ArticleJournal of Zhejiang University. Science. B2016
Protective effects of parecoxib on rat primary astrocytes from oxidative stress induced by hydrogen peroxide.
Article in Journal of Zhejiang University. Science. B, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Microfluidic device to study spatial and temporal response of astrocyte networks in response to changes in the biochemical milieu.Microsystems & nanoengineering · 2026Article
- Article
- Parecoxib mitigates lung ischemia-reperfusion injury in rats by reducing oxidative stress and inflammation and up-regulating HO-1 expression.Acta cirurgica brasileira · 2021Article
- Antioxidant Effects of Oleuropein on Hydrogen Peroxide-Induced Neuronal Stress- AnAnti-inflammatory & anti-allergy agents in medicinal chemistry · 2020Article
- Influence of Cyclooxygenase-2 Inhibitors on Kynurenic Acid Production in Rat Brain in Vitro.Neurotoxicity research · 2019Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the protective effects of parecoxib from oxidative stress induced by hydrogen peroxide (H2O2) in rat astrocytes in vitro.
methodsAll 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.
resultsCompared 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.
conclusionsOur results indicated that parecoxib provided a protective effect from oxidative stress induced by exposure to H2O2.
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