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Neuroprotective effect of 1′‐acetoxychavicol acetate against amyloid β induced toxicity is related with upregulation of proteasome activity
Author(s) -
Yaku Keisuke,
MatsuiYuasa Isao,
YuasaKojima Akiko
Publication year - 2013
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.27.1_supplement.637.4
Subject(s) - proteasome , neuroprotection , mg132 , neurotoxicity , chemistry , pharmacology , downregulation and upregulation , proteasome inhibitor , biochemistry , toxicity , biology , organic chemistry , gene
1′‐Acetoxychavicol acetate (ACA) naturally obtained from the rhizomes and the seeds of the Zingiberaceae plant such as Languas galangal and Alpinia galangal exhibits anti‐carcinogenesis effect. Though Alpinia galangal has neuroprotective effect in Alzheimer disease induced mice, the effect of ACA on neuroprotection is not clear. Proteasome activity is known to decrease with aging, and the loss of proteasome activity has relation to neurodegenerative process. The present study was conducted to examine the effects of ACA on amyloid β‐protein fragment 25–35 induced neurotoxicity and proteasome activity in PC12. Methods The cell number of PC12 was determined by MTT assay. The proteasome activity was measured by using Proteasome‐Glo™ Chymotrypsin‐Like proteasome activity assay kit. Results ACA recovered the cell number which was decreased by the addition of amyloid β Fragment in PC12. The effect of ACA on amyloid toxicity was decreased by MG132 which is one of the proteasome inhibitors. ACA induced proteasome activity at early stage and remained until at least 9 hours. Then it returned to control level within 24 hours. The structure‐activity relationship of ACA on proteasome activity was different from that on anti‐carcinogenesis. Conclusion ACA exhibited neuroprotective effect against amyloid β‐protein fragment 25–35 induced neurotoxicity via upregulation of proteasome activity.