2022
DOI: 10.1016/j.phymed.2022.154021
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Piperazine ferulate attenuates gentamicin-induced acute kidney injury via the NF-κB/NLRP3 pathway

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Cited by 11 publications
(2 citation statements)
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“…Indeed, excessive reactive oxygen species (ROS) production provokes deleterious cellular effects, including direct damage to lipids, oxidative damage of deoxyribonucleic acid (DNA), and protein oxidation. In addition, GEN-induced ROS overproduction is linked to nuclear factor-kappa B (NF-κB) activation, which results in the activation of several inflammatory components, particularly pro-inflammatory cytokines, eventually culminating in renal cell apoptosis and nephrotoxicity ( Balakumar et al, 2010 ; Randjelovic et al, 2017 ; Ahmed and Mohamed, 2019 ; Li et al, 2022 ). Since OS is an important event in the induction of GEN nephrotoxicity, activation of various antioxidant and cytoprotective enzymes is essential.…”
Section: Introductionmentioning
confidence: 99%
“…Indeed, excessive reactive oxygen species (ROS) production provokes deleterious cellular effects, including direct damage to lipids, oxidative damage of deoxyribonucleic acid (DNA), and protein oxidation. In addition, GEN-induced ROS overproduction is linked to nuclear factor-kappa B (NF-κB) activation, which results in the activation of several inflammatory components, particularly pro-inflammatory cytokines, eventually culminating in renal cell apoptosis and nephrotoxicity ( Balakumar et al, 2010 ; Randjelovic et al, 2017 ; Ahmed and Mohamed, 2019 ; Li et al, 2022 ). Since OS is an important event in the induction of GEN nephrotoxicity, activation of various antioxidant and cytoprotective enzymes is essential.…”
Section: Introductionmentioning
confidence: 99%
“…34) In acute kidney injury, activated NF-κB pathway induces downstream NLRP3 activation to promote inflammatory response. 35) In this study, the phosphorylation rates of IκB-α and NF-κB were significantly increased in the lung tissues of asthmatic mice induced by OVA. Our results further support the activation of the NF-κB pathway that mediates airway inflammation in asthma, and we also observed changes in NLRP3 and inflammatory factors following IκB/NF-κB activation in asthmatic mice.…”
Section: Discussionmentioning
confidence: 57%