Alogliptin attenuates cyclophosphamide-induced nephrotoxicity: a novel therapeutic approach through modulating MAP3K/JNK/SMAD3 signaling cascade

Salama, Rania M.; Nasr, Merihane M; Abdelhakeem, Jannatullah I; Roshdy, Omar K; ElGamal, Mohamed A

doi:10.1080/01480545.2020.1814319

Cited by 14 publications

(14 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CP significantly increased caspase-3 expression in rats compared to controls in the current study. This finding corroborates the reports that CPinduced oxidative stress leads to apoptosis through caspase-3 activation in kidney tissues of rats [8,30].…”

Section: Discussionsupporting

confidence: 92%

“…ILs and TNF-α are important inflammatory mediators in the pathogenesis of CP-mediated inflammation [1]. TNF-α levels in rat renal tissues were found to be significantly higher after CP administration, according to previous research [8,30]. In the current study, rats with CP-induced kidney damage had higher expression of the pro-inflammatory cytokine TNF-α than did control rats.…”

Section: Discussionsupporting

confidence: 74%

“…On day 2, the CP group received a single intraperitoneal (i.p.) dosage of 200 mg/kg CP to induce nephrotoxicity [8]. β-glucan group received β-glucan dissolved in distilled water at a dose of 50 mg/kg by oral gavage (o.g.)…”

Section: Experimental Procedures and Groupsmentioning

confidence: 99%

“…The toxic mechanism of CP is attributed to its main metabolites, phosphoramide mustard and acrolein, which cause an increase in free radicals [7]. Acrolein is responsible for inducing the reactive oxygen species (ROS) production that is crucial for DNA interstrand cross-links and the activation of multiple signaling molecules and inflammatory markers, specifically tumour necrosis factor-alpha (TNF-α) and interleukins (ILs); IL-1β and IL-6 [8,9]. It also leads to mitochondrial and endoplasmic reticulum dysfunction, as well as cell membrane disruption, resulting in apoptosis [10].…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

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

Metin¹,

TÜRK²,

Yalcin³

et al. 2023

J Surg Med

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 74%

Section: Experimental Procedures and Groupsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

Metin¹,

TÜRK²,

Yalcin³

et al. 2023

J Surg Med

View full text Add to dashboard Cite

show abstract

“…Then, c-Jun induces transcription of genes that mediate inflammatory response like tumor necrosis factor alpha (TNF-a). The activation of JNK/c-Jun pathway by exposure to toxic agents/drugs or cellular stresses led to renal fibrosis through stimulation of both inflammation and apoptosis [ 20 ].…”

Section: Mechanisms and Role Of Antioxidants In Cyclophosphamide-indu...mentioning

confidence: 99%

Potential Protective Effects of Antioxidants against Cyclophosphamide-Induced Nephrotoxicity

Ayza

Zewdie

Yigzaw

et al. 2022

International Journal of Nephrology

View full text Add to dashboard Cite

Cyclophosphamide is an alkylating antineoplastic agent, and it is one of the most successful drugs with wide arrays of clinical activity. It has been in use for several types of cancer treatments and as an immunosuppressive agent for the management of autoimmune and immune-mediated diseases. Nowadays, its clinical use is limited due to various toxicities, including nephrotoxicity. Even though the mechanisms are not well understood, cyclophosphamide-induced nephrotoxicity is reported to be mediated through oxidative stress. This review focuses on the potential role of natural and plant-derived antioxidants in preventing cyclophosphamide-induced nephrotoxicity.

show abstract

Roles of SIRT6 in kidney disease: a novel therapeutic target

Yang

Feng

Liang

et al. 2021

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Alogliptin attenuates cyclophosphamide-induced nephrotoxicity: a novel therapeutic approach through modulating MAP3K/JNK/SMAD3 signaling cascade

Cited by 14 publications

References 52 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

Potential Protective Effects of Antioxidants against Cyclophosphamide-Induced Nephrotoxicity

Roles of SIRT6 in kidney disease: a novel therapeutic target

Contact Info

Product

Resources

About