Berberine protects homocysteic acid-induced HT-22 cell death: involvement of Akt pathway.

Meihui Chen (1) , Min Tan (1, 2) , Minghua Jing (3) , Anmin Liu (4) , Qinyu Liu (4) , Shijun Wen (1, 5) , Ziwei Chen (1) , Xiaojuan Chao (1) , Xixin He (2) , Charles Ramassamy (6) , Youheng Gao (2) , Rongbiao Pi (1)

1 School of Pharmaceutical Sciences, Sun Yat-Sen University
2 Department of Traditional Chinese Medicine Chemistry, College of Chinese Materia Madica, Guangzhou University of Chinese Medicine
3 Department of Traditional Chinese Medicine, The First Affiliated Hospital, Sun Yat-Sen University
4 Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University
5 State Key Laboratory of Oncology in South China
6 INRS-IAF - Institut Armand Frappier

Berberine (BBR), one of the major constituents of Chinese herb Rhizoma coptidis, has been reported to exert beneficial effects to various diseases, including Alzheimer's disease (AD). In the present work, we aimed to investigate the effects of BBR on neuronal cell death induced by homocysteic acid (HCA), which was considered as a risk of AD. BBR significantly reduced HCA-induced reactive oxygen species (ROS) generation, lactate dehydrogenase release and subsequent cell death. LY294002, the PI3K inhibitor, blocked the protection as well as the up-regulation of Akt phosphorylation of BBR. Taken together, our results indicate that BBR protects HCA-induced HT-22 cell death partly via modulating Akt pathway, suggesting BBR may be a promising therapeutic agent for the treatment of HCA-related diseases, including AD.

Domaines: Sciences du Vivant [q-bio]

Meihui Chen, Min Tan, Minghua Jing, Anmin Liu, Qinyu Liu, et al.. Berberine protects homocysteic acid-induced HT-22 cell death: involvement of Akt pathway.. Metabolic Brain Disease, 2015, 30 (1), pp.137-42. ⟨10.1007/s11011-014-9580-x⟩. ⟨pasteur-01135521⟩