CLC number: R965
On-line Access: 2024-08-27
Received: 2023-10-17
Revision Accepted: 2024-05-08
Crosschecked: 2016-08-18
Cited: 0
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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.
[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
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