| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2051984 | FEBS Letters | 2007 | 7 Pages |
The protective effects of huperzine A against oxygen–glucose deprivation (OGD)-induced injury in C6 cells were investigated. OGD for 6 h and reoxygenation for 6 h enhanced phosphorylation and degradation of IκBα and nuclear translocation of nuclear factor-kappa B (NF-κB), triggered overexpression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and nitric oxide (NO) in C6 cells. Along with inhibiting acetylcholinesterase activity, treatment with 1 μM huperzine A inhibited activation of NF-κB, attenuated iNOS, COX-2 and NO overexpression, and promoted survival in C6 cells subjected to OGD insult. The protective effects of huperzine A were partly mediated by “cholinergic anti-inflammatory pathway” through α7 nicotinic acetylcholine receptor.
