Cannabinoid CB2 Receptor Mediates Nicotine-Induced Anti-Inflammation in N9 Microglial Cells Exposed to β Amyloid via Protein Kinase C
Background. Reducing β amyloid- (Aβ-) induced microglial activation is considered to be effective in treating Alzheimer's disease (AD). Nicotine attenuates Aβ-induced microglial activation; the mechanism, however, is still elusive. Microglia could be activated into classic activated state (M1 s...
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| Main Authors: | , , , , , , |
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| Format: | Book |
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Hindawi Limited,
2016-01-01T00:00:00Z.
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| LEADER | 00000 am a22000003u 4500 | ||
|---|---|---|---|
| 001 | doaj_c9e88bcc54d943e889da1608ca43fc3b | ||
| 042 | |a dc | ||
| 100 | 1 | 0 | |a Ji Jia |e author |
| 700 | 1 | 0 | |a Jie Peng |e author |
| 700 | 1 | 0 | |a Zhaoju Li |e author |
| 700 | 1 | 0 | |a Youping Wu |e author |
| 700 | 1 | 0 | |a Qunlin Wu |e author |
| 700 | 1 | 0 | |a Weifeng Tu |e author |
| 700 | 1 | 0 | |a Mingchun Wu |e author |
| 245 | 0 | 0 | |a Cannabinoid CB2 Receptor Mediates Nicotine-Induced Anti-Inflammation in N9 Microglial Cells Exposed to β Amyloid via Protein Kinase C |
| 260 | |b Hindawi Limited, |c 2016-01-01T00:00:00Z. | ||
| 500 | |a 0962-9351 | ||
| 500 | |a 1466-1861 | ||
| 500 | |a 10.1155/2016/4854378 | ||
| 520 | |a Background. Reducing β amyloid- (Aβ-) induced microglial activation is considered to be effective in treating Alzheimer's disease (AD). Nicotine attenuates Aβ-induced microglial activation; the mechanism, however, is still elusive. Microglia could be activated into classic activated state (M1 state) or alternative activated state (M2 state); the former is cytotoxic and the latter is neurotrophic. In this investigation, we hypothesized that nicotine attenuates Aβ-induced microglial activation by shifting microglial M1 to M2 state, and cannabinoid CB2 receptor and protein kinase C mediate the process. Methods. We used Aβ1-42 to activate N9 microglial cells and observed nicotine-induced effects on microglial M1 and M2 biomarkers by using western blot, immunocytochemistry, and enzyme-linked immunosorbent assay (ELISA). Results. We found that nicotine reduced the levels of M1 state markers, including inducible nitric oxide synthase (iNOS) expression and tumor necrosis factor α (TNF-α) and interleukin- (IL-) 6 releases; meanwhile, it increased the levels of M2 state markers, including arginase-1 (Arg-1) expression and brain-derived neurotrophic factor (BDNF) release, in the Aβ-stimulated microglia. Coadministration of cannabinoid CB2 receptor antagonist or protein kinase C (PKC) inhibitor partially abolished the nicotine-induced effects. Conclusion. These findings indicated that cannabinoid CB2 receptor mediates nicotine-induced anti-inflammation in microglia exposed to Aβ via PKC. | ||
| 546 | |a EN | ||
| 690 | |a Pathology | ||
| 690 | |a RB1-214 | ||
| 655 | 7 | |a article |2 local | |
| 786 | 0 | |n Mediators of Inflammation, Vol 2016 (2016) | |
| 787 | 0 | |n http://dx.doi.org/10.1155/2016/4854378 | |
| 787 | 0 | |n https://doaj.org/toc/0962-9351 | |
| 787 | 0 | |n https://doaj.org/toc/1466-1861 | |
| 856 | 4 | 1 | |u https://doaj.org/article/c9e88bcc54d943e889da1608ca43fc3b |z Connect to this object online. |