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Baicalein protects hippocampal neuronal HT22 cells from ER stress‐induced apoptosis by modulating unfolded protein responses‐associated proteins
Author(s) -
Choi Ji Hyun,
Kang Insug
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.lb218
Subject(s) - unfolded protein response , endoplasmic reticulum , thapsigargin , microbiology and biotechnology , brefeldin a , apoptosis , chemistry , neuroprotection , biology , golgi apparatus , biochemistry , pharmacology
The endoplasmic reticulum (ER) stress has been suggested to be involved in various neurodegenerative diseases including Alzheimer's disease and Parkinson's disease. Here we examined the effect of baicaleine (BE), a flavonoid, on ER stress‐induced apoptosis in mouse hippocampal neuronal cell line HT22. BE inhibited apoptosis induced by the ER stress inducers thapsigargin (TG) and brefeldin A (BFA). We showed that BE blocked ER stress‐induced unfolded protein response (UPR), including expression of CHOP and spliced form of XBP‐1 and phosphorylation of eIF2α, JNK, p38MAPK and the cleavage of ATF‐6. Moreover, we showed that BE blocked the accumulation of ROS and maintained mitochondrial membrane potential in ER stress‐induced HT 22 cells. Similar to the effect of BE, N‐acetyl‐cysteine (NAC), an antioxidant inhibited TG‐ or BFA‐induced apoptosis and changes in UPR‐associated proteins. Taken together, these results suggest that BE protects HT22 neuronal cells against ER stress‐induced apoptosis by inhibition of ROS accumulation and regulation of ER stress associated proteins. This work was supported by grants from KOSEF of Korea Government.