NO synthase inhibitors increased the exudate formation and inflammatory cell number, contributed to oxidative stress, induced an oxidant/antioxidant imbalance by maintaining high O2−, and enhanced the production of pro-inflammatory mediators. L-arginine and NOC-18 reversed the proinflammatory effects of NO synthase inhibitors, perhaps by reducing the expression of adhesion molecules on endothelial cells. Thus, our results indicate that NO is involved in blunting—not enhancing—the inflammatory response.
CiteULike: Involvement of Nitric Oxide in a Rat Model of Carrageenin-Induced Pleurisy: "Iwata, M., Suzuki, S., Asai, Y., Inoue, T., and Takagi, K. (2010). Involvement of nitric oxide in a rat model of carrageenin-induced pleurisy. Mediators of Inflammation, 2010."
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