Papers of the Week

Neuroinflammation and oxidative stress are key factors leading to neuronal injury. In this study, we investigated the role of S32, a novel 3-acetylaminocoumarin compound, in ameliorating neuronal injury induced by neuroinflammation and oxidative stress and . First, we found that S32 reduced the expression levels of p-P65 and p-P38, inhibited the nuclear translocation of P65, and lowered the levels of pro-inflammatory factors in LPS-induced BV2 cells, which indicated that S32 had an antineuroinflammatory effect. Second, BV2 cell culture medium was used as the conditioned medium to establish a model of oxidative damage in PC12 cells. It was found that S32 reduced the level of ROS and increased mitochondrial membrane potential of PC12 cells, which indicated that S32 can protect PC12 cells against conditioned medium-induced injury. Next, we found that S32 inhibited the decrease of cell viability of PC12 cells caused by HO, inhibited nuclear damage, decreased the level of ROS, increased MMP, activated the AKT and ERK pathways, increased Bcl-2 levels, and decreased Bax and Cleaved-Caspase3 expression levels, indicating that S32 ameliorated the damaging effects of HO-induced PC12 cells. Finally, we found that S32 exerted the antineuroinflammatory and apoptosis-inhibiting effects in LPS-induced mice. In conclusion, this study first demonstrated that S32, a novel 3-acetylaminocoumarin compound, can reduce neuroinflammation and neuroinflammation-induced neuronal injury, exerting an indirect protective effect on neurons, and also exert a direct protective effect on neurons by reducing oxidative stress.