Effect of Cyclooxygenase and Nitric Oxide Synthase Inhibitors on Streptozotocin-Induced Hyperalgesia in Rats

Bujalska, Magdalena; Tatarkiewicz, Jan; Cordé, Anna de; Gumulka, S. W.

doi:10.1159/000110787

Cited by 37 publications

(30 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The same authors observed that co-administration of two NSAIDs (indomethacin and celecoxib) also prevent this mechanical hyperalgesia. 70 These kind of results had already been observed with two other NSAIDs (ibuprofen and rofecoxib), 71 whereas NSAIDs did not showed analgesic effects. At last, IL-6, known to be implicated both in the neural degeneration and the regeneration process, displayed in the rat as a preventive effect on heat hypoalgesia.…”

Section: Preventive Strategiesmentioning

confidence: 69%

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

et al. 2009

View full text Add to dashboard Cite

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.

show abstract

Section: Preventive Strategiesmentioning

confidence: 69%

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

et al. 2009

View full text Add to dashboard Cite

show abstract

“…In vincristine-induced neuropathy, the reported effects of NO and nitric oxide synthase (NOS) on the pain are conflicting. Kamei et al (36) reported that vincristine administration decreased the levels of NO metabolites, cGMP and protein levels of neuronal NOS in the spinal cord, and a NOS inhibitor reversed the analgesic effect of a NOS substrate, while Bujalska and Gumułka reported that NOS inhibitors prevented the development of hyperalgesia induced by vincristine administration (37). In an inflammatory cellular model, Melilotus extract decreased the secretion of NO and expression of inducible NOS in a dose-dependent manner (38).…”

Section: Discussionmentioning

confidence: 99%

Anti-allodynic effect of theoesberiven F in a vincristine-induced neuropathy model

Bang

Kim

Jeong

2016

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Abstract. Allodynia is a main symptom of the peripheral neuropathy induced by vincristine treatment. Theoesberiven F, a combination of Melilotus extract and proxyphylline, is currently used for the treatment of inflammatory conditions due to its potent anti-inflammatory and analgesic properties. The anti-allodynic effect of theoesberiven F on mechanical and cold allodynia in a rat model of vincristine-induced neuropathy was investigated in the present study. Intraperitoneal vincristine injections were administered to male Sprague-Dawley rats at a dose of 0.1 mg/kg/day over 12 days (5 days of injection, a 2-day cessation and 5 days of injection). Rats that were allodynic following the vincristine injections were randomly allocated into four groups. Normal saline was injected into rats in the control group. Theoesberiven F (0.1, 0.25 and 0.5 mg/kg) was administered to rats in the three experimental groups, respectively. Mechanical and cold allodynia were measured at preadministration and at 15,30, 60, 90, 120, 150 and 180 min following the intraperitoneal administration of normal saline or theoesberiven F. The decreased paw withdrawal threshold induced by vincristine injection was increased by theoesberiven F administration. The increased withdrawal frequency to cold stimuli developed by vincristine was reduced by theoesberiven F administration. The results of this study suggest that the administration of theoesberiven F may be beneficial in reducing the mechanical and cold allodynia developed during vincristine treatment.

show abstract

“…So, the noted rise in serum nitrite levels in the present investigation suggests the enhanced expression of eNOS. Moreover, it has been documented that increase in nNOS is not responsible for diabetic neuropathy pain, 29) while its decreased expression may do so. 30) Further, it has also been noticed that net nitric oxide concentration is reduced during diabetes.…”

Section: Discussionmentioning

confidence: 99%

Possible Role of Spleen Derived Factors, Vanilloid Receptors and Calcitonin Gene-related Peptide in Diabetes Induced Hyperalgesia in Mice

2008

View full text Add to dashboard Cite

The present study was designed to investigate a possible role of vanilloid receptors, CGRP and spleen in the induction of diabetes induced hyperalgesia in mice. Tail ‰ick latency, an index of hyperalgesia, was assessed using analgesiometer. Serum nitrite levels and an index of nitric oxide were analyzed using Griess reaction. Mice were rendered diabetic with streptozotocin (200 mg/kg -1 , i.p.) and kept for 30 days for development of diabetic pain. To explore the involvement of spleen in diabetic pain, spleen homogenate supernatant (SHS) was prepared from spleen of 30 th day diabetic mice and administered in normal mice for 14 days. Both in diabetic and SHS treated mice, signiˆcant degree of hyperalgesia was developed, suggesting the possible role of spleen derived factor in induction of diabetic pain. Moreover, the levels of nitric oxide were also elevated in 30 day diabetic mice and SHS treated mice. Administration of ruthenium red (1 mg/kg -1 , i.p.), vanilloid receptor antagonist, and sumatriptan (50 mg/kg -1 , i.p.), a CGRP release inhibitor, attenuated diabetes and SHS induced decrease in nociceptive threshold and increase in serum nitrite oxide levels. These results suggest that spleen derived factor induced activation of vanilloid receptors and CGRP release may be contributing in the development of hyperalgesia in diabetic mice.

show abstract

Effect of Cyclooxygenase and Nitric Oxide Synthase Inhibitors on Streptozotocin-Induced Hyperalgesia in Rats

Cited by 37 publications

References 68 publications

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

Anti-allodynic effect of theoesberiven F in a vincristine-induced neuropathy model

Possible Role of Spleen Derived Factors, Vanilloid Receptors and Calcitonin Gene-related Peptide in Diabetes Induced Hyperalgesia in Mice

Contact Info

Product

Resources

About