Ubiquitin and ubiquitin-conjugated protein expression in the rat cerebral cortex and hippocampus following traumatic brain injury (TBI)

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Jiong Liu ◽  
Joseph T. McCabe
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Yaohua Li ◽  
Xin Chen ◽  
Shuyuan Yang ◽  
Jianning Zhang

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pp. 1687-1691 ◽  
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Takao Satou ◽  
Shigeo Hashimoto ◽  
Hiroyuki Ito

2002 ◽  
Vol 71 (2) ◽  
pp. 208-219 ◽  
Author(s):  
Vemuganti L. Raghavendra Rao ◽  
Vinay K. Dhodda ◽  
Guoqing Song ◽  
Kellie K. Bowen ◽  
Robert J. Dempsey

2018 ◽  
Vol 11 (1) ◽  
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Elvia Coballase-Urrutia ◽  
Marina Martinez-Vargas ◽  
Luz Navarro

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pp. 65-69 ◽  
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Xiang-Lan Yao ◽  
Jiong Liu ◽  
Eleanor Lee ◽  
Geoffrey S.F. Ling ◽  
Joseph T. McCabe

2021 ◽  
Vol 19 ◽  
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Anni Du ◽  
Rui Cai ◽  
Jingshan Shi ◽  
Qin Wu

Background: Neuroinflammation is central to the pathology of traumatic brain injury (TBI). Icariin (ICA) is a flavonoid derived from the genus Epimedium which is a traditional Chinese herb, a potential therapeutic drug for TBI. This study aims to explore the protective effect of ICA on TBI and its mechanism Methods: Sprague-Dawley rats were exposed to controlled cortical impact to produce a neuroinflammatory response. The treatment groups received ICA (15 mg/kg, 30 mg/kg and 60 mg/kg), while the sham group was gavaged with equal volumes of saline. The beam-balance testing and prehensile traction test were used for neurological scoring. Pathological changes were observed by H&E staining. The protein expression levels of inflammatory factors were measured by Western blot analysis Results: It was found that ICA significantly improved the neuroethology function and alleviated the pathological injury in TBI rats. The protein expression levels of inflammatory factors COX-2, IL-1β, and TNF-α and its regulatory proteins p-NF-κB-p65, p-ERK1/2, p-JNK, and p-p38 were increased in the cerebral cortex injured by TBI. The protein expression levels of inflammatory cytokines were markedly decreased in cerebral cortex of TBI rats when administrated with ICA. Conclusion: The present study demonstrates that ICA may be a promising therapeutic strategy for reducing inflammation in TBI.


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