Evaluation of Cisplatin Neurotoxicity in Cultured Rat Dorsal Root Ganglia via Cytosolic Calcium Accumulation

Erol, Kevser; Yiğitaslan, Semra; Ünel, Çiğdem Çengelli; Kaygisiz, Bilgin; Yıldırım, Engin

doi:10.5152/balkanmedj.2016.161110

Cited by 8 publications

(9 citation statements)

References 37 publications

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“…DRG (5 × 10 3 cells/well) were incubated overnight in 96‐well culture plates in drug‐free DMEM medium, and cisplatin was added to the wells with gradually increasing concentrations (100, 200, 500 μ m ) and incubated for 24 h. The neurotoxic effects of cisplatin were evaluated by incubating the cells with cisplatin alone and in combination with submaximal concentration of cisplatin (200 μ m ) and agmatine (10, 100, 500 μ m ). The MTT (3‐(4,5‐dimethylthiazolyl‐2)‐2,5‐diphenyltetrazolium bromide) assay was performed to detect cell viability of cultured cells . Cells were incubated with MTT solution (1 mg/mL) for 4 h at 37 °C.…”

Section: Methodsmentioning

confidence: 99%

“…The experimental procedures were performed after approval by the Local Ethical Committee of Eskisehir Osmangazi University for Animal Experimentation (11.02.2016/500). Effects of agmatine on cisplatin cytotoxicity were assessed in primary cultures of DRG by modifying our previous method . DRG were dissected out from 1‐day‐old Sprague Dawley rats purchased from Medical and Surgical Research Center of Eskisehir Osmangazi University and collected in sterile calcium‐ and magnesium‐free modified Hank's balanced salt solution (HBSS) (Sigma Aldrich; Lonza, Belgium).…”

Section: Methodsmentioning

confidence: 99%

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Agmatine co‐treatment attenuates allodynia and structural abnormalities in cisplatin‐induced neuropathy in rats

Dönertaş

Ünel

Aydın

et al. 2018

Fundamemntal Clinical Pharma

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Cisplatin is a widely used antineoplastic agent in the treatment of various cancers. Peripheral neuropathy is a well-known side effect of cisplatin and has potential to result in limiting and/or reducing the dose, decreasing the quality of life. Thus, effective treatments are needed. Agmatine is an endogenous neuromodulator that has been shown to exert antiallodynic effects in various animal studies. The first aim of this study was to investigate the in vitro effects of agmatine on cisplatin-induced neurotoxicity. Primary cultures of dorsal root ganglia (DRG) which are the primary target of drug injury were prepared. DRG cells were incubated with cisplatin (100, 200, 500 μm). Then, agmatine (10, 100, 500 μm) was administered with the submaximal concentration of cisplatin. Cisplatin caused concentration-dependent neurotoxicity, and agmatine did not alter this effect. The second aim was to investigate the effects of agmatine on cisplatin-induced peripheral neuropathy in rats and the influence of nitric oxide synthase (NOS) inhibitor, L-NAME, in this effect. Female Sprague Dawley rats received intraperitoneal saline (control), cisplatin (3 mg/kg), cisplatin+agmatine (100 mg/kg), or cisplatin+agmatine+L-NAME (10 mg/kg) once a week for 5 weeks. The mechanical allodynia, hot plate, and tail clip tests were performed, and DRG cells and sciatic nerves were analyzed. Agmatine and agmatine+L-NAME combination attenuated CIS-induced mechanical allodynia and degeneration in DRG cells and sciatic nerves. However, L-NAME did not potentiate the antiallodynic or neuroprotective effect of agmatine. These findings indicate that agmatine co-administration ameliorates cisplatin-induced neuropathy and may be a therapeutic alternative.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Agmatine co‐treatment attenuates allodynia and structural abnormalities in cisplatin‐induced neuropathy in rats

Dönertaş

Ünel

Aydın

et al. 2018

Fundamemntal Clinical Pharma

Self Cite

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“…There are some contradictory results in the literature, indicating that nimodipine has a neuroprotective effect on one hand [17], and increases neurotoxicity on the other hand [22].…”

Section: Discussionmentioning

confidence: 99%

“…Erol et al [22] reported that mitochondria played a crucial role in maintaining intracellular calcium homeostasis in combination with their buffering ability. Their study also indicated that the disruption of mitochondrial calcium homeostasis might be responsible for the neuropathy induced by cisplatin.…”

Section: Discussionmentioning

confidence: 99%

“…Their study also indicated that the disruption of mitochondrial calcium homeostasis might be responsible for the neuropathy induced by cisplatin. More importantly, it indicated a significant increase in neurotoxicity in the group where 300 μM nimodipine was co-administered with 600 μM cisplatin [22]. Another study reported that nimodipine, which prevents cytosolic calcium increase, may have cardiotoxic effects apart from its effects on neurons [23].…”

Section: Discussionmentioning

confidence: 99%

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Does Nimodipine, a Selective Calcium Channel Blocker, Impair Chondrocyte Proliferation or Damage Extracellular Matrix Structures?

Kaplan¹,

Yılmaz

Karaarslan

et al. 2019

CPB

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Background: The study aimed to investigate the effects of the active ingredient, nimodipine, on chondrocyte proliferation and extracellular matrix (ECM) structures in cartilage tissue cells. Methods: Chondrocyte cultures were prepared from tissues resected via surgical operations. Nimodipine was then applied to these cultures and molecular analysis was performed. The data obtained were statistically calculated. Results: Both, the results of the (3-(4,5 dimethylthiazol2-yl)-2,5-diphenyltetrazolium (MTT) assay and the fluorescence microscope analysis [a membrane permeability test carried out with acridine orange/ propidium iodide staining (AO/PI)] confirmed that the active ingredient, nimodipine, negatively affects the cell cultures. Conclusion: Nimodipine was reported to suppress cellular proliferation; chondroadherin (CHAD) and hypoxia-inducible factor-1 alpha (HIF-1α) expression thus decreased by 2.4 and 1.7 times, respectively, at 24 hrs when compared to the control group (p < 0.05). Furthermore, type II collagen (COL2A1) expression was not detected (p<0.05). The risk that a drug prescribed by a clinician in an innocuous manner to treat a patient by relieving the symptoms of a disease may affect the proliferation, differentiation, and viability of other cells and/or tissues at the molecular level, beyond its known side effects or adverse events, should not be forgotten.

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Pathogenesis of platinum-induced peripheral neurotoxicity: Insights from preclinical studies

Calls

Carozzi

Navarro

et al. 2020

Experimental Neurology

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Evaluation of Cisplatin Neurotoxicity in Cultured Rat Dorsal Root Ganglia via Cytosolic Calcium Accumulation

Cited by 8 publications

References 37 publications

Agmatine co‐treatment attenuates allodynia and structural abnormalities in cisplatin‐induced neuropathy in rats

Agmatine co‐treatment attenuates allodynia and structural abnormalities in cisplatin‐induced neuropathy in rats

Does Nimodipine, a Selective Calcium Channel Blocker, Impair Chondrocyte Proliferation or Damage Extracellular Matrix Structures?

Pathogenesis of platinum-induced peripheral neurotoxicity: Insights from preclinical studies

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