Effect of edaravone against cisplatin-induced chronic renal injury

Koike, Natsumi; Sasaki, A; Murakami, Tomoaki; Suzuki, Kazuhiko

doi:10.1080/01480545.2019.1604740

Cited by 12 publications

(8 citation statements)

References 28 publications

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“…Cisplatin (cis-diamminedichloroplatinum II) is a major chemotherapeutic agent used in the treatment of a different solid tumors such as head, neck and ovarian cancers (1). However, cisplatin chemotherapy results in side effects including nephrotoxicity (2) and ototoxicity (3). Studies have reported the cytotoxic mechanisms of cisplatin including DNA damage (4,5), production of reactive oxygen species (ROS) (6), cytoplasmic caspase activation (7) and mitochondrial dysfunction (8).…”

Section: Introductionmentioning

confidence: 99%

Targeting CXCL1 chemokine signaling for treating cisplatin ototoxicity

et al. 2023

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Cisplatin is chemotherapy used for solid tumor treatment like lung, bladder, head and neck, ovarian and testicular cancers. However, cisplatin-induced ototoxicity limits the utility of this agent in cancer patients, especially when dose escalations are needed. Ototoxicity is associated with cochlear cell death through DNA damage, the generation of reactive oxygen species (ROS) and the consequent activation of caspase, glutamate excitotoxicity, inflammation, apoptosis and/or necrosis. Previous studies have demonstrated a role of CXC chemokines in cisplatin ototoxicity. In this study, we investigated the role of CXCL1, a cytokine which increased in the serum and cochlea by 24 h following cisplatin administration. Adult male Wistar rats treated with cisplatin demonstrated significant hearing loss, assessed by auditory brainstem responses (ABRs), hair cell loss and loss of ribbon synapse. Immunohistochemical studies evaluated the levels of CXCL1 along with increased presence of CD68 and CD45-positive immune cells in cochlea. Increases in CXCL1 was time-dependent in the spiral ganglion neurons and organ of Corti and was associated with progressive increases in CD45, CD68 and IBA1-positive immune cells. Trans-tympanic administration of SB225002, a chemical inhibitor of CXCR2 (receptor target for CXCL1) reduced immune cell migration, protected against cisplatin-induced hearing loss and preserved hair cell integrity. We show that SB225002 reduced the expression of CXCL1, NOX3, iNOS, TNF-α, IL-6 and COX-2. Similarly, knockdown of CXCR2 by trans-tympanic administration of CXCR2 siRNA protected against hearing loss and loss of outer hair cells and reduced ribbon synapses. In addition, SB225002 reduced the expression of inflammatory mediators induced by cisplatin. These results implicate the CXCL1 chemokine as an early player in cisplatin ototoxicity, possibly by initiating the immune cascade, and indicate that CXCR2 is a relevant target for treating cisplatin ototoxicity.

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Section: Introductionmentioning

confidence: 99%

Targeting CXCL1 chemokine signaling for treating cisplatin ototoxicity

et al. 2023

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“…Edaravone is a free radical scavenger that possesses combined properties of vitamin C and D in preventing free radical-induced peroxidation in both the lipid and aqueous phases [ 19 ]. Edaravone reduces oxidative damage and cell apoptosis in models of retinal diseases, spinal cord injury, ischemic cerebral injury, and chronic renal injury [ 20 - 24 ]. The therapeutic effects of edaravone have also been proven in lung injury under various conditions.…”

Section: Discussionmentioning

confidence: 99%

Edaravone alleviates lung damage in mice with hypoxic pulmonary hypertension by increasing nitric oxide synthase 3 expression

Zheng

Wei

et al. 2023

Korean J Physiol Pharmacol

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This study is to determine the regulation of nitric oxide synthase 3 (NOS3) by edaravone in mice with hypoxic pulmonary hypertension (HPH). C57BL/6J mice were reared in a hypoxic chamber. HPH mice were treated with edaravone or edaravone + L-NMMA (a NOS inhibitor). Lung tissue was collected for histological assessment, apoptosis analysis, and detection of malondialdehyde, superoxide dismutase, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and NOS3. The levels of serum TNF-α and IL-6 were also measured. Immunohistochemistry was used to visualize the expression of α-smooth muscle actin (SMA) in pulmonary arterioles. Edaravone treatment improved hemodynamics, inhibited right ventricular hypertrophy, increased NOS3 expression, and reduced pathological changes, pulmonary artery wall thickness, apoptotic pulmonary cells, oxidative stress, and the expression of TNF-α, IL-6, and α-SMA in HPH mice. L-NMMA treatment counteracted the lung protective effects of edaravone. In conclusion, edaravone might reduce lung damage in HPH mice by increasing the expression of NOS3.

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“…In contrast, experimental animal studies have suggested that edaravone treatment improves hepatic injury following ischemia/reperfusion injury, partial hepatectomy, or endotoxin administration[ 19 ]. Other researchers have shown that edaravone has beneficial effects on kidney injury induced by ischemia/reperfusion or cisplatin[ 20 - 22 ]. It is possible that edaravone and edaravone-peroxy radicals, which are metabolic products of edaravone, are responsible for these adverse effects; however, the underlying mechanisms remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Edaravone administration and its potential association with a new clinical syndrome in cerebral infarction patients: Three case reports

Liu¹,

Xu²,

Wang³

et al. 2023

World J Clin Cases

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BACKGROUND Edaravone is a widely used treatment for patients with cerebral infarction and, in most cases, edaravone-induced side effects are mild. However, edaravone-related adverse reactions have been receiving increasing attention. CASE SUMMARY We treated three patients with acute cerebral infarction who died following treatment with edaravone. Edaravone is a widely used treatment for patients with cerebral infarction and, in most cases, edaravone-induced side effects are mild. However, edaravone-related adverse reactions have been receiving increasing attention. CONCLUSION Our cases highlight the importance of educating clinicians regarding the new edaravone-induced clinical syndromes of cerebral infarction as potentially fatal adverse drug reactions. Considering that no laboratory or confirmatory test exists to diagnose edaravone-induced death from cerebral infarction, clinicians’ knowledge is the key element in recognizing this phenomenon.

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Effect of edaravone against cisplatin-induced chronic renal injury

Cited by 12 publications

References 28 publications

Targeting CXCL1 chemokine signaling for treating cisplatin ototoxicity

Targeting CXCL1 chemokine signaling for treating cisplatin ototoxicity

Edaravone alleviates lung damage in mice with hypoxic pulmonary hypertension by increasing nitric oxide synthase 3 expression

Edaravone administration and its potential association with a new clinical syndrome in cerebral infarction patients: Three case reports

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