Melatonin receptor activation provides cerebral protection after traumatic brain injury by mitigating oxidative stress and inflammation via the Nrf2 signaling pathway

2019 ◽  
Vol 131 ◽  
pp. 345-355 ◽  
Author(s):  
Junmin Wang ◽  
Chao Jiang ◽  
Kun Zhang ◽  
Xi Lan ◽  
Xuemei Chen ◽  
...  
Neuropeptides ◽  
2018 ◽  
Vol 72 ◽  
pp. 58-64 ◽  
Author(s):  
Fayin Li ◽  
Xiaodong Wang ◽  
Zhikui Deng ◽  
Xianlong Zhang ◽  
Pengfei Gao ◽  
...  

2020 ◽  
Vol 45 (8) ◽  
pp. 1839-1850
Author(s):  
Wei Zhu ◽  
Guangqiang Cui ◽  
Tuo Li ◽  
Hongguang Chen ◽  
Jian Zhu ◽  
...  

2011 ◽  
Vol 71 (3) ◽  
pp. 680-686 ◽  
Author(s):  
Wei Jin ◽  
Jun Wu ◽  
Handong Wang ◽  
Jie Kong ◽  
Hongbin Ni ◽  
...  

2020 ◽  
Vol 34 (9) ◽  
pp. 831-843
Author(s):  
Yunliang Tang ◽  
Xiaoyang Dong ◽  
Gengfa Chen ◽  
Wen Ye ◽  
Junwei Kang ◽  
...  

Background Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Oxidative stress, inflammation, and apoptosis are vital pathophysiological features post-TBI. Objectives Research has shown that vagus nerve stimulation (VNS) can attenuate oxidative stress in various diseases. However, the critical role of VNS in TBI is still not completely understood. This study investigated the protective effects and potential mechanism of VNS on TBI. Methods Male Sprague-Dawley rats were randomized into 3 groups: sham, TBI, and TBI + VNS. The TBI model was induced in rats by the free-fall drop method. The vagal nerve trunk was separated, and VNS was performed after establishing the TBI model. Results The results showed that VNS significantly ameliorated tissue damage, neurological deficits, and cerebral edema, compared with the sham VNS group. Additionally, VNS alleviated oxidative stress, inflammation, and apoptosis in the pericontusive cortex of rats after TBI. VNS also significantly suppressed expression of the nuclear factor-κB (NF-κB) protein in the nucleus and activation of the nucleotide-binding domain–like receptor protein 3 (NLRP3) inflammasome. Conclusions Taken together, the present study indicates that VNS may attenuate brain damage after TBI by inhibiting oxidative stress, inflammation, and apoptosis, possibly through the NF-κB/NLRP3 signaling pathway.


2018 ◽  
Vol 43 (12) ◽  
pp. 2435-2445 ◽  
Author(s):  
Man Zhang ◽  
Li-Li Huang ◽  
Chen-Huai Teng ◽  
Fang-Fang Wu ◽  
Li-yun Ge ◽  
...  

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