依达拉奉联合缺血后处理对大鼠脑缺血再灌注损伤的影响

Abstract
Figure/Table
References (22)
Related Citation (5)

Download: PDF (965 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To investigate the effect of Edaravone (Eda) combined with ischemic postconditioning (IP) on cerebral ischemia-reperfusion injury (I/R), and to evaluate whether Eda combined with IP have superimpose protective effects on I/R compared with IP alone. Methods Thirty-six SD rats were selected and divided into the control group (I/R group), IP group and IP+Eda group according to the random number table method, with 12 rats in each group. The rat I/R model was established in the I/R group by suture method. The rat I/R model was established by suture method in the IP group with IP intervention. The rat I/R model was established by suture method in the IP+Eda group with Eda and IP intervention. At 48 h after the operation, the rats were evaluated for neurological deficits and the volume of cerebral infarction was measured. By fluorescence quantitative PCR, Western blot and immunohistochemical method the expression of tissue angiotensin Ⅱ with type 1 and type 2 receptor (AT1, AT2) in the rat brain tissue was detected. The inhibition rate of superoxide dismutase (SOD) of rats in each group was detected. Results Compared with I/R group, IP+Eda group and IP group showed a decrease in neurological deficit score, a decrease in cerebral infarction volume, a decrease in mRNA and protein expression of AT1 and AT2, a decrease in the number of AT1 and AT2 positive cells, and an increase in SOD inhibition rate, with statistically significant differences (P ＜ 0.01 or P ＜ 0.05). There was no significant difference in the above indicators between the IP+Eda group and the IP group (P ＞ 0.05). Conclusion The IP+Eda group can protect rat I/R, but the combination of the two groups does not produce a superimposed protective effect.

Key words： Cerebral ischemia-reperfusion injury Edaravone Ischemic postconditioning Angiotensin Ⅱ type 1 receptor Angiotensin Ⅱ type 2 receptor

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	WANG Ying ZHOU Hongqun YIN Mei MIAO Wei ZHU Yuhong

Cite this article:

WANG Ying ZHOU Hongqun YIN Mei MIAO Wei ZHU Yuhong. Effect of Edaravone combined with ischemic postconditioning on cerebral ischemia-reperfusion injury in rats[J]. 中国医药导报, 2020, 17(5): 13-17.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2020/V17/I5/13

[1] Wu MY，Yiang GT，Liao WT，et al. The Current Mechanistic Concepts in Ischemia and Reperfusion Injury [J]. Cell Physiol Biochem，2018，46（4)：1650-1667.
[2] 黄丽，朱彩霞，张芹欣，等.四种开窍药对急性不完全性脑缺血再灌注损伤模型大鼠的脑保护作用[J].中国比较医学杂志，2018，28（8）：77-82.
[3] 曾兆禄，韩继超，薛云，等.针刺结合丹红注射液对大鼠脑缺血再灌注损伤的保护作用[J].中国比较医学杂志，2016，26（2）：62-66.
[4] Zhao H，Sapolsky RM，Steinberg GK. Interrupting reperfusion as a stroke therapy：ischemic postconditioning reduces infarct size after focal ischemia in rats [J]. J Cereb Blood Flow Metab，2006，26：1114-1121.
[5] 徐波.HO-1在缺血后处理抗肺缺血再灌注损伤中的作用及其对STAT-3表达的影响[J].中国实验动物学报，2013，21（4）：81-85.
[6] 王荣亮，赵海苹，罗玫.远程缺血后适应对大鼠脑缺血再灌注损伤后MIP-1α表达的影响[J].中国比较医学杂志，2013，23（8）：24-29，后插1.
[7] Wang Y，Ge P，Yang L，et al. Protection of ischemic post conditioning against transient focal ischemia-induced brain damage is associated with inhibition of neuroinflammation via modulation of TLR2 and TLR4 pathways [J]. J Neuroinflammation，2014，11：15.
[8] Sun MS， Jin H，Sun X，et al. Free Radical Damage in Ischemia-Reperfusion Injury：An Obstacle in Acute Ischemic Stroke after Revascularization Therapy [J]. Oxid Med Cell Longev，2018：3804979.
[9] Dringen R. Metaolism and functions of glutathione in brain. Prog Neurobiol，2000，62（6）：649-671.
[10] 韩遵华，段淼，李清香.依达拉奉对缺氧缺血性脑病新生大鼠脑水肿及CD163/HO-1信号通路的影响[J].中国比较医学杂志，2019，29（4）：34-40.
[11] 米艳，高小平，朱清风，等.依达拉奉对大鼠脑缺血再灌注损伤的机制研究[J].中国医药导报，2019，16（13）：16-19.
[12] Belayev L，Alonso OF，Busto R，et al. Middle cerebral artery occlusion in the rat by intraluminal suture [J]. Stroke，1996，27（9）：1616-1622.
[13] Yang T，Xu C. Physiology and Pathophysiology of the Intrarenal Renin-Angiotensin System: An Update [J]. J Am Soc Nephrol，2017，28（4）：1040-1049.
[14] Tao MX，Xue X，Gao L，et al. Involvement of angiotensin-(1-7) in the neuroprotection of captopril against focal cerebral ischemia [J]. Neurosci Lett，2018，687：16-21.
[15] 李蓓华，鲁国洲，黄新武.血管性痴呆大鼠肾素-血管紧张素-醛固醇系统的动态变化[J].中国老年学杂志，2017， 37（14）：3423-3425.
[16] Gebre AK，Altaye BM，Atey TM，et al. Targeting Renin-Angiotensin System Against Alzheimer′s Disease [J]. Front Pharmacol，2018，9：440.
[17] Tang M，Zhao L，Chen Y，et al. Angiotensin Ⅱ protects cortical neurons against oxygen-glucose deprivation-induced injury in vitro [J]. Biomed Rep，2014，2（1）：112-116.
[18] Wu CY，Zha H，Xia QQ，et al. Expression of angiotensin Ⅱ and its receptors in activated microglia in experimentally induced cerebral ischemia in the adult rats [J]. Mol Cell Biochem，2013，382（1/2）：47-58.
[19] Alhusban A，Kozak A，Eldashan W，et al. Artery reopening is required for the neurorestorative effects of angiotensin modulation after experimental stroke [J]. Exp Transl Stroke Med，2016，8：4.
[20] Rodríguez-Lara SQ，García-Benavides L，Miranda-Díaz AG. The Renin-Angiotensin-Aldosterone System as a Therapeutic Target in Late Injury Caused by Ischemia-Reperfusion [J]. Int J Endocrinol，2018，2018：3614303.
[21] Wang ZF，Wang NP，Harmouche S，et al. Postconditioning attenuates coronary perivascular and interstitial fibrosis through modulating angiotensin Ⅱ receptors and angiotensin-converting enzyme 2 after myocardial infarction [J]. J Surg Res，2017，211：178-190.
[22] Zhang WW，Bai F，Wang J，et al. Edaravone inhibits pressure overload-induced cardiac fibrosis and dysfunction by reducing expression of angiotensin II AT1 receptor [J]. Drug Des Devel Ther，2017，11：3019-3033.