Saikosaponin a protects TBI rats after controlled cortical impact and the underlying mechanism.


The inflammatory response plays a significant role in neuronal cell death and functional deficits after Traumatic brain injury (TBI). Importantly, anti-inflammatory agents have neuroprotective effects. To date, however, no studies have investigated the neuroprotective effects of Saikosaponin a (SSa) after TBI. In the present study, rats with controlled cortical impact (CCI) were used to investigate the neuroprotective effects of SSa. The results showed that SSa reduced body weight loss, improved neurological functions andcognition, and reduced brain edema and blood brain barrier permeability after CCI. Moreover, SSa inhibited aquaporin-4 (AQP-4), matrix metalloprotein-9 (MMP-9), mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (c-JNK), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The reduction in the loss of occludin mediated by SSa may partially account for its neuroprotective effects. Together, our results suggest that SSa appears to counteract the inflammatory response and neurological function deficits after TBI and possibly via an anti-inflammatory response and inhibition of the MAPK signaling pathway.

Cite this paper

@article{Mao2016SaikosaponinAP, title={Saikosaponin a protects TBI rats after controlled cortical impact and the underlying mechanism.}, author={Xiang Mao and Guozhuan Miao and Xiaogang Tao and Shuyu Hao and Hao Zhang and Huan Li and Zonggang Hou and Runfa Tian and Te Ling Lu and Jun Ma and Xiaodong Zhang and Hongwei Cheng and Baiyun Liu}, journal={American journal of translational research}, year={2016}, volume={8 1}, pages={133-41} }