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. 2013 Mar;34(3):345-55.
doi: 10.1007/s10072-012-1007-z. Epub 2012 Mar 23.

Therapeutic effect of SN50, an inhibitor of nuclear factor-κB, in treatment of TBI in mice

Yu-Xia Sun  1 , Ding-Kun Dai, Ran Liu, Tao Wang, Cheng-Liang Luo, Hai-Jun Bao, Rui Yang, Xue-Ying Feng, Zheng-Hong Qin, Xi-Ping Chen, Lu-Yang Tao
Affiliations

Therapeutic effect of SN50, an inhibitor of nuclear factor-κB, in treatment of TBI in mice

Yu-Xia Sun et al. Neurol Sci. 2013 Mar.

Abstract

NF-κB upregulation has been demonstrated in neurons and glial cells in response to experimental injury and neuropathological disorders, where it has been related to both neurodegenerative and neuroprotective activities. It has been generally recognized that NF-κB plays important roles in the regulation of apoptosis and inflammation as well as innate and adaptive immunity. However, the regulatory mechanism of NF-κB in apoptosis remained to be determined. The present study sought to first investigate the effect of a NF-κB inhibitor SN50, which inhibits NF-κB nuclear translocation, on cell death and behavioral deficits in our mice traumatic brain injury (TBI) models. Additionally, we tried to elucidate the possible mechanisms of the therapeutic effect of SN50 through NF-κB regulating apoptotic and inflammatory pathway in vivo. Encouragingly, the results showed that pretreatment with SN50 remarkably attenuated TBI-induced cell death (detected by PI labeling), cumulative loss of cells (detected by lesion volume), and motor and cognitive dysfunction (detected by motor test and Morris water maze). To analyze the mechanism of SN50 on cell apoptotic and inflammatory signaling pathway, we thus assessed expression levels of TNF-α, cathepsin B and caspase-3, Bid cleavage and cytochrome c release in SN50-pretreated groups compared with those in saline vehicle groups. The results imply that through NF-κB/TNF-α/cathepsin networks SN50 may contribute to TBI-induced extrinsic and intrinsic apoptosis, and inflammatory pathways, which partly determined the fate of injured cells in our TBI model.

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