Effects of the Prostaglandin E1 Analog Limaprost on Mechanical Allodynia Caused by Chemotherapeutic Agents in Mice

Gauchan, Punam; Andoh, Tsugunobu; Kato, Atsushi; Sasaki, Atsushi; Kuraishi, Yasushi

doi:10.1254/jphs.08325sc

Cited by 47 publications

(56 citation statements)

References 16 publications

(16 reference statements)

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“…55 Finally, concerning the opioid system, administration of a complete inhibitor of enkephalincatabolizing enzymes (PL37) also induced an antinociceptive and anti-allodynic effect, but were not effective on cold allodynia. 57 More recently, to investigate if blood flow reduction is involved in this neuropathy, Gauchan et al 58 assessed the effect of limaprost, a prostaglandin E1 analog, on mechanical allodynia without effectiveness.…”

Section: Treatment Strategiesmentioning

confidence: 99%

“…26,63 Repeated administration of limaprost, contrary to vincristine, significantly inhibited the late phase of mechanical allodynia induced by a single injection of paclitaxel. 58 Therefore, repeated administration of acetyl-L-carnitine (ALC) displayed a significant attenuation of established paclitaxel-induced mechanical hypersensitivity, but this analgesic effect dissipated shortly after ALC discontinuation.…”

Section: Treatment Strategiesmentioning

confidence: 99%

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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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Section: Treatment Strategiesmentioning

confidence: 99%

Section: Treatment Strategiesmentioning

confidence: 99%

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

et al. 2009

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“…The recommended dose of paclitaxel is 210 mg/m 2 body surface area (package insert of Taxol ® ; Bristol-Myers Squibb, New York City, NY, U.S.A.), which corresponds to 5.9 mg/kg when the height and body weight are 170 cm and 60 kg, respectively. 11) In in vitro experiments, paclitaxel was dissolved in 100% dimethyl sulfoxide (DMSO), which was diluted in the medium so that the final concentration of DMSO was 1%. Aucubin (Wako Pure Chemical Industries, Ltd., Osaka, Japan: Lot.…”

Section: Methodsmentioning

confidence: 99%

Prophylactic Administration of Aucubin Inhibits Paclitaxel-Induced Mechanical Allodynia <i>via</i> the Inhibition of Endoplasmic Reticulum Stress in Peripheral Schwann Cells

Andoh

Uta

Kato

et al. 2017

Biological & Pharmaceutical Bulletin

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Paclitaxel is a chemotherapeutic agent that causes peripheral neuropathy as its major dose-limiting side effect. However, the peripheral neuropathy is difficult to manage. A study we recently conducted showed that repetitive administration of aucubin as a prophylactic inhibits paclitaxel-induced mechanical allodynia. However, the mechanisms underlying the anti-allodynic activity of aucubin, which is a major component of Plantaginis Semen, was unclear. In addition to mechanical allodynia, aucubin inhibited spontaneous and mechanical stimuli-induced firing in spinal dorsal horn neurons; however, catalpol, a metabolite of aucubin, did not show these effects. Furthermore, paclitaxel induced the expression of CCAAT/enhancer-binding protein homologous protein, a marker of endoplasmic reticulum (ER) stress, in the sciatic nerve and a Schwann cell line (LY-PPB6 cells); however, this effect was inhibited by aucubin. These results suggest that aucubin inhibits paclitaxel-induced mechanical allodynia through the inhibition of ER stress in peripheral Schwann cells. Key words paclitaxel; mechanical allodynia; aucubin; firing; Schwann cell; stressPaclitaxel is an anti-microtubule agent originally isolated from the bark of the Pacific yew tree (Taxus brevifolia) and is wildly used to treat solid neoplasms such as breast, ovarian, and lung cancers.1,2) However, in spite of its useful anticancer effect, paclitaxel causes peripheral neuropathy, which is characterized by mechanical allodynia, spontaneous pain, shooting and burning pain, tingling, and numbness, with a stocking-and-glove distribution.3) The peripheral neuropathy is a major dose-limiting side effect, which disturbs cancer treatment with paclitaxel. Therefore, relief of the neuropathy is very important for improving both the QOL and cancer treatment with paclitaxel. Several drugs, including gabapentin and amifostine, have failed to relieve paclitaxel-induced peripheral neuropathy [4][5][6] ; therefore, alternative therapeutic agents are need.Goshajinkigan is a traditional herbal formulation that consists of 10 herbal medicines (Rehmanniae Radix, Achyranthis Radix, Corni Fructus, Dioscoreae Rhizoma, Plantaginis Semen, Alismatis Rhizoma, Poria, Moutan Cortex, Cinnamoni Cortex, and Processi Aconiti Radix). It has been shown to attenuate the progression of peripheral neuropathy induced by docetaxel and paclitaxel/carboplatin treatments in cancer patients.7,8) Our previous study has been shown that repetitive administration of goshajinkigan extract as a prophylactic inhibits the exacerbation of paclitaxel-induced mechanical allodynia in mice.9) We also showed that aucubin, which is an iridoid glycoside and the main component of Plantaginis Semen, plays an important role in the anti-allodynic action of goshajinkigan.10) However, the mechanisms underlying the anti-allodynic activity of aucubin are not understood completely. It was reported in a previous study that paclitaxel decreased peripheral blood flow and induced mechanical allodynia in mice.11) The study also demonstra...

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“…Furthermore, paclitaxel-and vincristine-evoked neuropathic pain is reduced by both the T-type channel calcium blocker, ethosuximide, and the 2 calcium channel subunit antagonist, gabapentin [30,31]. In addition, paclitaxel has been reported to increase the expression level of 2 -1 mRNA in the dorsal spinal cord [30,32]. Accordingly, it has been proposed that 2 -1 subunit in the spinal dorsal horn and DRG is a main site where gabapentin inhibits paclitaxel-induced allodynia [33].…”

Section: Introductionmentioning

confidence: 99%

“…A recent study demonstrated a correlation between the increase in interleukin 6 (IL-6) and the appearance of bortezomibinduced neuropathic pain [44]. Further, the administration of the prostaglandin E 1 (PGE 1 ) analog, limaprost, attenuated mechanical allodynia induced by paclitaxel and oxaliplatin (but not by vincristine) [32]. An increase in skin Langerhans cells (LC) has been associated with the development of pain in vincristine-and paclitaxel-evoked neuropathy [21].…”

Section: Introductionmentioning

confidence: 99%

Transient Receptor Potential Channels in Chemotherapy-Induced Neuropathy

Nassini¹,

Benemei²,

Fusi³

et al. 2013

TOPAINJ

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Chemotherapy-Induced Peripheral Neuropathy (CIPN) is a common dose-limiting side effect of many chemotherapeutic drugs, including platinum-based compounds (e.g., cisplatin and oxaliplatin), taxanes (e.g., paclitaxel), vinca alkaloids (e.g., vincristine), and the first-in-class proteasome inhibitor, bortezomib. Among the various sensory symptoms of CIPN, paresthesia, dysesthesia, spontaneous pain, and mechanical and thermal hypersensitivity are prominent. Inflammation, oxidative stress, loss of intraepidermal nerve fibers, modifications of mitochondria, and various ion channels alterations are part of the several mechanisms contributing to CIPN. Because attempts to mitigate chemotherapeutic-induced acute neuronal hyperexcitability and the subsequent peripheral neuropathy have yielded unsatisfactory results, a more in-depth understanding of the mechanism(s) responsible for the neurotoxic action of anticancer drugs is required.Some members of the transient receptor potential (TRP) family of channels, as the TRPV1 and TRPV4 (vanilloid), TRPA1 (ankyrin) and TRPM8 (melastatin) are expressed on the plasma membrane of primary sensory neurons (nociceptors), where they are activated by an unprecedented series of physical and chemical stimuli. There is evidence that TRPV1, TRPV4, TRPA1 and TRPM8 are prominent contributors of mechanical and thermal hypersensitivity in models of CIPN. In particular, in vitro and in vivo studies have pointed out the unique role of TRPA1 and oxidative stress in the mechanism responsible for cold and mechanical hyperalgesia in rodent models of CIPN.

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Effects of the Prostaglandin E1 Analog Limaprost on Mechanical Allodynia Caused by Chemotherapeutic Agents in Mice

Cited by 47 publications

References 16 publications

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

Prophylactic Administration of Aucubin Inhibits Paclitaxel-Induced Mechanical Allodynia <i>via</i> the Inhibition of Endoplasmic Reticulum Stress in Peripheral Schwann Cells

Transient Receptor Potential Channels in Chemotherapy-Induced Neuropathy

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