Potential Protective Effects of Antioxidants against Cyclophosphamide-Induced Nephrotoxicity

Ayza, Muluken Altaye; Zewdie, Kaleab Alemayehu; Yigzaw, Elias Fitsum; Ayele, Solomon Gashaw; Tesfaye, Bekalu Amare; Tafere, Gebrehiwot Gebremedhin; Abrha, Muzey Gebreyohannes

doi:10.1155/2022/5096825

Cited by 27 publications

(20 citation statements)

References 92 publications

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“…These outcomes are consistent with the nephrotoxicity observed in the renal tissues of rats treated with CP in the current study. Several natural and other antioxidants are beneficial and effective source for preventing renal damage [27]. Previous studies have revealed the beneficial potential of βglucan, a natural product on kidney [16][17][18].…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory and anti-apoptotic potential of beta-glucan on chemotherapy-induced nephrotoxicity in rats

Metin¹,

TÜRK²,

Yalcin³

et al. 2023

J Surg Med

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Background/Aim: Cyclophosphamide (CP) is an anti-cancer agent that mediates nephrotoxicity. Beta (β)-glucan has restorative effects on kidney toxicities through its antioxidant potential; however, the effects of β-glucan on CP-induced renal injury remain unknown. In an experimental nephrotoxicity model using rats, we sought to examine the potential protective action of β-glucan on kidney histomorphology, apoptosis, and TNF-α expression. Methods: Male albino Wistar rats were divided equally into four groups: control, CP, β-glucan, and CP+β-glucan. The kidney tissues of the rats were examined for TNF-α and caspase-3 immunostaining to evaluate inflammation and apoptosis, respectively. Hematoxylin and eosin (H&E) and periodic acid–Schiff (PAS) staining were used for histopathological analyses. Results: The CP group showed severe histopathological damage in the renal tissues of rats. In the renal tissue of the CP group, immunoreactivities for TNF-α (1.25 [0.079] and caspase-3 (1.506 [0.143] were also higher than the control group (0.117 [0.006] and 0.116 [0.002], respectively; P<0.001). In the CP+β-glucan group, the histopathological changes significantly improved. Conclusion: Beta-glucan has therapeutic potential against CP-induced nephrotoxicity in rat kidney.

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Section: Discussionmentioning

confidence: 99%

Anti-inflammatory and anti-apoptotic potential of beta-glucan on chemotherapy-induced nephrotoxicity in rats

Metin¹,

TÜRK²,

Yalcin³

et al. 2023

J Surg Med

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“…If it is necessary to use drugs with significant potential nephrotoxicity, detailed recommendations are developed to prevent their harmful effects on the kidneys. For example, reference can be made to the prophylactic use of antioxidant compounds (vitamin E, vitamin C, flavonoids, melatonin, N-acetylcysteine, luteolin, lycopene, or coenzyme Q10) that reduce free radical damage in the course of the use of drugs that increase oxidative stress in kidney tissues, e.g., during treatment with vancomycin [ 101 ], cyclophosphamide [ 102 ], colistin [ 103 ], cyclosporine A [ 104 ], tacrolimus [ 105 ], contrast media [ 106 ], and cisplatin [ 107 ]. Antioxidants, vitamins, and minerals were also demonstrated to prevent gentamicin-induced nephrotoxicity [ 108 ].…”

Section: Preventive Factors Of Drug-induced Nephrotoxicitymentioning

confidence: 99%

A Synopsis of Current Theories on Drug-Induced Nephrotoxicity

Dobrek

2023

Life

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The overriding goal of the treatment of patients is its effectiveness and safety. However, all medications currently being used also exert some adverse pharmaceutical reactions, which may be regarded as an unintended but inevitable cost of pharmacotherapy. The kidney, as the main organ that eliminates xenobiotics, is an organ especially predisposed and vulnerable to the toxic effects of drugs and their metabolites during their excretion from the body. Moreover, some drugs (e.g., aminoglycosides, cyclosporin A, cisplatin, amphotericin B, and others) have a “preferential” nephrotoxicity potential, and their use is associated with an increased risk of kidney damage. Drug nephrotoxicity is, therefore, both a significant problem and a complication of pharmacotherapy. It should be noted that, currently, there is no generally recognized definition of drug-induced nephrotoxicity and no clear criteria for its diagnosis. This review briefly describes the epidemiology and diagnosis of drug-induced nephrotoxicity and characterizes its pathomechanisms, including immunological and inflammatory disturbances, altered kidney blood flow, tubulointerstitial injury, increased lithogenesis–crystal nephropathy, rhabdomyolysis, and thrombotic microangiopathy. The study also lists the basic drugs with nephrotoxicity potential and provides a short overview of the preventive methods for reducing the risk of drug-related kidney damage developing.

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“…7 Preclinical evidence also emphasizes the increased apoptosis where increased caspases, cytochrome C, dysfunctional mitochondria, and calcium overload were found. 4,5,7,8 In addition to increased oxidative stress, inflammation, and apoptosis, CPM administration is also reported to cause renal fibrosis and increased levels of transforming growth factor beta 1 (TGF-β1). 6 Hence, a multifactorial approach exists for the management of CPM-induced nephrotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Nephroprotective Effect of Bergapten Against Cyclophosphamide-Mediated Renal Stress, Inflammation, and Fibrosis in Wistar Rats: Probable Role of NF-kB and TGF-β1 Signaling Molecules

Mohsin,

Akhtar,

Alkahtani

et al. 2024

ACS Omega

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Cyclophosphamide (CPM) is a well-established antineoplastic drug with marked clinical outcomes in various types of cancers. Despite being a promising drug, its use is associated with significant renal toxicity and often limits its use, leading to compromised clinical outcomes. Therefore, this study explored the renal protective effect of bergapten (BGP), a natural bioactive compound that showed marked antioxidant, anti-inflammatory, anticancer, and neuroprotective effects. Till now, BGP has not been studied for its renal protective effect in an in vivo model. Animals were divided into control, toxic, BGP-3, BGP-10, and BGP Per se. The control group was treated with normal saline for 2 weeks. To the toxic group, CPM 200 mg/kg was given on day 7 as i.p. To BGP-3, 10, and Per se, BGP-3 and 10 mg/kg, ip was given 2 weeks with a single shot of CPM 200 day 7. To the Per se group, only BGP 10 mg/kg, ip was given from day 1 to day 14. After 14 days, animals were sacrificed, and kidneys were removed and studied for the markers of oxidative stress, inflammation, renal injury, renal fibrosis, and renal damage using biochemical, histopathological, and immunohistochemical studies. We found that BGP-10 effectively reversed the damage toward normal, whereas BGP-3 failed to exhibit a significant renal protective effect. We conclude that bergapten could be a potential renal protective drug, and hence, more detailed cellular molecular-based studies are needed to bring this drug from the bench to the bedside.

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Potential Protective Effects of Antioxidants against Cyclophosphamide-Induced Nephrotoxicity

Cited by 27 publications

References 92 publications

Anti-inflammatory and anti-apoptotic potential of beta-glucan on chemotherapy-induced nephrotoxicity in rats

Anti-inflammatory and anti-apoptotic potential of beta-glucan on chemotherapy-induced nephrotoxicity in rats

A Synopsis of Current Theories on Drug-Induced Nephrotoxicity

Nephroprotective Effect of Bergapten Against Cyclophosphamide-Mediated Renal Stress, Inflammation, and Fibrosis in Wistar Rats: Probable Role of NF-kB and TGF-β1 Signaling Molecules

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