Objective To study the cell apoptosis and expression of Omi/HtrA2 in brain of neonatal rats after asphyxia and to evaluate the effects of Salvia miltorrhiza bunge( SMB ) on it. Methods A total of 75 SD rats aged 7 days were randomly divided into the following groupscontrol group, asphyxia group and SMB treatment group, then the brain tissues were taken from the rats in the three groups at 6, 12, 24, 48 hours and 72 hours after the asphyxia.The apoptotic cells were detected by the TUNEL staining method, The Omi/HtrA2 protein expression was detected with the immunhistochemistry method. Results The number of apoptotic cells and the expression of Omi/HtrA2 were higher in asphyxia groups than those in control group (P<0.05).In asphyxia groups, the expression of Omi/HtrA2 reached peak at 12 h after asphyxia(10.98±1.34), and the number of apoptotic cells reached peak at 24 h after asphyxia (12.1±2.66).But compared with asphyxia group, the expression of Omi/HtrA2 and the number of apoptotic cells were significantly decreased in SMB treatment group, and the differences were significant(P<0.05), but all parameters were not restored to the levels of control group(P<0.05). Conclusion Asphyxia can induce the apoptosis of neuronal, Omi/HtrA2 may be involved in this process.SMB can reduce the number of apoptotic cells by inhibiting the expression of Omi/HtrA2 in brain, and thus it can play a protective role in asphyxia brain damage of neonatal rats.
Key words
asphyxia /
neonatal rat /
neuron /
apoptosis /
Omi/HtrA2 /
Salvia miltiorrhiza Bunge
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References
[1] Wang B, Armstrong JS, Lee JH, et al.Rewarming from therapeutic hypothermia induces cortical neuron apoptosis in a swine model of neonatal hypoxic-ischemic encephalopathy[J].Journal of Cerebral Blood Flow & Metabolism, 2015, 7(1):1020-1038.
[2] Xu Z, Chen Y, Xu G, et al.Omi/HtrA2 pro-apoptotic marker differs in various hepatocellular carcinoma cell lines owing to ped/pea-15 expression level[J].Oncology Reports, 2015, 33(2):905-912.
[3] 林少珠, 陈广斌, 吴铁, 等.丹参素对新生大鼠缺氧缺血性脑损伤脑组织 SOD、MDA 的影响[J].中国实用医药, 2012, 24(7):12-14.
[4] 邹礼乐, 雷小平, 韩艺, 等.促红细胞生成素对窒息新生大鼠脑组织Omi/HtrA2表达水平及细胞凋亡的影响[J].中国儿童保健杂志, 2013, 21(2):144-147.
[5] 陈宇清, 薛梅, 张亚明.丹参注射液对新生鼠缺氧缺血性脑损伤神经细胞的保护作用研究[J].中国药房, 2011, 21(47):4439-4441.
[6] Liu J, Feng ZC.Increased umbilical cord plasma interleukin-1β levels was correlated with adverse outcomes of neonatal hypoxic-ischemic encephalopathy[J].J Trop Pediatr, 2010, 56(6):178-182.
[7] Mimura K, Tomimatsu T, Minato K, et al.Ceftriaxone preconditioning confers neuroprotection in neonatal rats through glutamate transporter 1 upregulation[J].Reproductive Sciences, 2011, 18(12):1193-1201.
[8] 张琴芬, 屠文娟.李红新, 等.人脐带间充质干细胞联用神经节苷酯GM1治疗新生大鼠缺氧缺血性脑损伤[J].中国儿童保健杂志, 2014, 22(8):819-825.
[9] Kibride SM, Prehn JH.Central roles of apoptosis proteins in mitochon-drial function[J].Oncogene, 2013, 32(22):2703-2711.
[10] Sano R, Reed JC.ER stress-induced cell death mechanisms[J].Biochim Biophys Acta, 2013, 1833(12):3460-3470.
[11] Wang K, Zhang J, Liu J, et al.Variations in the protein level of Omi/HtrA2 in the heart of aged rats may contribute to the increased suscep-tibility of cardiomyocytes to ischemia / reperfusion injury and cell death:Omi/HtrA2 and aged heartinjury[J].Age(Dordr), 2013, 35(3):733-746.
[12] Xin L, Ke W, Huirong L.GW25-e3224 Omi/HtrA2 Cause Cardiomyocyte Apoptosis via Release of Cytochrome C in Aging Rats[J].Journal of the American College of Cardiology, 2014, 64(16S):C22.
[13] 吴庆庆.丹参酮ⅡA 对肺腺癌 NCI-H460 细胞增殖和凋亡的影响[J].实用医学杂志, 2012, 28(6):877-879.
[14] 张秋玲, 孙远标, 王海英, 等.白花丹参对大鼠脑缺血再灌注致线粒体损伤及细胞凋亡的影响[J].中国病理生理杂志, 2010, 26(4):725-729.
[15] 任宏强, 赵利, 王忠, 等.复方丹参滴丸对急性心肌梗死大鼠心肌细胞凋亡和凋亡相关蛋白的影响[J].中国动脉硬化杂志, 2013, 21(12):1084-1088.