Protective effect of empagliflozin on gentamicin-induced acute renal injury via regulation of SIRT1/NF-κB signaling pathway

Botros, Sandy R; Matouk, Asmaa I.; Mohamed, Alia F; Khalifa, Mohamed M.; Heeba, Gehan H.

doi:10.1016/j.etap.2022.103907

Cited by 13 publications

(13 citation statements)

References 53 publications

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“…It is likely that GTNinduced ROS overproduction stimulates the expression of inducible nitric oxide synthase (iNOS) leading to high NO levels [27]. Our finding, in line with other studies, suggests the role of oxidative stress and NO in gentamicin mediated cytotoxicity [2,28,29]. Literature confirmed that, under physiological conditions, NO is predominantly released by endothelial nitric oxide synthase enzyme (eNOS) causing vasorelaxation and maintaining of the endothelial function.…”

Section: Discussionsupporting

confidence: 89%

“…It is important to mention that, the upregulation of NF-κB and TNF-α expression in aortic tissues strongly matches the previously reported increase in their renal levels upon GTN administration. This indicates the role of inflammatory mediators in mediating GTN toxicity [2,43].…”

Section: Discussionmentioning

confidence: 84%

“…and given carboxymethyl cellulose, p.o., 0.5 % w/v (vehicle of DHM). GTN group: rats were injected gentamicin (100 mg/kg/day, i.p) [2,18] and given 0.5 % w/v carboxymethyl cellulose p.o. GTN+DHM: animals were injected by gentamicin (100 mg/kg/day, i.p.)…”

Section: Experimental Designmentioning

confidence: 99%

“…Unfortunately, the clinical use of gentamicin is limited due to its nephrotoxic side effect [1]. Oxidative stress and inflammation have been considered the main causes of gentamicin induced renal damage [2,3]. However, there is a growing interest in the role of vascular dysfunction in the pathogenesis of GTN-induced nephrotoxicity since decreased renal blood flow (RBF) results in decreased glomerular filtration rate and impairs renal function.…”

mentioning

confidence: 99%

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Dihydromyricetin alleviates gentamicin induced vascular dysfunction through inhibition of ROS/NF-κB activation

Anter

Awad

Kamed

et al. 2023

Journal of advanced Biomedical and Pharmaceutical Sciences

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Gentamicin causes an impairment of vascular function due to endothelial cell damage. Renal injury by gentamicin may contribute to the development of vascular dysfunction due to decreased NO bioavailability as well as increased oxidative stress and inflammation. In this study we investigate the role of DHM on vascular dysfunction induced by gentamicin. Male Wistar rats were divided into 3 groups (n= 6, each); control group; received the vehicle, gentamicin group; given gentamicin (100 mg/kg/day i.p) for 8 days and gentamicin + dihydromyricetin group; rats were treated with dihydromyricetin (200 mg/kg, p.o) concurrently with gentamicin. DHM reversed the GTN-induced histopathological changes of aortic rings. In addition, administration of DHM to GTN treated rats improved the vascular functions evident as enhanced vasorelaxation and vasoconstriction responses to acetylcholine and phenylephrine, respectively. Further, DHM increased the vascular levels of GSH and total antioxidant activity. Immunohistochemical analysis of aortic sections revealed that DHM treatment downregulated NF-κB, TNF-α and caspase-3 expression. Our data provide a new evidence for the protective effects of DHM against gentamicin-induced vascular dysfunction via provoking antioxidant, anti-inflammatory and antiapoptotic effects.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 84%

Section: Experimental Designmentioning

confidence: 99%

mentioning

confidence: 99%

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Dihydromyricetin alleviates gentamicin induced vascular dysfunction through inhibition of ROS/NF-κB activation

Anter

Awad

Kamed

et al. 2023

Journal of advanced Biomedical and Pharmaceutical Sciences

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“…(2) EMPA group: received EMPA (10 mg/kg/day) p.o. dissolved in distilled water for 28 days [39,40]. (3) HAL group: received HAL (2 mg/kg/day) p.o.…”

Section: Animals and Experimental Designmentioning

confidence: 99%

Empagliflozin Protects against Haloperidol Experimentally-Induced Ovarian Toxicity

et al. 2023

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The present experiment aimed to identify the potential protective role of empagliflozin (EMPA) on haloperidol (HAL)-induced ovarian damage in female rats because of its anti-inflammatory, antioxidant, and antiapoptotic effects. EMPA was administered in the presence and absence of HAL. Thirty-two adult female albino rats were divided into four groups. Control group, EMPA group: received EMPA (10 mg/kg/day) p.o., HAL group: received HAL (2 mg/kg/day) p.o., HAL + EMPA group: HAL (2 mg/kg/day) combined with EMPA for 28 days. Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and anti-mullerian hormone (AMH) levels were measured. Ovarian oxidative stress parameters, besides inflammatory and apoptotic biomarkers, and ovarian Sirtuin-1 (Sirt-1) were evaluated. Ovarian histopathological examination and heat shock protein 70 (Hsp70) immunohistochemical study were performed. HAL significantly increased serum levels of FSH, LH, and ovarian inflammatory, apoptotic, and oxidative stress biomarkers and decreased serum AMH levels and Sirt-1 expression. Histopathological findings of ovarian damage and high Hsp70 immunoexpression were detected. EMPA significantly normalized the distributed hormonal levels, oxidative stress, inflammatory, and apoptotic biomarkers with a prompt improvement in the histopathological picture and a decrease in Hsp70 immunoexpression. Accordingly, EMPA protected against HAL-induced ovarian toxicity by modulating the Sirt-1/Hsp70/TNF-α/caspase-3 signaling pathway.

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The ameliorative effect of vinpocetine against gentamicin-induced uterine-injury in rats involves the inflammasome/caspase-1/IL-1β pathway

Geddawy,

Attya,

Hegazy

et al. 2024

Mol Biol Rep

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Protective effect of empagliflozin on gentamicin-induced acute renal injury via regulation of SIRT1/NF-κB signaling pathway

Cited by 13 publications

References 53 publications

Dihydromyricetin alleviates gentamicin induced vascular dysfunction through inhibition of ROS/NF-κB activation

Dihydromyricetin alleviates gentamicin induced vascular dysfunction through inhibition of ROS/NF-κB activation

Empagliflozin Protects against Haloperidol Experimentally-Induced Ovarian Toxicity

The ameliorative effect of vinpocetine against gentamicin-induced uterine-injury in rats involves the inflammasome/caspase-1/IL-1β pathway

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