Bioactive Ingredients from Nitraria tangutorun Bobr. Protect Against Cerebral Ischemia/Reperfusion Injury Through Attenuation of Oxidative Stress and the Inflammatory Response

被引:5
|
作者
Wang, Hailiang [1 ]
Zhou, Jianhong [2 ]
Bi, Hongtao [3 ]
Yang, Xiaoyu [2 ]
Chen, Wenlong [1 ]
Jiang, Kuijun [1 ]
Yao, Yang [4 ]
Ni, Weihua [2 ]
机构
[1] Second Hosp Jilin Univ, Changchun, Peoples R China
[2] Jilin Univ, Coll Basic Med Sci, Changchun, Peoples R China
[3] Chinese Acad Sci, Northwest Inst Plateau Biol, Key Lab Tibetan Med Res, Xining, Peoples R China
[4] Tianjin Med Univ Gen Hosp, Dept Neurol, Tianjin 300052, Peoples R China
基金
中国国家自然科学基金;
关键词
anti-inflammatory; blood-brain barrier; focal cerebral ischemia; neuroprotection; Nitraria tangutorun Bobr; oxidative stress; NF-KAPPA-B; ANTHOCYANINS; EXTRACTION; STROKE; ISCHEMIA; FOOD; SEED; IDENTIFICATION; ANTIOXIDANTS; EVOLUTION;
D O I
10.1089/jmf.2020.4848
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Nitraria tangutorun Bobr. has been used for thousands of years as a native folk medicine to alleviate dizziness and neurasthenia due to oxygen. In our previous study, natural antioxidant components (namely, NJBE) were isolated from industrial N. tangutorun Bobr. juice byproducts (NJBE) from the Qinghai-Tibet plateau. The current investigation assessed the effects of NJBE on ischemic stroke in mice and the potential mechanisms. C57BL/6 mice received NJBE (25, 50, or 100 mg/Kg) by gavage for 14 days and then stroke was induced by the middle cerebral artery occlusion (MCAO) model, followed by reperfusion for 72 h. The evaluation of brain infarct size, behavioral tests, and functional assessments was conducted to assess the effects of NJBE after MCAO. Our results suggested that NJBE significantly decreases infarct size, improves neurological deficits, as well as reduces the number of GFAP(+) and Iba-1(+) cells after MCAO. NJBE inhibited nitric oxide and malondialdehyde production in the ischemic brain. Meanwhile, it attenuated the expressions of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Also, NJBE significantly attenuated the expression levels of proinflammatory indicators, including TNF-alpha, IL-1 beta, IL-6, and IL-12. This process was accompanied by the downregulation of TLR4, TRAF6, pI kappa B/pI kappa B, and MMP9 expression and the upregulation of claudin-5 expression. NJBE induced improvements in brain injury. The neuroprotective effect of NJBE provides evidence for its potential application in stroke treatment.
引用
收藏
页码:686 / 696
页数:11
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