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Pretreatment with SN50 results in a significant reduction in amount of PI-positive cells at 12, 24, and 48 h time-point post TBI compared with vehicle-treated groups. Topical SN50 suppresses nuclear factor-κB activation in local cells and reduces the incidence of epithelial defects/ulceration in healing corneas. Myofibroblast generation, macrophage invasion, activity of matrix metalloproteinases, basement membrane destruction, and expression of cytokines are all decreased in treated corneas compared with controls. Treating the human gastric cancer cells SGC7901 with SN50 could significantly enhance the effects of LY294002 on inducing cell death after 24 h. SN50 can inhibit translocation of NF-kB and production of inflammatory cytokines that are implicated in lipopolysaccharide (LPS)-induced lung injury.

Treatment with SN50 accelerates the recovery of motor functional outcome from 1st to 4th day. Animals subjected to SN50 pretreatment demonstrate a significant decrease in the visuospatial learning latencies relative to the control group at 7 and 8 days post-TBI. Pretreatment with SN50 results in a significant reduction of NF-κB p65 protein levels from 6 to 48 h post-TBI and TNF-a protein levels from 12 to 48 h post-TBI.