片仔癀对局灶性脑缺血/再灌注大鼠皮质中NMDAR1和GluR2表达的影响
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摘要
目的研究片仔癀对局灶性脑缺血/再灌注大鼠皮质中NMDAR1、GluR2 mRNA及蛋白表达的影响。方法健康成年♂SD大鼠40只,随机分为假手术组、模型对照组、片仔癀给药组,用线栓法建立局灶性脑缺血/再灌注大鼠模型(MCAO)。Zea-Longa标准评分法评价大鼠神经功能损伤;TTC染色法评价脑梗死体积变化;qPCR法和Western blot法分别检测大鼠缺血侧脑组织皮质中NMDAR1、GluR2 mRNA及蛋白的表达。结果与MCAO组比较,片仔癀能明显改善大鼠的神经功能损伤,降低大鼠脑梗死体积,促进NMDAR1、GluR2 mRNA及蛋白的表达。结论片仔癀可能通过抑制局灶性脑缺血/再灌注大鼠皮质NMDAR1、GluR2 mRNA及蛋白的下调而发挥脑保护作用。
Aim To investigate the effects of Pien-Tze-Huang(PZH) on mRNA and protein expression of NMDAR1 and GluR2 in cortex of MCAO rats.Methods Forty healthy adult male Sprague-Dawley rats were randomly divided into three groups: sham, MCAO, MCAO+PZH groups. The rats were subjected to focal cerebral ischemia/reperfusion with suture-occluded method. Neurological deficit testing was performed with Zea Longa scale. The volume of cerebral infarction was evaluated by TTC staining. The mRNA and protein expression of NMDAR1 and GluR2 in cortex of side cerebral ischemic tissues were determined using qPCR and Western blot analysis.Results Compared with MCAO group, PZH significantly improved the neurological deficit, decreased the volume of cerebral infarction, and up-regulated the mRNA and protein expression of NMDAR1 and GluR2.Conclusions PZH attenuates the down-regulation of mRNA and protein expression of NMDAR1 and GluR2 after focal cerebral ischemic injury in rats, which may be associated with the cerebral protective effect of PZH.
Aim To investigate the effects of Pien-Tze-Huang(PZH) on mRNA and protein expression of NMDAR1 and GluR2 in cortex of MCAO rats.Methods Forty healthy adult male Sprague-Dawley rats were randomly divided into three groups: sham, MCAO, MCAO+PZH groups. The rats were subjected to focal cerebral ischemia/reperfusion with suture-occluded method. Neurological deficit testing was performed with Zea Longa scale. The volume of cerebral infarction was evaluated by TTC staining. The mRNA and protein expression of NMDAR1 and GluR2 in cortex of side cerebral ischemic tissues were determined using qPCR and Western blot analysis.Results Compared with MCAO group, PZH significantly improved the neurological deficit, decreased the volume of cerebral infarction, and up-regulated the mRNA and protein expression of NMDAR1 and GluR2.Conclusions PZH attenuates the down-regulation of mRNA and protein expression of NMDAR1 and GluR2 after focal cerebral ischemic injury in rats, which may be associated with the cerebral protective effect of PZH.
引文
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[2] Corbyn Z. Statistics: a growing global burden[J]. Nature, 2014, 510(7506):S2-3.
[3] 国家药典委员会.中华人民共和国药典(一部)[S].北京:中国医药科技出版社, 2015:144. Chinese Pharmacopoeia Commission. The Pharmacopoeia of the People′s Republic of China(a)[S].Beijing: China Medical Science and Technology Press, 2015:144.
[4] 黄希艳.片仔癀对大鼠大脑中动脉阻断所致局灶性脑梗死的影响研究[D].北京:北京中医药大学,2012. Huang X Y. Effect of Pien Tze Huang on focal cerebral infarction induced by occlusion of middle cerebral artery in rats[D]. Beijing: Beijing University of Chinese Medicine, 2012.
[5] 李倩.片仔癀对大脑中动脉局灶性梗死大鼠的影响及机理研究[D]. 北京:北京中医药大学,2012. Li Q. Effects and mechanism of Pien Tze Huang on focal cerebral infarction rats[D]. Beijing: Beijing University of Chinese Medicine, 2012.
[6] Zhang X Q, Zhang Y P, Tang S Q, et al. Pien-Tze-Huang protects cerebral ischemic injury by inhibiting neuronal apoptosis in acute ischemic stroke rats[J]. J Ethnopharmacol, 2018, 219:117-225.
[7] 张小琴,苗学蒸,周丽英,等.红景天苷对局灶性脑缺血/再灌注大鼠轴突再生及Akt/GSK-3β/CRMP-2表达的影响[J].中国药理学通报,2017,33(9):1320-4. Zhang X Q, Miao X Z, Zhou L Y, et al. Salidroside regulates the Akt/GSK-3β/CRMP-2 expression and axonal regeneration in MCAO rats[J]. Chin Pharmacol Bull, 2017, 33(9):1320-4.
[8] 许力伟,应雄,李茗菊,等. 红景天苷对局灶性脑缺血/再灌注大鼠脑组织Ephb3、Ephb6 mRNA表达的影响[J].福建中医药,2016,47(5):9-10. Xu L W, Ying X, Li M J, et al. The effect of salidroside on expression of Ephb3 and Ephb6 mRNA in MCAO rats[J]. Fujian J Tradit Chin Med, 2016, 47(5):9-10.
[9] Longa E Z, Weinstein P R, Carlson S, Cummins R. Reversible middle cerebral artery occlusion without craniectomy in rats[J]. Stroke, 1989, 20(1):84-91.
[10] 左玮,梅丹.高血糖通过抑制线粒体自噬加重大鼠脑缺血/再灌注损伤[J].中国药理学通报,2016,32(6):846-53. Zuo W, Mei D. Hyperglycemia aggravated cerebral ischemia/reperfusion injury by inhibiting mitophagy[J]. Chin Pharmacol Bull, 2016, 32(6):846-53.
[11] 朱贤富,王振华.脑缺血/再灌注损伤机制的研究现状[J].医学综述,2010, 16(18):2786-9. Zhu X F, Wang Z H. Progress on the mechanisms of cerebral ischemia/reperfusion injury[J]. Med Recapitulate, 2010, 16(18):2786-9.
[12] Traynelis S F, Wollmuth L P, McBain C J, et al. Glutamate receptor ion channels: structure, regulation, and function[J]. Pharmacol Rev, 2010, 62(3):405-96.
[13] Kutsuwada T, Kashiwabuchi N, Mori H, et al. Molecular diversity of the NMDA receptor channel[J]. Nature, 1992, 358(6381):36-41.
[14] Parsons M P, Raymond L A. Extrasynaptic NMDA receptor involvement in central nervous system disorders[J]. Neuron, 2014, 82(2):279-93.
[15] Pellegrini-Giampietro D E, Gorter J A, Bennett M V, et al. The GluR2(GluR-B) hypothesis: Ca2+-permeable AMPA receptors in neurological disorders[J]. Trends Neurosci, 1997, 20(10):464-70.