Suramin protects from cisplatin-induced acute kidney injury.

Dupre, Tess V.

doi:10.18297/etd/2217

Cited by 5 publications

(5 citation statements)

References 44 publications

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“…Therefore, it is still necessary to identify novel effective strategies to minimize the renal cytotoxicity of CDDP. Of all these approaches used, natural compounds have been shown to provide promising protection [17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Ganoderma lucidum Prevents Cisplatin-Induced Nephrotoxicity through Inhibition of Epidermal Growth Factor Receptor Signaling and Autophagy-Mediated Apoptosis

Mahran

Hassan

2020

Oxidative Medicine and Cellular Longevity

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Background. Cisplatin (cis-diaminedichloroplatinum, CDDP) is a broad-spectrum antineoplastic agent. However, CDDP has been blamed for its nephrotoxicity, which is the main dose-limiting adverse effect. Ganoderma lucidum (GL), a medicinal mushroom, has antioxidant and inflammatory activities. Therefore, this study is aimed at finding out the potential nephroprotection of GL against CDDP-induced nephrotoxicity in rats and the possible molecular mechanisms including the EGFR downstream signaling, apoptosis, and autophagy. Methods. Rats were given GL (500 mg/kg) for 10 days and a single injection of CDDP (12 mg/kg, i.p). Results. Nephrotoxicity was evidenced by a significant increase in renal indices and oxidative stress markers. Additionally, CDDP showed a plethora of inflammatory and apoptotic responses as evidenced by a profound increase of HMGB-1, NF-κB, and caspase-3 expressions, whereas administration of GL significantly improved all these indices as well as the histopathological insults. Renal expression of EGFR showed a similar trend after GL administration. Furthermore, activation of autophagy protein, LC3 II, was found to be involved in GL-mediated nephroprotection correlated with the downregulation of apoptotic signaling, caspase-3 and terminal deoxynucleotidyl transferase (TDT) renal expressions. Conclusion. These results suggest that GL might have improved CDDP-induced nephrotoxicity through antioxidant, anti-inflammatory, and autophagy-mediated apoptosis mechanisms and that inhibition of EGFR signaling might be involved in nephroprotection.

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Section: Introductionmentioning

confidence: 99%

Ganoderma lucidum Prevents Cisplatin-Induced Nephrotoxicity through Inhibition of Epidermal Growth Factor Receptor Signaling and Autophagy-Mediated Apoptosis

Mahran

Hassan

2020

Oxidative Medicine and Cellular Longevity

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“…Injury and death of renal tubular epithelial cells are characteristics of AKI induced by ischemia/reperfusion (I/ R). Epithelial cells in the proximal tubule are commonly affected when ischemia occurs in the kidney [17]. Characteristic changes in histology in tubular cells include dilatation of the tubular lumen, loss or effacement of the tubular brush border, and formation of casts because of apoptosis [18].…”

Section: Cg 4hmentioning

confidence: 99%

“…Studies have demonstrated that the inhibition of overexpression of CHOP can decrease cell apoptosis and alleviate AKI. For example, when cisplatin was administered to mice to develop an AKI model, AKI was associated with activation of ERS, and kidney function increased and renal cell apoptosis decreased with the inhibition of expression of CHOP [17]. In another animal experiment, tunicamycin, a type of antibiotic, is known to lead to ERS and is used to induce AKI.…”

Section: Cg 4hmentioning

confidence: 99%

The Mechanisms of the Herbal Components of CRSAS on HK‐2 Cells in a Hypoxia/Reoxygenation Model Based on Network Pharmacology

Xie

Yang

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Background. Acute kidney injury is a global problem, which brings a great burden to the society and family. The component of rhubarb, Salvia miltiorrhiza, Astragalus membranaceus, and safflower (CRSAS) has been proved as an useful agent to treat acute kidney injury (AKI) patients in China. Objective. To assess the effect of CRSAS on human renal tubular epithelial cells (HK-2) after the hypoxia/reoxygenation (H/R) and investigate the potential mechanisms. Methods. Network pharmacology was used to predict the potential pathways shared by CRSAS and AKI. Cell counting kit-8 (CCK-8) was used to assess the HK-2 vitality. Apoptosis of HK-2 cells was detected by carboxyfluorescein succinimidyl ester/propidium iodide (CFSF/PI) staining. Expression of GRP78, CHOP, caspase-3, and Bax was detected by western blot and quantitative real-time RT-PCR. Result. CRSAS and AKI shared the endoplasmic reticulum stress (ERS) pathway based on network pharmacology analysis. CRSAS increases the vitality of HK-2 cells and reduces the apoptosis of HK-2 cells induced by H/R injury. The expression of GRP78 and CHOP in CRSAS groups was lower than that of control groups. Conclusions. H/R can induce HK-2 cell apoptosis and ERS. CRSAS can reduce HK-2 cell apoptosis by inhibiting the ERS. Therefore, CRSAS might be able to treat kidney disease due to I/R injury. Animal experiment should be done to further prove our finding.

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“…Approximately one-third of patients treated with cisplatin suffered from renal dysfunction and injury, especially acute kidney injury (AKI), which has become the most di cult problem in the application of cisplatin [3]. Unfortunately, there is currently no effective treatment to prevent cisplatin-induced AKI [4].…”

Section: Introductionmentioning

confidence: 99%

Cisplatin induces acute kidney injury and pyroptosis in mice through the exosome miR-122/ELAVL1 regulatory axis

Zhu¹,

Ye²,

Gao³

et al. 2020

Preprint

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Background Although cisplatin is an effective chemotherapeutic drug for the treatment of various cancers, its clinical application is limited due to its side effects, especially nephrotoxicity. Unfortunately, Acute kidney injury (AKI) caused by cisplatin remains one of the main obstacles to cancer treatment. Increasing evidence suggests that renal inflammation and pyroptotic inflammatory cell death of tubular epithelial cells (RTECs) mainly determine the progression and outcome of cisplatin-induced AKI. However, it is not clear how cisplatin regulates the pyroptosis of RTECs cells in AKI. The current study aimed to determine the regulation mechanism of AKI induced by cisplatin. In vivo, cisplatin was used to induce AKI. H&E staining of mouse kidney tissue sections and serological indicators of kidney injury (including BUN, serum creatinine and TNF-α) were detected. The important substrate protein GSDMD and key target caspase-1 of pyroptosis were detected by immunohistochemistry and western blot, respectively. In vitro, cisplatin significantly induces HK-2 cells pyroptosis. Furthermore, Cisplatin transmits HK2 cells pyroptosis signals to surrounding cells in the form of exosomes. Previous studies have shown that exosomes are involved in kidney physiology and the pathogenesis of various kidney diseases/disorders. MicroRNAs (miRNAs) are the main functional components of exosomes. Results Further research shows that exosome miR-122 negatively regulates the pyrolysis of HK2 cells. Finally, we elucidated that exosome miR-122 participates in cisplatin induced AKI regulation by regulating ELAVL1 expression. Conclusions In conclusion, these results suggest that exosome miR-122 inhibits pyroptosis and AKI by targeting ELAVL1 under cisplatin treatment, which will provide a potential target for the treatment of AKI.

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Suramin protects from cisplatin-induced acute kidney injury.

Cited by 5 publications

References 44 publications

Ganoderma lucidum Prevents Cisplatin-Induced Nephrotoxicity through Inhibition of Epidermal Growth Factor Receptor Signaling and Autophagy-Mediated Apoptosis

Ganoderma lucidum Prevents Cisplatin-Induced Nephrotoxicity through Inhibition of Epidermal Growth Factor Receptor Signaling and Autophagy-Mediated Apoptosis

The Mechanisms of the Herbal Components of CRSAS on HK‐2 Cells in a Hypoxia/Reoxygenation Model Based on Network Pharmacology

Cisplatin induces acute kidney injury and pyroptosis in mice through the exosome miR-122/ELAVL1 regulatory axis

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