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NAD+ blocks H2O2‐induced HMGB1 translocation of PC12 cells and decreases survival of microglia
Author(s) -
Chen Heyu,
Han Jin,
Shao Jiaxiang,
Xia Weiliang,
Ying Weihai
Publication year - 2010
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.24.1_supplement.lb469
Subject(s) - nad+ kinase , microglia , chromosomal translocation , inflammation , hmgb1 , chemistry , medicine , microbiology and biotechnology , pharmacology , biology , biochemistry , enzyme , gene
We have reported that NAD+ administration can profoundly decrease ischemic brain injury. However, the mechanisms underlying the protection remain unclear. Because inflammation plays a crucial role in ischemic brain damage, we hypothesized that NAD+ may decrease ischemic brain injury partially by affecting the inflammation. Because HMGB1 translocation outside of the nucleus has been suggested as a key signal activating inflammatory responses, we determined the effects of NAD+ on the HMGB1 translocation in PC12 cells. Our study has suggested that NAD+ treatment could decrease the H2O2‐induced HMGB1 translocation. Our study using microglial BV2 cell lines has also found that NAD+ treatment can significantly decrease the number of surviving microglial cells. Treatment of relatively high density (80–90%) microglia cultures with 0.1 mM or 1 mM NAD+ for 24 hrs decreased the number of surviving cells by 30% and 50%, respectively. Treatment of relatively low density (50–60%) microglia cultures with 0.01 mM or 0.1 mM NAD+ decreased the number of surviving cells by 30% and 40%, respectively. These observations suggest that NAD+ administration may attenuate ischemic brain injury partially by inhibiting inflammatory reactions. (Supported by a key basic research grant from Shanghai Municipal Scientific Committee (to W.Y.), and a National 973 grant #2010CB834306 (to W.Y.)).