2020
DOI: 10.1111/1440-1681.13334
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Abstract: Gentamicin is an aminoglycoside antibiotic commonly administrated to patients with Gram‐negative infections. Gentamicin induced nephrotoxicity by functional and structural impairment. Toll‐like receptors (TLRs) as key mediators in the innate and adaptive immune system response involved in gentamicin‐induced nephrotoxicity. The present study aimed to investigate the gene expression of TLR2 and pro‐inflammatory cytokines in the renal tissues and buffy coat of the whole blood in gentamicin‐treated rats. Twenty ad… Show more

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Cited by 9 publications
(3 citation statements)
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“…Previous studies, in agreement with our data, reported the correlation of the inflammatory response to GNT in clinical and animal studies 30,31 . Karimi et al, 32 reported that GNT treatment induced a significant systemic inflammation, which may be linked to the associated increase of pro‐inflammatory chemokines and cytokines like TNF‐α and IL‐1.…”
Section: Discussionsupporting
confidence: 92%
“…Previous studies, in agreement with our data, reported the correlation of the inflammatory response to GNT in clinical and animal studies 30,31 . Karimi et al, 32 reported that GNT treatment induced a significant systemic inflammation, which may be linked to the associated increase of pro‐inflammatory chemokines and cytokines like TNF‐α and IL‐1.…”
Section: Discussionsupporting
confidence: 92%
“…First, male gonadal involvement and a subsequent inflammation in testes are possible complications of SARS-CoV-2 (Fan et al, 2020;Ma et al, 2020;Ren et al, 2020;Rival et al, 2006;Xu et al, 2006). Inflammation can lead to excessive production of ROS, and this product can lead to sperm DNA damage (Anifandis et al, 2020;Evenson & Wixon, 2006;Homa et al, 2019;Karimi et al, 2020). Moreover, SARS-CoV-2 infection causes psychological stress, which is a major cause of systemic oxidative stress (Li et al, 2020).…”
Section: Sperm Dfi As a Promising Determiner Of Male Infertilitymentioning
confidence: 99%
“…The necrosis and apoptosis of the proximal tubular epithelium is the leading feature of GEN‐induced kidney injury 11,12 . Recently, inflammatory pathways including toll‐like receptors (TLR2 and TLR4), nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB)/NOD‐like receptor family, pyrin domain containing 3 (NLRP3) and januskinase 1/signal transducer and activator of transcription 3 (JAK1/STAT‐3) are found involved in GEN‐induced renal injury 13,14 . However, blunting these inflammatory pathways or inhibiting apoptosis only partially improves GEN‐induced renal damage in animals 15,16 .…”
Section: Introductionmentioning
confidence: 99%