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

Abstract

Abstract:Objective: To investigate the protective effects of parecoxib from oxidative stress induced by hydrogen peroxide (H 2 O 2 ) in rat astrocytes in vitro. Methods: All experiments included 4 groups: (1) negative control (NC) group, without any treatment; (2) H 2 O 2 treatment group, 100 μmol/L H 2 O 2 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 H 2 O 2 . 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 H 2 O 2 resulted in significant morphological changes, which could be reversed by pretreatment of parecoxib. In addition, H 2 O 2 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 H 2 O 2 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 H 2 O 2 .

Parecoxib mitigates lung ischemia-reperfusion injury in rats by reducing oxidative stress and inflammation and up-regulating HO-1 expression

“…It is found that parecoxib can resist the oxidative stress in body 17 . Results of the present study showed that, compared with sham-operated group, in LIRI and LIRI+parecoxib groups the lung tissue MDA content was significantly increased, and the lung tissue SOD and MPO activities were significantly decreased.…”

Influence of Cyclooxygenase-2 Inhibitors on Kynurenic Acid Production in Rat Brain in Vitro

“…First, inhibitory effect in our study was achieved at 100-μM parecoxib and niflumic acid concentration. Similarly, 80- and 160-μM parecoxib concentrations were shown to be neuroprotective in rat astrocytes in vitro (Ling et al 2016 ). Additionally, niflumic acid up to 160-μM concentration was examined in human-monocyte derived dendritic cells (Svajger et al 2008 ).…”

Involvement of DAAO Overexpression in Delayed Hippocampal Neuronal Death

“…Meanwhile, our results indicated that both TRP calcium channels and H 2 O 2 are involved in DAAO-induced neuronal apoptosis. H 2 O 2 can cause astrocytic metabolism disorder, induce an increase in active oxygen free radicals, and decrease BDNF expression [ 10 , 11 ]. Hence, it is supposed that the high level of ROS and reduced BDNF in ACM might elicit apoptosis in neuronal cells.…”

“…DAAO inhibitors or siRNA/DAAO could effectively alleviate brain injury by suppressing levels of the byproduct hydrogen peroxide, which implies that DAAO might be involved in the process of ischemic stroke. D-Ser is found at high physiological levels in the cerebrum and can be degraded by DAAO to increase levels of the byproduct hydrogen peroxide, which is one of the most stable reactive oxygen species (ROS), thus causing cytotoxicity to induce neuronal apoptosis as well as to reduce the expression of brain-derived neurotrophic factor (BDNF) [ 10 , 11 ]. In our previous study, we reported that cortical DAAO is upregulated following MCAO and is predominantly expressed in astrocytes.…”