Full Text:   <2739>

Summary:  <2073>

Suppl. Mater.: 

CLC number: R965

On-line Access: 2016-09-07

Received: 2016-01-16

Revision Accepted: 2016-04-10

Crosschecked: 2016-08-18

Cited: 0

Clicked: 5132

Citations:  Bibtex RefMan EndNote GB/T7714

 ORCID:

Ye Zhang

http://orcid.org/0000-0001-6328-8003

-   Go to

Article info.
Open peer comments

Journal of Zhejiang University SCIENCE B 2016 Vol.17 No.9 P.692-702

http://doi.org/10.1631/jzus.B1600017


Protective effects of parecoxib on rat primary astrocytes from oxidative stress induced by hydrogen peroxide


Author(s):  Yun-zhi Ling, Xiao-hong Li, Li Yu, Ye Zhang, Qi-sheng Liang, Xiao-di Yang, Hong-tao Wang

Affiliation(s):  Department of Anesthesiology, First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, China; more

Corresponding email(s):   yuli95@163.com, zhang_ye011@163.com

Key Words:  Parecoxib, Primary astrocyte, Hydrogen peroxide (H2O2), Brain-derived neurotrophic factor (BDNF), Bax, Bcl-2


Yun-zhi Ling, Xiao-hong Li, Li Yu, Ye Zhang, Qi-sheng Liang, Xiao-di Yang, Hong-tao Wang. Protective effects of parecoxib on rat primary astrocytes from oxidative stress induced by hydrogen peroxide[J]. Journal of Zhejiang University Science B, 2016, 17(9): 692-702.

@article{title="Protective effects of parecoxib on rat primary astrocytes from oxidative stress induced by hydrogen peroxide",
author="Yun-zhi Ling, Xiao-hong Li, Li Yu, Ye Zhang, Qi-sheng Liang, Xiao-di Yang, Hong-tao Wang",
journal="Journal of Zhejiang University Science B",
volume="17",
number="9",
pages="692-702",
year="2016",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1600017"
}

%0 Journal Article
%T Protective effects of parecoxib on rat primary astrocytes from oxidative stress induced by hydrogen peroxide
%A Yun-zhi Ling
%A Xiao-hong Li
%A Li Yu
%A Ye Zhang
%A Qi-sheng Liang
%A Xiao-di Yang
%A Hong-tao Wang
%J Journal of Zhejiang University SCIENCE B
%V 17
%N 9
%P 692-702
%@ 1673-1581
%D 2016
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1600017

TY - JOUR
T1 - Protective effects of parecoxib on rat primary astrocytes from oxidative stress induced by hydrogen peroxide
A1 - Yun-zhi Ling
A1 - Xiao-hong Li
A1 - Li Yu
A1 - Ye Zhang
A1 - Qi-sheng Liang
A1 - Xiao-di Yang
A1 - Hong-tao Wang
J0 - Journal of Zhejiang University Science B
VL - 17
IS - 9
SP - 692
EP - 702
%@ 1673-1581
Y1 - 2016
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1600017


Abstract: 
Objective: To investigate the protective effects of parecoxib from oxidative stress induced by hydrogen peroxide (H2O2) in rat astrocytes in vitro. Methods: All experiments included 4 groups: (1) negative control (NC) group, without any treatment; (2) H2O2 treatment group, 100 μmol/L H2O2 treatment for 24 h; (3) and (4) parecoxib pretreatment groups, 80 and 160 μmol/L parecoxib treatment for 24 h, respectively, and then treated with 100 μmol/L H2O2. Several indices were investigated, and the expressions of bax, bcl-2, and brain-derived neurotrophic factor (BDNF) were quantified. Results: Compared to the NC group, exposure to H2O2 resulted in significant morphological changes, which could be reversed by pretreatment of parecoxib. In addition, H2O2 treatment led to loss of viability (P=0.026) and increased intracellular reactive oxygen species (ROS) levels (P<0.001), and induced apoptosis (P<0.01) in the primary astrocytes relative to the NC group. However, in the parecoxib pretreatment groups, all the above changes reversed significantly (P<0.05) as compared to the H2O2 treatment group, and were nearly unchanged when compared to the NC group. Mechanical investigation showed that dysregulated bax, bcl-2, and BDNF could be implicated in these changes. Conclusions: Our results indicated that parecoxib provided a protective effect from oxidative stress induced by exposure to H2O2.

帕瑞昔布对过氧化氢诱导的原代星形胶质细胞氧化应激的保护作用

目的:评估帕瑞昔布对过氧化氢诱导的大鼠原代星形胶质细胞氧化应激状态的保护作用,并初步探讨其作用机制。
创新点:首次在大鼠原代星形胶质细胞中证实帕瑞昔布对过氧化氢诱导的氧化应激具有保护作用,且此作用可能与Bax、Bcl-2和BDNF的失调有关。
方法:设立如下四组对照:(1)阴性对照组;(2)100 µmol/L H2O2处理组(处理时间为24 h);(3)80 µmol/L 帕瑞昔布处理组;(4)160 µmol/L帕瑞昔布处理组(第三和第四组先用帕瑞昔布处理24 h,再用100 µmol/L H2O2处理24 h)。用荧光显微镜观察星形胶质细胞的形态,用MTT法检测星形胶质细胞的存活率,用荧光探针二氯荧光黄双乙酸盐(DCDHF-DA)检测星形胶质细胞内氧自由基的含量,并用碘化丙啶(PI)染色检测细胞的凋亡状态。最后用反转录酶聚合酶链反应(RT-PCR)和蛋白质印迹(Western blot)检测Bax、Bcl-2和BDNF三种蛋白在4组中的表达水平。
结论:H2O2处理可以导致星形胶质细胞的形态发生改变(图1)和存活率降低(图2),提高星形胶质细胞内的氧自由基水平(图3),同时诱导细胞凋亡(图4)。然而,所有这些变化都可以被帕瑞昔布逆转。此外,我们发现,Bax、Bcl-2和BDNF的表达水平在H2O2处理时失调,而在帕瑞昔布预处理时恢复正常。综上所述,帕瑞昔布对H2O2诱导的氧化应激具有保护作用。

关键词:帕瑞昔布;原代星形胶质细胞;过氧化氢;Bax;Bcl-2;BDNF

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

[1]An, L.N., Yue, Y., Guo, W.Z., et al., 2013. Surgical trauma induces iron accumulation and oxidative stress in a rodent model of postoperative cognitive dysfunction. Biol. Trace Elem. Res., 151(2):277-283.

[2]Arora, S.S., Gooch, J.L., Garcia, P.S., 2014. Postoperative cognitive dysfunction, Alzheimer’s disease, and anesthesia. Int. J. Neurosci., 124(4):236-242.

[3]Barres, B.A., 2008. The mystery and magic of glia: a perspective on their roles in health and disease. Neuron, 60(3):430-440.

[4]Cao, Y., Jiang, Z., Zeng, Z., et al., 2016. Bcl-2 silencing attenuates hypoxia-induced apoptosis resistance in pulmonary microvascular endothelial cells. Apoptosis, 21(1):69-84.

[5]Guan, J.J., Zhang, X.D., Sun, W., et al., 2015. DRAM1 regulates apoptosis through increasing protein levels and lysosomal localization of BAX. Cell Death Dis., 6:e1624.

[6]Hernandez, R.V., Puro, A.C., Manos, J.C., et al., 2016. Transgenic mice with increased astrocyte expression of IL-6 show altered effects of acute ethanol on synaptic function. Neuropharmacology, 103:27-43.

[7]Jia, S.N., Lin, C., Chen, D.F., et al., 2016. The transcription factor p8 regulates autophagy in response to palmitic acid stress via a mammalian target of rapamycin (mTOR)-independent signaling pathway. J. Biol. Chem., 291(9):4462-4472.

[8]Jin, W.J., Feng, S.W., Feng, Z., et al., 2014. Minocycline improves postoperative cognitive impairment in aged mice by inhibiting astrocytic activation. Neuroreport, 25(1):1-6.

[9]Kim, G.H., Kim, J.E., Rhie, S.J., et al., 2015. The role of oxidative stress in neurodegenerative diseases. Exp. Neurobiol., 24(4):325-340.

[10]Li, R.L., Zhang, Z.Z., Peng, M., et al., 2013. Postoperative impairment of cognitive function in old mice: a possible role for neuroinflammation mediated by HMGB1, S100B, and RAGE. J. Surg. Res., 185(2):815-824.

[11]Li, Y., Wang, S., Ran, K., et al., 2015. Differential hippocampal protein expression between normal aged rats and aged rats with postoperative cognitive dysfunction: a proteomic analysis. Mol. Med. Rep., 12(2):2953-2960.

[12]Lu, J., Liu, Z., Xia, K., et al., 2015. Effect of preemptive analgesia with parecoxib sodium in patients undergoing radical resection of lung cancer. Int. J. Clin. Exp. Med., 8(8):14115-14118.

[13]Pellerin, L., Bouzier-Sore, A.K., Aubert, A., et al., 2007. Activity-dependent regulation of energy metabolism by astrocytes: an update. Glia, 55(12):1251-1262.

[14]Phillips, E.C., Croft, C.L., Kurbatskaya, K., et al., 2014. Astrocytes and neuroinflammation in Alzheimer’s disease. Biochem. Soc. Trans., 42(5):1321-1325.

[15]Pruchniak, M.P., Arazna, M., Demkow, U., 2016. Biochemistry of oxidative stress. Adv. Exp. Med. Boil., 878:9-19.

[16]Rundshagen, I., 2014. Postoperative cognitive dysfunction. Dtsch. Arztebl. Int., 111(8):119-125.

[17]Salloum, F.N., Hoke, N.N., Seropian, I.M., et al., 2009. Parecoxib inhibits apoptosis in acute myocardial infarction due to permanent coronary ligation but not due to ischemia-reperfusion. J. Cardiovasc. Pharmacol., 53(6):495-498.

[18]Shen, L., Zhu, J., Chen, F., et al., 2015. RUNX1-Evi-1 fusion gene inhibited differentiation and apoptosis in myelopoiesis: an in vivo study. BMC Cancer, 15(1):970.

[19]Smith, C.C., Guevremont, D., Williams, J.M., et al., 2015. Apoptotic cell death and temporal expression of apoptotic proteins Bcl-2 and Bax in the hippocampus, following binge ethanol in the neonatal rat model. Alcohol. Clin. Exp. Res., 39(1):36-44.

[20]Takeda, K., Kermani, P., Anastasia, A., et al., 2013. BDNF protects human vascular endothelial cells from TNFα-induced apoptosis. Biochem. Cell Biol., 91(5):341-349.

[21]Valvassori, S.S., Arent, C.O., Steckert, A.V., et al., 2015. Intracerebral administration of BDNF protects rat brain against oxidative stress induced by ouabain in an animal model of mania. Mol. Neurobiol., 52(1):353-362.

[22]Yu, H.T., Zhen, J., Pang, B., et al., 2015. Ginsenoside Rg1 ameliorates oxidative stress and myocardial apoptosis in streptozotocin-induced diabetic rats. J. Zhejiang Univ.-Sci. B (Biomed. & Biotechnol.), 16(5):344-354.

[23]Zhang, N., Cheng, G.Y., Liu, X.Z., et al., 2014. Expression of Bcl-2 and NF-κB in brain tissue after acute renal ischemia-reperfusion in rats. Asian Pac. J. Trop. Med., 7(5):386-389.

[24]List of electronic supplementary materials

[25]Fig. S1 Identification of primary astrocytes using GFAP staining

Open peer comments: Debate/Discuss/Question/Opinion

<1>

Please provide your name, email address and a comment





Journal of Zhejiang University-SCIENCE, 38 Zheda Road, Hangzhou 310027, China
Tel: +86-571-87952783; E-mail: cjzhang@zju.edu.cn
Copyright © 2000 - 2024 Journal of Zhejiang University-SCIENCE