Lycium Barbarum Polysaccharides Decrease Hyperglycemia-Aggravated Ischemic Brain Injury through Maintaining Mitochondrial Fission and Fusion Balance.
Lycium Barbarum Polysaccharides Decrease Hyperglycemia-Aggravated Ischemic Brain Injury through Maintaining Mitochondrial Fission and Fusion Balance.
复制标题
枸杞多糖通过维持线粒体裂变和融合平衡减少高血糖加重的缺血性脑损伤
DOI：
10.7150/ijbs.18404
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发表时间：
2017
影响因子：
9.2
通讯作者：
Zhang JZ
中科院分区：
文献类型：
--
作者：
Liu WJ;Jiang HF;Rehman FU;Zhang JW;Chang Y;Jing L;Zhang JZ
虽然已经报道了枸杞多糖具有神经保护作用，但对其改善高血糖加重的缺血/再灌注脑损伤的能力知之甚少。本研究比较了正常血糖（NG）和高血糖（HG）大鼠在大脑中动脉闭塞（MCAO）30分钟后，再灌注24或27小时，以及用枸杞多糖（LBP）或胰岛素预处理的HG大鼠。在每一组中，神经功能缺损，梗死体积，病理组织学，蛋白质，Opa 1和Drp 1的表达进行了评估，以确定LBP在减轻高血糖加重缺血/再灌注脑损伤的疗效。我们的结果表明，与NG组相比，HG组在再灌注24和/或72小时时神经功能缺损、梗死体积和神经元固缩的证据增加（P<0.05），并且LBP预处理降低了这些效应（P<0.05）。此外，免疫组化结果显示，与NG组相比，HG组再灌注24和72 h后Drp 1阳性神经元增加，Opa 1阳性神经元减少。LBP处理防止了HG诱导的Drp-1和Opa 1表达的改变。Western印迹进一步证实了这些发现，表明HG引起磷酸化Drp 1的增加和Opa 1的减少，随后通过LBP的加入而逆转。这些结果表明，高血糖症加重缺血性脑损伤与线粒体动力学的改变和LBP预处理改善高血糖症增强缺血性脑损伤，通过维持线粒体动态平衡。
Although it has been reported that polysaccharides found in Lycium barbarum possess neuroprotective effects, little is known of their ability to ameliorate hyperglycemia-aggravated ischemia/reperfusion brain injury. In this study, normoglycemic (NG) and hyperglycemic (HG) rats were compared after 30 minutes of middle cerebral artery occlusion (MCAO), followed by 24 or 27 hours of reperfusion, with HG rats pretreated with lyceum barbarum polysaccharides (LBP) or insulin. In each group, the neurological deficit, infarct volume, pathohistology, and expression of proteins, Opa1 and Drp1, were assessed to determine the efficacy of LBP in alleviating hyperglycemia-aggravated ischemia/reperfusion brain injury. Our results show that, compared to the NG group, the HG group had increases in neurological deficits, infarct volume, and evidence of neuronal pyknosis at 24- and/or 72-h of reperfusion (P<0.05) and that pre-treatment with LBP decreased these effects (P<0.05). In addition, immunohistochemistry revealed an increase of Drp1 and a decrease of Opa1 positive neurons in the HG group after 24 and 72 hours of reperfusion when compared to the NG group. LBP treatment prevented the HG-induced alterations in Drp-1 and Opa1 expression. Western blots further confirmed these findings showing that HG caused an increase in phospho-Drp1 and a decrease in Opa1 which were subsequently reversed by LBP addition. These results suggest that hyperglycemia-aggravated ischemic brain damage is associated with an alteration of mitochondrial dynamics and that pre-treatment with LBP ameliorates the hyperglycemia-enhanced ischemic brain damage through maintaining mitochondrial dynamic balance.
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影响因子：
8.3
作者：
Baek SH;Noh AR;Kim KA;Akram M;Shin YJ;Kim ES;Yu SW;Majid A;Bae ON
通讯作者：
Bae ON
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DOI：
10.1258/ebm.2011.010400
发表时间：
2011-09
期刊：
Experimental biology and medicine (Maywood, N.J.)
影响因子：
--
作者：
Tang L;Zhang Y;Jiang Y;Willard L;Ortiz E;Wark L;Medeiros D;Lin D
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Lin D
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影响因子：
1.5
作者：
Ten VS;Starkov A
通讯作者：
Starkov A
DOI：
10.1016/j.mcn.2016.08.010
发表时间：
2016-10
期刊：
Molecular and cellular neurosciences
影响因子：
--
作者：
Kumar R;Bukowski MJ;Wider JM;Reynolds CA;Calo L;Lepore B;Tousignant R;Jones M;Przyklenk K;Sanderson TH
通讯作者：
Sanderson TH
影响因子：
4
作者：
Ho, Yuen-Shan;Yu, Man-Shan;Chang, Raymond Chuen-Chung
通讯作者：
Chang, Raymond Chuen-Chung