Vincamine protects against cisplatin induced nephrotoxicity via activation of Nrf2/HO-1 and hindering TLR4/ IFN-γ/CD44 cells inflammatory cascade

El‐Sayed, Rehab M.; Gheit, Rehab E. Abo El; Badawi, Ghada A.

doi:10.1016/j.lfs.2021.119224

Cited by 28 publications

(17 citation statements)

References 57 publications

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“…And embelin, an antiinflammatory drug, can alleviate cisplatin-induced nephrotoxicity by activating the signaling pathway of Nrf2/ HO-1 and impeding NF-κB (Qin et al, 2019). Some studies have found that vinorelbine protects against cisplatin-induced acute kidney injury (AKI) by activating Nrf2/HO-1 signaling pathway and hindering TLR4-IFN-γ-CD44 cell inflammatory cascade when investigating the molecular mechanism of renal protection against nephrotoxicity (El-Sayed et al, 2021). Accumulating evidence suggests that the antioxidant mechanism protecting against enucleation-induced nephrotoxicity involves the Nrf2/HO-1 signaling pathway (Younis et al, 2020).…”

Section: Cisplatin-induced Nephrotoxicitymentioning

confidence: 99%

Dissecting the Crosstalk Between Nrf2 and NF-κB Response Pathways in Drug-Induced Toxicity

Gao

Guo

Yang

et al. 2022

Front. Cell Dev. Biol.

116

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Nrf2 and NF-κB are important regulators of the response to oxidative stress and inflammation in the body. Previous pharmacological and genetic studies have confirmed crosstalk between the two. The deficiency of Nrf2 elevates the expression of NF-κB, leading to increased production of inflammatory factors, while NF-κB can affect the expression of downstream target genes by regulating the transcription and activity of Nrf2. At the same time, many therapeutic drug-induced organ toxicities, including hepatotoxicity, nephrotoxicity, cardiotoxicity, pulmonary toxicity, dermal toxicity, and neurotoxicity, have received increasing attention from researchers in clinical practice. Drug-induced organ injury can destroy body function, reduce the patients’ quality of life, and even threaten the lives of patients. Therefore, it is urgent to find protective drugs to ameliorate drug-induced injury. There is substantial evidence that protective medications can alleviate drug-induced organ toxicity by modulating both Nrf2 and NF-κB signaling pathways. Thus, it has become increasingly important to explore the crosstalk mechanism between Nrf2 and NF-κB in drug-induced toxicity. In this review, we summarize the potential molecular mechanisms of Nrf2 and NF-κB pathways and the important effects on adverse effects including toxic reactions and look forward to finding protective drugs that can target the crosstalk between the two.

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Section: Cisplatin-induced Nephrotoxicitymentioning

confidence: 99%

Dissecting the Crosstalk Between Nrf2 and NF-κB Response Pathways in Drug-Induced Toxicity

Gao

Guo

Yang

et al. 2022

Front. Cell Dev. Biol.

116

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“…Since OS is an important event in the induction of GEN nephrotoxicity, activation of various antioxidant and cytoprotective enzymes is essential. The nuclear factor erythroid 2-related factor 2 (Nrf2) is among the possible druggable targets that can prevent oxidative tissue injury induced by various redox insults ( Satta et al, 2017 ; El-Sayed et al, 2021 ). It is a critical coordinator of the cellular stress reaction by modulating the expression of a plethora of cytoprotective and antioxidant enzymes ( Shelton et al, 2013 ; He et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Formononetin Ameliorates Renal Dysfunction, Oxidative Stress, Inflammation, and Apoptosis and Upregulates Nrf2/HO-1 Signaling in a Rat Model of Gentamicin-Induced Nephrotoxicity

et al. 2022

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Gentamicin (GEN) is a bactericidal aminoglycoside known to cause nephrotoxicity. Formononetin (FN) is a potent flavonoid that exhibits numerous promising pharmacological activities. In this study, we have assessed the nephroprotective efficacy of FN against GEN-induced renal injury in rats. Rats were orally administered with FN (60 mg/kg/day, for 2 weeks) and were co-treated with intraperitoneal (i.p.) injection of GEN (100 mg/kg/day) during the days 8–14. GEN-treated rats demonstrated increased urea and creatinine levels in serum associated with marked histopathological changes in the kidney. Malondialdehyde (MDA) and protein carbonyl contents were elevated, whereas glutathione concentration and catalase and superoxide dismutase activities were lowered in GEN-administered rats. The FN largely prevented tissue damage, attenuated renal function, reduced MDA and protein carbonyl, and enhanced antioxidant capacity in the kidney of GEN-administrated animals. The kidney of GEN-treated rats demonstrated elevated Bax and caspase-3 protein expression, accompanied by lowered Bcl-2 protein expression, an effect that FN attenuated. Moreover, FN treatment caused upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) expression in renal tissue of GEN-intoxicated animals. Collectively, FN protects against GEN-caused renal damage via exhibiting antioxidant, anti-inflammatory, and antiapoptotic activities and augmenting Nrf2 signaling, suggesting FN as a promising agent for preventing drug-induced organ damage.

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“…In this study, 72 h after cisplatin administration was selected to be the suitable time point for analysis. The choice was made with reference to the selection that most researchers use to analyze the toxicity of cisplatin [ 50 , 51 , 52 , 53 , 54 , 55 ]. Moreover, our previous work analyzed the toxicity at different time points of cisplatin administration, and found that the toxicity became severe and the protein glutathionylation level had a significant increase in the kidney at 72 h [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Selenium Status in Diet Affects Nephrotoxicity Induced by Cisplatin in Mice

et al. 2022

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Cisplatin is one of the most active chemotherapy drugs to treat solid tumors. However, it also causes various side effects, especially nephrotoxicity, in which oxidative stress plays critical roles. Our previous studies found that cisplatin selectively inhibited selenoenzyme thioredoxin reductase1 (TrxR1) in the kidney at an early stage and, subsequently, induced the activation of Nrf2. However, the effects of selenium on cisplatin-induced nephrotoxicity are still unclear. In this study, we established mice models with different selenium intake levels to explore the effects of selenoenzyme activity changes on cisplatin-induced nephrotoxicity. Results showed that feeding with a selenium-deficient diet sensitize the mice to cisplatin-induced damage, whereas selenium supplementation increased the activities of selenoenzymes TrxR and glutathione peroxidase (GPx), changed the renal cellular redox environment to a reduced state, and exhibited protective effects. These results demonstrated the correlation of selenoenzymes with cisplatin-induced side effects and provided a basis for the potential approach to alleviate cisplatin-induced renal injury.

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Vincamine protects against cisplatin induced nephrotoxicity via activation of Nrf2/HO-1 and hindering TLR4/ IFN-γ/CD44 cells inflammatory cascade

Cited by 28 publications

References 57 publications

Dissecting the Crosstalk Between Nrf2 and NF-κB Response Pathways in Drug-Induced Toxicity

Dissecting the Crosstalk Between Nrf2 and NF-κB Response Pathways in Drug-Induced Toxicity

Formononetin Ameliorates Renal Dysfunction, Oxidative Stress, Inflammation, and Apoptosis and Upregulates Nrf2/HO-1 Signaling in a Rat Model of Gentamicin-Induced Nephrotoxicity

Selenium Status in Diet Affects Nephrotoxicity Induced by Cisplatin in Mice

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