Immunostimulation protects microglial cells from nitric oxide-mediated apoptosis.
Cellular oxidative stress from excess free radicals can initiate apoptosis in some cell types. Thus, we hypothesize that cells expressing nitric oxide synthase (NOS) will also express anti-oxidative stress mechanisms, in order to prevent self-intoxication by the free radical, nitric oxide (NO). To test this hypothesis, we investigated the vulnerability of microglial cells (BV-2 line) to NO produced by the NO donor sodium nitroprusside. Damage to the cells was measured by an in situ detection method of DNA fragmentation, an indicator of apoptosis. Activation by lipopolysaccharide (LPS) dose-dependently protected BV-2 cells against NO toxicity (up to 67%) while unactivated BV-2 cells were vulnerable to NO. Our results indicate that activation of BV-2 cells induces protection mechanisms against NO toxicity.
Sugaya
K
K
Department of Pharmacology, Mayo Clinic Jacksonville, FL 32224, USA.
Chouinard
M
M
McKinney
M
M
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002478:Cells, Cultured / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D007114:Immunization; D008070:Lipopolysaccharides / Q000494:pharmacology*; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism; D009569:Nitric Oxide / Q000633:toxicity*; D009573:Nitrites / Q000378:metabolism
D008070:Lipopolysaccharides; D009573:Nitrites; D009569:Nitric Oxide