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155. Dexamethasone exacerbates cisplatin‐induced muscle atrophy

Author

Sakai, Hiroyasu, primary, Kimura, Minami, additional, Tsukimura, Yuka, additional, Yabe, Saori, additional, Isa, Yosuke, additional, Kai, Yuki, additional, Sato, Fumiaki, additional, Kon, Risako, additional, Ikarashi, Nobutomo, additional, Narita, Minoru, additional, Chiba, Yoshihiko, additional, and Kamei, Junzo, additional

Published
2018
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170. Dexamethasone exacerbates cisplatin‐induced muscle atrophy.

Author

Sakai, Hiroyasu, Kimura, Minami, Tsukimura, Yuka, Yabe, Saori, Isa, Yosuke, Kai, Yuki, Sato, Fumiaki, Kon, Risako, Ikarashi, Nobutomo, Narita, Minoru, Chiba, Yoshihiko, and Kamei, Junzo

Subjects
DEXAMETHASONE, DISEASE exacerbation, CISPLATIN, MUSCULAR atrophy, ANTINEOPLASTIC agents, ANTIEMETICS
Abstract

Summary: Dexamethasone for antiemetic therapy is typically administered with anticancer drugs such as cisplatin. We previously reported that cisplatin upregulates the muscle‐specific E3 ubiquitin ligase genes, namely muscle ring‐finger protein 1 (MuRF1) and atrophy gene‐1 (atrogin‐1), and promotes muscle atrophy in mice. It is well known that dexamethasone causes upregulation of MuRF1 and Atrogin‐1 expression in skeletal muscles. Although it is speculated that a combination of dexamethasone and cisplatin worsens muscle atrophy, there are no reports based on research. We thereby investigated the effects of cisplatin and dexamethasone, alone or in combination, on the expression of MuRF1 and Atrogin‐1 in murine skeletal muscles and C2C12 myotubes. Mice were intraperitoneally injected with cisplatin or the vehicle control once daily for 4 days. Dexamethasone or the vehicle control was subcutaneously administered 30 minutes prior to the administration of cisplatin. Dexamethasone enhanced MuRF1 and Atrogin‐1 gene expression upregulated by cisplatin in murine quadriceps muscles and C2C12 myotubes. Cisplatin‐caused upregulation of myostatin and downregulation of IGF‐1 gene expression were also enhanced by co‐administration of dexamethasone in murine quadriceps muscles and C2C12 myotubes. This study shows that the combination treatment of cisplatin and dexamethasone exacerbated muscle atrophy in mice. Therefore, this treatment regimen might exacerbate muscle atrophy in cancer patients. [ABSTRACT FROM AUTHOR]

Published
2019
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171. Mechanical stimulation by postnasal drip evokes cough

Author

40447975, 30805817, 60359809, Iwata, Toshiyuki, Ito, Isao, Niimi, Akio, Ikegami, Koji, Marumo, Satoshi, Tanabe, Naoya, Nakaji, Hitoshi, Kanemitsu, Yoshihiro, Matsumoto, Hisako, Kamei, Junzo, Setou, Mitsutoshi, Mishima, Michiaki, 40447975, 30805817, 60359809, Iwata, Toshiyuki, Ito, Isao, Niimi, Akio, Ikegami, Koji, Marumo, Satoshi, Tanabe, Naoya, Nakaji, Hitoshi, Kanemitsu, Yoshihiro, Matsumoto, Hisako, Kamei, Junzo, Setou, Mitsutoshi, and Mishima, Michiaki

Abstract

Cough affects all individuals at different times, and its economic burden is substantial. Despite these widespread adverse effects, cough research relies on animal models, which hampers our understanding of the fundamental cause of cough. Postnasal drip is speculated to be one of the most frequent causes of chronic cough; however, this is a matter of debate. Here we show that mechanical stimuli by postnasal drip cause chronic cough. We distinguished human cough from sneezes and expiration reflexes by airflow patterns. Cough and sneeze exhibited one-peak and two-peak patterns, respectively, in expiratory airflow, which were also confirmed by animal models of cough and sneeze. Transgenic mice with ciliary dyskinesia coughed substantially and showed postnasal drip in the pharynx; furthermore, their cough was completely inhibited by nasal airway blockade of postnasal drip. We successfully reproduced cough observed in these mice by injecting artificial postnasal drip in wild-type mice. These results demonstrated that mechanical stimulation by postnasal drip evoked cough. The findings of our study can therefore be used to develop new antitussive drugs that prevent the root cause of cough.

Published
2015

172. Antihyperalgesic effects of ProTx-II, a Nav1.7 antagonist, and A803467, a Nav1.8 antagonist, in diabetic mice

Author

Tanaka,Ken-ichiro, Sekino,Shota, Ikegami,Megumi, Ikeda,Hiroko, Kamei,Junzo, Tanaka,Ken-ichiro, Sekino,Shota, Ikegami,Megumi, Ikeda,Hiroko, and Kamei,Junzo

Abstract

Ken-ichiro Tanaka,1,2, Shota Sekino,1 Megumi Ikegami,1 Hiroko Ikeda,1 Junzo Kamei11Department of Pathophysiology and Therapeutics, School of Pharmacy and Pharmaceutical Sciences, Hoshi University, Tokyo, Japan; 2Department of Endocrinology and Metabolism, Graduate School of Medicine, Yokohama City University, Yokohama, JapanAbstract: The present study investigated the effects of intrathecal administration of ProTx-II (tarantula venom peptide) and A803467 (5-[4-chloro-phenyl]-furan-2-carboxylic acid [3,5-dimethoxy-phenyl]-amide), selective Nav1.7 and Nav1.8 antagonists, respectively, on thermal hyperalgesia in a painful diabetic neuropathy model of mice. Intrathecal administration of ProTx-II at doses from 0.04 to 4 ng to diabetic mice dose-dependently and significantly increased the tail-flick latency. Intrathecal administration of A803467 at doses from 10 to 100 ng to diabetic mice also dose-dependently and significantly increased the tail-flick latency. However, intrathecal administration of either ProTx-II (4 ng) or A803467 (100 ng) had no effect on the tail-flick latency in nondiabetic mice. The expression of either the Nav1.7 or Nav1.8 sodium channel protein in the dorsal root ganglion in diabetic mice was not different from that in nondiabetic mice. The present results suggest that ProTx-II and A803467, highly selective blockers of Nav1.7 and Nav1.8 sodium channels, respectively, in the spinal cord, can have antihyperalgesic effects in diabetic mice.Keywords: painful diabetic neuropathy, Nav1.7, Nav1.8, ProTx-II, A803467

Published
2015

173. Mechanical Stimulation by Postnasal Drip Evokes Cough

Author

Iwata, Toshiyuki, primary, Ito, Isao, additional, Niimi, Akio, additional, Ikegami, Koji, additional, Marumo, Satoshi, additional, Tanabe, Naoya, additional, Nakaji, Hitoshi, additional, Kanemitsu, Yoshihiro, additional, Matsumoto, Hisako, additional, Kamei, Junzo, additional, Setou, Mitsutoshi, additional, and Mishima, Michiaki, additional

Published
2015
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175. Effects of 8-hydroxy-2-(di-n-propylamino)tetraEin, a selective agonist of 5-HT1A receptors, on the cough reflex in rats

Author

Kamei Junzo, Mori Tomoko, Igarashi Hironori, and Kasuya Yutaka

Subjects
Male, Agonist, Spiperone, Ketanserin, Tetrahydronaphthalenes, medicine.drug_class, Injections, Subcutaneous, Methysergide, Pharmacology, Dextromethorphan, Reflex, medicine, Animals, Drug Interactions, 5-HT receptor, 8-Hydroxy-2-(di-n-propylamino)tetralin, Codeine, Chemistry, Rats, Inbred Strains, Dihydrocodeine, Rats, Antitussive Agents, Cough, Antitussive Agent, Receptors, Serotonin, Capsaicin, Injections, Intraperitoneal, medicine.drug
Abstract

The effects of the agonist of 5-HT1A receptors, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), on the capsaicin-induced cough reflex in rats were studied. I.p. injection of 8-OH-DPAT, at doses of 0.1 and 0.3 mg/kg, significantly decreased the number of coughs in a dose-dependent manner. The antitussive effect of 8-OH-DPAT (0.3 mg/kg) was blocked by prior injection of methysergide (3 mg/kg i.p.) and spiperone (0.3 mg/kg i.p.), whereas ketanserin (3 mg/kg i.p.) had no effect on the antitussive effect of 8-OH-DPAT. The antitussive effects of dihydrocodeine (1 mg/kg i.p.) and dextromethorphan (3 mg/kg i.p.) were also antagonized by methysergide and spiperone. However, these cough-depressant effects were not reduced by ketanserin. These results suggest that the antitussive action of 8-OH-DPAT may be related to the enhancement of the function of 5-HT1A receptors, and that antitussives interact with the 5-HT1A receptors.

Published
1991
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176. IGF2 Preserves Osteosarcoma Cell Survival by Creating an Autophagic State of Dormancy That Protects Cells against Chemotherapeutic Stress

Author

Shimizu, Takatsune, primary, Sugihara, Eiji, additional, Yamaguchi-Iwai, Sayaka, additional, Tamaki, Sakura, additional, Koyama, Yuko, additional, Kamel, Walied, additional, Ueki, Arisa, additional, Ishikawa, Tomoki, additional, Chiyoda, Tatsuyuki, additional, Osuka, Satoru, additional, Onishi, Nobuyuki, additional, Ikeda, Hiroko, additional, Kamei, Junzo, additional, Matsuo, Koichi, additional, Fukuchi, Yumi, additional, Nagai, Toshihiro, additional, Toguchida, Junya, additional, Toyama, Yoshiaki, additional, Muto, Akihiro, additional, and Saya, Hideyuki, additional

Published
2014
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178. The dipeptide Phe-Phe amide attenuates signs of hyperalgesia, allodynia and nociception in diabetic mice using a mechanism involving the sigma receptor system

Author

Ohsawa, Masahiro, Carlsson, Anna, Asato, Megumi, Koizumi, Takayuki, Nakanishi, Yuki, Fransson, Rebecca, Sandström, Anja, Hallberg, Mathias, Nyberg, Fred, Kamei, Junzo, Ohsawa, Masahiro, Carlsson, Anna, Asato, Megumi, Koizumi, Takayuki, Nakanishi, Yuki, Fransson, Rebecca, Sandström, Anja, Hallberg, Mathias, Nyberg, Fred, and Kamei, Junzo

Abstract

Background: Previous studies have demonstrated that intrathecal administration of the substance P amino-terminal metabolite substance P1-7 (SP1-7) and its C-terminal amidated congener induced antihyperalgesic effects in diabetic mice. In this study, we studied a small synthetic dipeptide related to SP1-7 and endomorphin-2, i.e. Phe-Phe amide, using the tail-flick test and von Frey filament test in diabetic and non-diabetic mice. Results: Intrathecal treatment with the dipeptide increased the tail-flick latency in both diabetic and non-diabetic mice. This effect of Phe-Phe amide was significantly greater in diabetic mice than non-diabetic mice. The Phe-Phe amide-induced antinociceptive effect in both diabetic and non-diabetic mice was reversed by the σ1 receptor agonist (+)-pentazocine. Moreover, Phe-Phe amide attenuated mechanical allodynia in diabetic mice, which was reversible by (+)-pentazocine. The expression of spinal σ1 receptor mRNA and protein did not differ between diabetic mice and non-diabetic mice. On the other hand, the expression of phosphorylated extracellular signal-regulated protein kinase 1 (ERK1) and ERK2 proteins was enhanced in diabetic mice. (+)-Pentazocine caused phosphorylation of ERK1 and ERK2 proteins in non-diabetic mice, but not in diabetic mice. Conclusions: These results suggest that the spinal σ1 receptor system might contribute to diabetic mechanical allodynia and thermal hyperalgesia, which could be potently attenuated by Phe-Phe amide.

Published
2011
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183. Tubulin Tyrosine Ligase-Like Family Member 1 Gene Knockout Mice Spontaneously Cough Due To Post Nasal Drip

Author

Iwata, Toshiyuki, primary, Ito, Isao, additional, Niimi, Akio, additional, Ikegami, Koji, additional, Marumo, Satoshi, additional, Nakaji, Hitoshi, additional, Tanabe, Naoya, additional, Matsumoto, Hisako, additional, Oguma, Tsuyoshi, additional, Inoue, Hideki, additional, Tajiri, Tomoko, additional, Nagasaki, Tadao, additional, Kanemitsu, Yoshihiro, additional, Kamei, Junzo, additional, Setou, Mitsutoshi, additional, and Mishima, Michiaki, additional

Published
2012
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196. Structure−Antitussive Activity Relationships of Naltrindole Derivatives. Identification of Novel and Potent Antitussive Agents

Author

Sakami, Satoshi, primary, Maeda, Masayuki, additional, Kawai, Koji, additional, Aoki, Takumi, additional, Kawamura, Kuniaki, additional, Fujii, Hideaki, additional, Hasebe, Ko, additional, Nakajima, Mayumi, additional, Endo, Takashi, additional, Ueno, Shinya, additional, Ito, Tsuyoshi, additional, Kamei, Junzo, additional, and Nagase, Hiroshi, additional

Published
2008
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198. Antidepressant-like effects of the delta-opioid receptor agonist SNC80 ([(+)-4-[(alphaR)-alpha-[(2S,5R)-2,5-dimethyl-4-(2-propenyl)-1-piperazinyl]-(3-methoxyphenyl)methyl]-N,N-diethylbenzamide) in an olfactory bulbectomized rat model

Author

Saitoh, Akiyoshi, primary, Yamada, Mitsuhiko, additional, Yamada, Misa, additional, Takahashi, Kou, additional, Yamaguchi, Kazumasa, additional, Murasawa, Hiroyasu, additional, Nakatani, Akiko, additional, Tatsumi, Yoshimi, additional, Hirose, Noritaka, additional, and Kamei, Junzo, additional

Published
2008
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