Figure 4.

NOS and ROS inhibitors improve microglial viability and reduce NO accumulation. A panel of NO (AG, 1 mM; LNMA, 1 mM) and ROS (APO, 1 mM; ALO, 50 μM; INDO, 10 μM) inhibitors as well as minocycline (MINO, 10 μM) known to have anti-inflammatory properties and NOHA (an arginase inhibitor, 10 μM) were studied in BV2 cells exposed to LPS (1 μg/ml). BV2 cell viability as assessed by MTT showed that all of the ROS and NOS inhibitors protected the cells, but not MINO or NOHA (A). LPS-induced NO in BV2 cells was attenuated by some (APO, ALO, AG, MINO, LNMA) but not all inhibitors (B). Neither NOS inhibitor inhibited LPS induced increases in iNOS (C), shown is a representative blot of at least 3 independent experiments. (AG: aminoguanidine, a relatively selective iNOS inhibitor; LNMA: L-NNMA, a non selective NOS inhibitor APO: apocynin, a NADPH oxidase inhibitor; ALO: allopurinol, a xanthine oxidase inhibitor; INDO: indomethacin, a COX inhibitor) n = 12 independent observations, *P < 0.0001 versus control; #P < 0.0001 versus LPS.

Kacimi et al. Journal of Inflammation 2011 8:7   doi:10.1186/1476-9255-8-7
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