activated protein kinase activity. These findings suggest that attenuation of Aβ25?35-induced inflammatory responses by downregulating the NF-κB signaling pathway might be a valuable strategy for both Alzheimer's disease prevention and/or treatment.

키워드

Alzheimer's disease; beta-amyloid peptide; corilagin; inflammation; NF-κB

원문 및 링크아웃 정보

등재저널 정보