WIN 55,212-2 prevents mechanical allodynia but not alterations in feeding behaviour induced by chronic cisplatin in the rat

Vera, Gema; Chiarlone, Anna; Cabezos, P. A.; Pascual, David W.; Martı́n, Marı́a Isabel; Abalo, Raquel

doi:10.1016/j.lfs.2007.06.012

Cited by 67 publications

(113 citation statements)

References 58 publications

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“…Animal models exist for cisplatin-induced sensory peripheral neuropathy (Verdú et al, 1999; Authier et al, 2003; Vera et al, 2007), or cisplatin induced-nephrotoxicity (Vickers et al, 2004) and there are experimental data about the cardiac toxicity produced by acute administration of this antitumoral agent (Al-Majed et al, 2006; Yüce et al, 2007). However, to our knowledge, no experimental data has been reported so far about the cardiovascular alterations that may be developed after chronic administration of cisplatin.…”

Section: Introductionmentioning

confidence: 99%

Characterization of Cardiovascular Alterations Induced by Different Chronic Cisplatin Treatments

et al. 2017

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In the last years, many clinical studies have revealed that some cisplatin-treated cancer survivors have a significantly increased risk of cardiovascular events, being cisplatin-induced cardiovascular toxicity an increasing concern. The aim of the present work was to evaluate the cardiovascular alterations induced by different chronic cisplatin treatments, and to identify some of the mechanisms involved. Direct blood pressure, basal cardiac (left ventricle and coronary arteries) and vascular (aortic and mesenteric) functions were evaluated in chronic (5 weeks) saline- or cisplatin-treated male Wistar rats. Three different doses of cisplatin were tested (1, 2, and 3 mg/kg/week). Alterations in cardiac and vascular tissues were also investigated by immunohistochemistry, Western Blot, and or quantitative RT-PCR analysis. Cisplatin treatment provoked a significant modification of arterial blood pressure, heart rate, and basal cardiac function at the maximum dose tested. However, vascular endothelial dysfunction occurred at lower doses. The expression of collagen fibers and conexin-43 were increased in cardiac tissue in cisplatin-treated rats with doses of 2 and 3 mg/kg/week. The expression of endothelial nitric oxide synthase was also modified in cardiac and vascular tissues after cisplatin treatment. In conclusion, chronic cisplatin treatment provokes cardiac and vascular toxicity in a dose-dependent manner. Besides, vascular endothelial dysfunction occurs at lower doses than cardiac and systemic cardiovascular toxicity. Moreover, some structural changes in cardiac and vascular tissues are also patent even before any systemic cardiovascular alterations.

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Section: Introductionmentioning

confidence: 99%

Characterization of Cardiovascular Alterations Induced by Different Chronic Cisplatin Treatments

et al. 2017

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“…73 WIN 55,212-2, a synthetic CB1/CB2 agonist that has previously showed antinociceptive effect in vincristine and paclitaxel-induced neuropathy, also prevented the development of mechanical allodynia induced by chronic cisplatin administration. 84 Finally, the recently discovered hormone, Ghrelin, a potent GH secretagogue mainly secreted from the stomach, with neuroprotective properties, displayed an inhibition of the cisplatin-induced mechanical hyperalgesia, correlated to the decrease in insulin-like growth factor-1 levels (Table 4). 85 …”

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confidence: 99%

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

et al. 2009

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Summary:This review examines recent preclinical research on toxic peripheral neuropathy and potential therapeutic developments. Chemotherapy-induced peripheral neurotoxicity is a major clinical problem because it represents the dose-limiting side effects of a significant number of antineoplastic drugs. Patients are unable to complete full or optimal treatment schedules. The incidence of chemotherapy-induced peripheral neuropathy varies depending on the drugs and schedules used, and this can be quite high, particularly when neurophysiological methods are used to make a diagnosis. However, even when chemotherapy-induced peripheral neuropathy is not a doselimiting side effect, its onset may severely affect the quality of life of cancer patients and cause chronic discomfort. As such, improved understanding of the pathophysiology of chemotherapy-induced neurotoxicity need for animal models is clinically relevant and will assist in the development of future neuroprotective strategies and also in the design of novel chemotherapies with improved toxicity profiles. In this review, the features of animal models of chemotherapy-induced painful neuropathy developed for 20 years, due to the administration of the most widely used drugs, such as platinum drugs, taxanes, and vinca alkaloids, will be discussed. In a second part, data available on neuroprotectants and treatment strategies, evaluated using these previous animal models in the attempt to prevent neuropathic pain, will be summarized.

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“…Cisplatin leads to anorexia, [35] and this could be the reason underlying weight loss following its administration.…”

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Pretreatment with Oxygen Protects Rat Kidney from Cisplatin Nephrotoxicity

et al. 2010

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Cisplatin (CP) nephrotoxicity is mainly due to reactive oxygen species. Oxygen pre-exposure as a mild oxidative stress may enhance some endogenous defense mechanisms, so its effect on cisplatininduced acute renal failure was investigated in present study.Twenty-four rats were divided into four groups. The O 2 + CP and Air + CP groups were were subjected to i.p. injection of 5 mg/kg cisplatin, and in the Air + Saline and O 2 + Saline groups, saline was injected instead of cisplatin. O 2 + CP and O 2 + Saline groups were pretreated with oxygen (3h/d for two days), and the other two groups were pretreated with room air. Cisplatin was administered 24 h after last pretreatment session. Three days after cisplatin injection, plasma samples were obtained, and parts of kidney tissue were frozen for biochemical analysis or fixed in formalin for histological assessments. Preconditioning with oxygen prior to cisplatin administration led to reduced tubular necrosis and luminal cast formation and improvement of renal function, as was evidenced by significant reduction in plasma creatinine and urea levels. Oxygen pretreatment also significantly reversed cisplatin-induced reduction in renal catalase activity and glutathione level. It could be concluded that oxygen pretreatment could have a delayed protective effect against cisplatin nephrotoxicity, and that increased renal catalase activity may be involved in this protective effect of hyperoxia.

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WIN 55,212-2 prevents mechanical allodynia but not alterations in feeding behaviour induced by chronic cisplatin in the rat

Cited by 67 publications

References 58 publications

Characterization of Cardiovascular Alterations Induced by Different Chronic Cisplatin Treatments

Characterization of Cardiovascular Alterations Induced by Different Chronic Cisplatin Treatments

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

Pretreatment with Oxygen Protects Rat Kidney from Cisplatin Nephrotoxicity

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