Abstract：Objective To investigate the protective effects of baicalin on damaged SH-SY5Y cells induced by H2O2 through antioxygenation. Methods According to the different culture methods, SH-SY5Y cells were divided into five groups: control group (normal culture media), model group (200 μmol/L H2O2), low, medium, high dose of baicalin groups (protected by 50, 100, 200 μmol/L baicalin first, then damaged by H2O2). The survival rate of the SH-SY5Y cells were determined by MTT. The expression of thioredoxin protein (Trx) in cells was detected by Western blot. The contents of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and lipid oxidative malonaldehyde (MDA) were detected by kits. Results The absorbancy and cell survival rate in the model group were significantly lower than those of control group (P ＜ 0.01). Compared with model group, the absorbancy and cell survival rate of different doses of baicalin groups were all increased to different degrees, among which, there were highly statistically significant differences of low, medium doses of baicalin groups cpmpared with model group (P ＜ 0.01). Compared with control group, the MDA of model group increased significantly, while the Trx, SOD and GSH-Px decreased significantly (P ＜ 0.01). Compared with model group, the MDA of low, medium doses of baicalin groups decreased, while the Trx, SOD and GSH-Px increased, there were statistically significant differences (P ＜ 0.05 or P ＜ 0.01). Conclusion Baicalin has protective effects on the damaged SH-SY5Y cells induced by H2O2, the mechanism may be related to antioxidation.
吴宜艳 韩杨 李玲玉 唐春银 袁晓环. 黄芩苷通过抗氧化对H2O2诱导的SH-SY5Y细胞损伤的保护作用[J]. 中国医药导报, 2018, 15(27): 8-11.
WU Yiyan HAN Yang LI Lingyu TANG Chunyin YUAN Xiaohuan. The protective effect of baicalin on the damaged SH-SY5Y cells induced by H2O2 through antioxygenation. 中国医药导报, 2018, 15(27): 8-11.
[1] Son JW，Choi H，Yoo A，et al. Activation of the phosphatidylinositol 3-kinase pathway plays important roles in reduction of cerebral infarction by cilnidipine [J]. J Neurochem，2015，135（1）：186-193.
[2] Qu ZS，Zhang QD，Li L. Impact of low-dose urokinase in peritoneal dialysis on serum oxidative stress，nitric oxide and endothelin in cerebral infarction complicated with uremia [J]. Int J Clin Exp Med，2015，8（1）：1333-1341.
[3] Moore DJ，West AB，Dawson VL，et al. Molecular pathophysioligy of Parkinson′s disease [J]. Annu Rev Neurosci，2005，28：57-87.
[4] Sun ZW，Zhang L，Zhu SJ，et al. Excitotoxicity effects of glutamate on human neuroblastoma SH-SY5Y cells via oxidative damage [J]. Neurosci Bull，2010，26（1）：8-16.
[5] Nakaso K，Ito S，Nakashima K. Caffeine activates the PI3K/Akt pathway and prevents apoptotic cell death in a Parkinson′s disease model of SH-SY5Y cells [J]. Neurosci Lett，2008，432（2）：146-150.
[6] Lopes FM，Schr?觟dera R，da Frota ML Jr，et al. Comparison between proliferative and neuron-like SH-SY5Y cells as an in vitro model for Parkinson disease studies [J]. Brain Res，2010，1337：85-94.
[7] 余涓，胡桂芳，翁绳美，等.13-甲基十四烷酸对H2O2诱导SH-SY5Y神经细胞损伤的保护作用[J].中国临床药理学与治疗学，2010，15（6）：622-626.
[8] 张陆军，邢东明，王伟，等.静脉注射黄芩总苷后黄芩苷在大鼠血浆及大脑皮层的药物动力学比较[J].中国药理学通报，2005，21（6）：765-766.
[9] 李敏，曹慧，王斌，等.基于AQP-4、GFAP的黄芩苷、栀子苷配伍抗脑缺血大鼠神经功能损伤的研究[J].中药药理与临床2017，33（2）：56-59.
[10] 李筱筱，魏芬芬，孙雅煊，等.胰岛素信号通路参与阿尔兹海默症发病机制的研究进展[J].生命的化学，2017， 37（3）：386-390.
[11] 匡涛，刘旭，朱家伟，等.脑出血患者血清基质金属蛋白酶和氧化－抗氧化因子的动态变化研究[J].重庆医学，2016，45（32）：4558-4561.
[12] Lappalainen Z，Lappalainen J，Oksala NK，et al. Diabetes impairs exercise training-associated thioredoxin response and glutathione status in rat brain [J]. J Appl Physiol（1985），2009，106（2）：461-467.
[13] Tonissen KF，Di Trapani G. Thioredoxin system inhibitors as mediators of apoptosis for cancer therapy [J]. Mol Nutr Food Res，2009，53（1）：87-103.
[14] Calabrese V，Guagliano E，Sapienza M，et al. Redox regulation of cellular stress response in aging and neurodegenerative disorders：role of vitagenes [J]. Neurochem Res，2007，32（4/5）：757-773.
[15] Joshi MB，Ivanov D，Philippova M，et al. A requirement for Thiore-doxin in redox-sensitive modulation of T-cadherin expression in endothelial cells [J]. Biochem J，2008，416（2）：271-280.
[16] Kabe Y，Ando K，Hirao S，et al. Redox regulation of NF-kappaB activation：distinct redox regulation between the cytoplasm and the nucleus [J]. Antioxid Redox Signal，2005， 7（3/4）：395-403.
[17] 郑俊超，畅洪昇，马素亚，等.天丝饮中多糖成分对H2O2损伤SH-SY-5Y的保护作用对比研究[J].中华中医药杂志，2017，32（8）：3717-3720.
[18] 陈宇琼，孙东岳，吴恒芳，等.黄芪甲苷改善过氧化氢诱导的人主动脉内皮细胞氧化应激损伤的研究[J].南京医科大学学报：自然科学版，2017，37（8）：949-954.
[19] 颜明，赵冰海，张春雷，等.黄芩苷通过硫氧还原蛋白介导对SH-SY5Y细胞保护作用[J].医药导报，2013，32（10）：1278-1281.
[20] 徐妍，严旺，蔡雅卫，等.异钩藤碱通过mTOR非依赖性途径诱导SH-SY5Y细胞自噬发生[J].中国现代医生，2016，54（17）：28-34.
[21] 颜明，刘洁婷，李洪志，等.黄芩苷对H2O2诱导的SH-SY5Y细胞损伤的保护作用及其对Trx表达的影响[J].中国生化药物杂志，2012，33（5）：574-577.
2018, Vol. 15 
京公网安备 11010502046598号