p-Coumaric acid and ursolic acid from Corni fructus attenuated β-amyloid(25-35)-induced toxicity through regulation of the NF-κB signaling pathway in PC12 cells

• Published in: Journal of agricultural and food chemistry Vol. 62; no. 21; p. 4911
• Main Authors: Yoon, Jeong-Hyun, Youn, Kumju, Ho, Chi-Tang, Karwe, Mukund V, Jeong, Woo-Sik, Jun, Mira
• Format: Journal Article
• Language: English
• Published: United States 28.05.2014
• Subjects: Alzheimer Disease - drug therapy; Alzheimer Disease - metabolism; Alzheimer Disease - physiopathology; Amyloid beta-Peptides - toxicity; Animals; Apoptosis - drug effects; Cornus - chemistry; Coumaric Acids - pharmacology; Humans; MAP Kinase Signaling System - drug effects; Neuroprotective Agents - pharmacology; NF-kappa B - metabolism; Phosphorylation - drug effects; Plant Extracts - pharmacology; Propionates; Rats; Triterpenes - pharmacology; Ursolic Acid
• ISSN: 1520-5118
• DOI: 10.1021/jf501314g

Neuroinflammatory responses induced by amyloid-beta peptide (Aβ) are important causes in the pathogenesis of Alzheimer's disease (AD). Blockade of Aβ has emerged as a possible therapeutic approach to control the onset of AD. This study investigated the neuroprotective effects and molecular mechanisms of p-coumaric acid (p-CA) and ursolic acid (UA) from Corni fructus against Aβ(25-35)-induced toxicity in PC12 cells. p-CA and UA significantly inhibited the expression of iNOS and COX-2 in Aβ(25-35)-injured PC12 cells. Blockade of nuclear translocation of the p65 subunit of nuclear factor κB (NF-κB) and phosphorylation of IκB-α was also observed after p-CA and UA treatment. For the upstream kinases, UA exclusively reduced ERK1/2, p-38, and JNK phosphorylation, but p-CA suppressed ERK1/2 and JNK phosphorylation. Both compounds comprehensively inhibited NF-κB activity, but possibly with different upstream pathways. The results provide new insight into the pharmacological modes of p-CA and UA and their potential therapeutic application to AD.