ArticleIranian journal of pharmaceutical research : IJPR2021
Inhibition of Different Pain Pathways Attenuates Oxidative Stress in Glial Cells: A Mechanistic View on Neuroprotective Effects of Different Types of Analgesics.
Article in Iranian journal of pharmaceutical research : IJPR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 2 citations in OpenAlex.
- GDPD3 Deficiency Alleviates Neuropathic Pain and Reprograms Macrophagic Polarization Through PGE2 and PPARγ Pathway.Neurochemical research · 2024Article
- Hydrogen Sulfide Interacting with Cannabinoid 2 Receptors during Sciatic Nerve Injury-Induced Neuropathic Pain.Antioxidants (Basel, Switzerland) · 2023Article
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6 authors at 2 institutions in 1 country.
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Abstract
Neuropathic pain results from trauma or diseases affecting the central nervous system (CNS) and triggers a cascade of events in different CNS parts that eventually lead to oxidative injury. This study was aimed to investigate the protective effects of some selected analgesics in neuropathic pain-induced oxidative damage in the isolated glial cells of the rat brain. In this experiment, rats were randomly divided into 5 main groups. Rats in group 1 received no medication, whereas rats in groups 2 to 5 received ASA (aspirin), celecoxib, morphine, and etanercept daily, respectively. Each main group divides into 3 subgroups: normal, sham, and neuropathic pain model rats. The glial cells of the rat brain were isolated at different time points. Our results demonstrate that neuropathic pain induces ROS generation as the major cause of mitochondrial membrane potential collapse (%∆Ψm) and lysosomal membrane rupture, which result in oxidative damage of the glial cells. In addition, ASA and celecoxib had protective effects on the neuropathic pain-induced oxidative stress markers, including ROS production, mitochondrial membrane potential collapse, and lysosomal membrane leakiness at different time points. Furthermore, the oxidative damage markers were significantly decreased by morphine and etanercept in all investigated days. Since arachidonic acid metabolites and TNF-α are produced during neuropathic pain and inflammation, it can be concluded that the inhibition of the substances production or inhibition of the ligands binding with their receptors would help to decrease the destructive effects of neuropathic pain in the glial cells of rat brain.
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