1.上海中医药大学科技实验中心(上海 201203)
2.上海市金山区中西医结合医院(上海 201501)
3.上海中医药大学针灸推拿学院(上海 201203)
4.上海市中医文献馆(上海 200025)
5.上海中医药大学附属龙华医院针灸科(上海 201203)
郭润杰,男,在读硕士生,主要从事针刺治疗视网膜疾病的基础研究
田雪松,研究员,硕士生导师;E-mail:xuesong.tian@shutcm.edu.cn
扫 描 看 全 文
郭润杰,陈平,符甜甜等.δ⁃阿片受体在电针抗视网膜缺血再灌注致视网膜细胞坏死性凋亡中的作用[J].上海中医药大学学报,2022,36(05):52-59.
GUO Runjie,CHEN Ping,FU Tiantian,et al.Role of δ⁃opioid receptors in electroacupuncture against retinal ischemia⁃reperfusion induced retinal cell necroptosis[J].Academic Journal of Shanghai University of Traditional Chinese Medicine,2022,36(05):52-59.
郭润杰,陈平,符甜甜等.δ⁃阿片受体在电针抗视网膜缺血再灌注致视网膜细胞坏死性凋亡中的作用[J].上海中医药大学学报,2022,36(05):52-59. DOI: 10.16306/j.1008-861x.2022.05.010.
GUO Runjie,CHEN Ping,FU Tiantian,et al.Role of δ⁃opioid receptors in electroacupuncture against retinal ischemia⁃reperfusion induced retinal cell necroptosis[J].Academic Journal of Shanghai University of Traditional Chinese Medicine,2022,36(05):52-59. DOI: 10.16306/j.1008-861x.2022.05.010.
目的,2,探讨δ-阿片受体(DOR)在电针抗高眼压(HIOP)诱导视网膜缺血再灌注损伤致视网膜细胞坏死性凋亡中的作用。,方法,2,55只Wistar大鼠随机分为 5 组:空白对照组、HIOP 6 h组、HIOP 12 h组、HIOP 24 h组、HIOP 72 h组,PI染色检测上述时间点大鼠视网膜细胞坏死性凋亡数量,Western blot检测p-Rip1、p-Rip3表达。另取55只Wistar大鼠随机分为 5 组:空白对照组、HIOP组、电针+HIOP组、假电针+HIOP组、DOR 拮抗剂+HIOP+电针组,除空白对照组外,其余各组均采用HIOP法致大鼠视网膜缺血再灌注,缺血 1 h再灌 24 h。DOR 拮抗剂+HIOP+电针组缺血前 1 h 玻璃体腔注射DOR拮抗剂Naltrindole,再灌注开始及再灌注12 h,电针“水沟”“睛明”穴两次,每次30 min,再灌注 24 h,PI染色检测视网膜中坏死性凋亡细胞数量,Western blot检测p-Rip1、p-Rip3表达。,结果,2,HIOP 6、12、24、72 h,视网膜坏死性凋亡细胞数量明显增多,在12 h达到高峰,视网膜中p-Rip1和p-Rip3蛋白表达亦显著增加,其中p-Rip1峰值出现在12 h,p-Rip3在24 h表达最高;再灌注24 h,电针+HIOP组坏死性凋亡细胞数量、p-Rip1和p-Rip3蛋白表达均显著低于HIOP组,假电针+HIOP组和DOR 拮抗剂+HIOP+电针组与HIOP组比较,坏死性凋亡细胞数量、p-Rip1和p-Rip3蛋白表达均无显著性差异。,结论,2,在HIOP法诱导的视网膜缺血再灌注损伤中,电针“水沟”“睛明”两穴可显著减少视网膜细胞坏死性凋亡,对视网膜具有保护作用,且电针的抗视网膜细胞坏死性凋亡作用可能和DOR密切相关。
Objective: To investigate the role of delta-opioid receptor (DOR) in electroacupuncture (EA) against retinal cell necroptosis caused by retinal ischemia-reperfusion induced by high intraocular pressure (HIOP).,Methods,2,Fifty-five Wistar rats were randomly divided into five groups: blank control group, HIOP 6 h group, HIOP 12 h group, HIOP 24 h group and HIOP 72 h group. PI staining was used to detect the number of necroptotic cells in rats’ retina at the above timings, and Western blot was used to detect the expressions of p-Rip1 and p-Rip3. Another fifty-five Wistar rats were randomly divided into 5 groups: blank control group, HIOP group, EA+HIOP group, sham EA+HIOP group, and DOR antagonist+HIOP+EA group. Except for the blank control group, HIOP was used in the other groups to induce retinal ischemia-reperfusion in rats, and the ischemia lasted for 1 h, then reperfused for 24 h. DOR antagonist+HIOP+EA group received intravitreal injection of DOR antagonist Naltrindole 1 h before ischemia. At the beginning of reperfusion and 12 h after reperfusion, EA was performed at acupoints “Shuigou” and “Jingming” twice, 30 min each time. 24 h after reperfusion, the number of necroptotic cells in retina was detected by PI staining, and the expressions of p-Rip1 and p-Rip3 were detected by Western blot.,Result,2,After HIOP for 6 h, 12 h, 24 h and 72 h, the number of retinal necroptotic cells was increased significantly, and reached a peak at 12 h. The protein expressions of p-Rip1 and p-Rip3 in the retina were also significantly increased, and the peak of p-Rip1 expression appeared at 12 h and the expression of p-Rip3 was the highest at 24 h. After 24 h of reperfusion, the number of necroptotic cells and the protein expressions of p-Rip1 and p-Rip3 in the EA+HIOP group were all significantly lower than those in the HIOP group. Compared with the HIOP group, there was no significant difference in the number of necroptotic cells or the protein expressions of p-Rip1 and p-Rip3 in the sham EA+HIOP group and the DOR antagonist+HIOP+EA group.,Conclusion,2,In retinal ischemia-reperfusion injury induced by HIOP, EA at acupoints “Shuigou” and “Jingming” can significantly reduce retinal cell necroptosis and protect the retina, and the anti-retinal cell necroptosis effect of EA may be closely related to DOR.
电针视网膜缺血再灌注损伤δ阿片受体坏死性凋亡
electroacupunctureretinal ischemia-reperfusion injuryδ-opioid receptornecroptosis
OSBORNE N N. Pathogenesis of ganglion “cell death” in glaucoma and neuroprotection: focus on ganglion cell axonal mitochondria[J]. Prog brain Res, 2008, 173: 339-352.
VERMA D. Pathogenesis of diabetic retinopathy--the missing link?[J]. Med Hypotheses, 1993, 41(3): 205-210.
MATEI N, LEAHY S, BLAIR N P, et al. Assessment of retinal oxygen metabolism, visual function,thickness and degeneration markers after variable ischemia/reperfusion in rats[J]. Exp Eye Res, 2021, 213: 108838.
ROSENBAUM D M, DEGTEREV A, DAVID J, et al. Necroptosis, a novel form of caspase-independent cell death, contributes to neuronal damage in a retinal ischemia-reperfusion injury model[J]. J Neuroscience Res, 2009, 88(7): 1569-1576.
ZIESCHE A, BERGELT J, DEUBEL H, et al. Pre- and post-saccadic stimulus timing in saccadic suppression of displacement - A computational model[J]. Vision Res, 2017, 138: 1-11.
DVORIANTCHIKOVA G, DEGTEREV A, IVANOV D. Retinal ganglion cell (RGC) programmed necrosis contributes to ischemi-reperfusion-induced retinal damage[J]. Exp Eye Res, 2014, 123: 1-7.
DEGTEREV A, HUANG Z, BOYCE M, et al. Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury[J]. Nat chem biol,2005, 1(2): 112-119.
WANG H Y, SUN L M, SU L J, et al. Mixed lineage kinase domain-like protein MLKL causes necrotic membrane disruption upon phosphorylation by RIP3[J]. Mol cell, 2014, 54(1): 133-146.
樊远志,吴耀持. 远近配穴结合电针对降低青光眼高眼压影响的临床观察[J]. 中国中医药现代远程教育,2020, 18(5): 73-75.
梁凯霞. 针刺联合电针治疗视网膜动脉阻塞疗效观察[J]. 航空航天医学杂志,2017, 28(9): 1067-1069.
田雪松,周飞,杨茹,等. 电针上调δ阿片受体的表达减轻大鼠急性缺血性脑损伤[J]. 中西医结合学报,2008(6): 632-638.
田雪松,周飞,杨茹,等. 大鼠脑内δ-阿片受体在累加电针抗缺血性脑损伤中的作用[J]. 上海中医药杂志,2008, 42(6): 71-74.
GENG Y,CHEN Y T,SUN W,et al. Electroacupuncture Ameliorates Cerebral I/R-Induced Inflammation through DOR-BDNF/TrkB Pathway[J]. Evid Based Complement Alternat Med,2020, 2020: 3495836.
田雪松,周飞,杨茹, 等. 大鼠侧脑室注射δ-阿片受体拮抗剂naltrindole或激动剂TAN-67对急性脑缺血的影响[J]. 生理学报,2008, 60(4): 475-484.
TIAN X S, GUO J C, ZHU M, et al. δ-Opioid receptor activation rescues the functional TrkB receptor and protects the brain from ischemia-reperfusion injury in the rat[J]. PloS one, 2013, 8(7): e69252.
TIAN X S, HUA F, SANDHU H K, et al. Effect of δ-opioid receptor activation on BDNF-TrkB vs. TNF-α in the mouse cortex exposed to prolonged hypoxia[J]. Int J mol Sci, 2013, 14(8): 15959-15976.
CHENG M,GENG Y,CHEN Y T, et al. δ-Opioid receptor activation ameliorates lipopolysaccharide-induced inflammation and apoptosis by inhibiting the MAPK/caspase-3 pathway in BV2 microglial cells[J]. Exp Brain Res, 2021, 239(2): 401-412.
HUSAIN S, LIOU G I, CROSSON C E. Opioid receptor activation: suppression of ischemia/reperfusion-induced production of TNF-α in the retina[J]. Invest Ophthalmol Vis Sci, 2011, 52(5): 2577-2583.
HARTSOCK M J,CHO H K,WU L J,et al. A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure[J]. J Vis Exp, 2016(113): 54065.
郭承伟,吕璐. 《内经》络脉理论与眼科应用探讨[J]. 中国中医眼科杂志,2010, 20(4): 237-239.
徐红,张进,王海丽,等. 眼病针灸简史[J]. 中医文献杂志,2016, 34(1): 56-60.
徐红,张进,王海丽,等. 眼病针灸简史(续完)[J]. 中医文献杂志,2016, 34(2): 59-65.
裘沛然,陈汉平. 新编中国针灸学[M]. 上海:上海科学技术出版社,1992.
魏媛媛,樊小农,王舒,等. “水沟”穴干预MCAO大鼠脑梗死面积的特异性效应及针刺参数研究[J]. 中国针灸,2010, 30(3): 221-225.
崔培秀. 醒脑开窍针刺法配合血府逐瘀胶囊治疗中心性浆液性脉络膜视网膜病变18例[J]. 吉林中医药,2008, 28(7): 516-517.
史军月,张伯儒,张春红. 针刺治疗视网膜中央动脉阻塞型失明28例[J]. 上海针灸杂志,2015, 34(2): 164.
王淑娟. 睛明穴的应用体会[J]. 上海针灸杂志,2009, 28(7): 426-427.
GALLUZZI L,KEPP O,CHAN F K,et al. Necroptosis:Mechanisms and Relevance to Disease[J]. Annual Review of Pathology:Mechanisms of Disease, 2017, 12: 103-130.
WONG W W,GENTLE I E,NACHBUR U,et al. RIPK1 is not essential for TNFR1-induced activation of NF-κB[J]. Cell Death & Differentiation, 2010, 17(3): 482-487.
TING A T, BERTRAND M J. More to life than NF-κB in TNFR1 signaling[J]. Trends Immunol, 2016, 37(8): 535-545.
SUN L M, WANG H Y, WANG Z G, et al. Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase[J]. Cell, 2012, 148(1-2): 213-227.
0
浏览量
226
下载量
0
CSCD
0
CNKI被引量
关联资源
相关文章
相关作者
相关机构