ライフサイエンスコーパス: inflammatory pain

1 d structural plasticity during the course of inflammatory pain.

2 of neuropathic pain and carrageenan model of inflammatory pain.

3 NF-alpha secretion, synaptic plasticity, and inflammatory pain.

4 ility that underlies chronic neuropathic and inflammatory pain.

5 hich implicates endogenous Cat-S and PAR2 in inflammatory pain.

6 zepine site agonist HZ166 in neuropathic and inflammatory pain.

7 upport the hypothesis of cytokine release in inflammatory pain.

8 on following noxious thermal stimulation and inflammatory pain.

9 ice show enhanced sensitivity to thermal and inflammatory pain.

10 activity in vivo in several rodent models of inflammatory pain.

11 n of nociceptor excitability and relief from inflammatory pain.

12 plications for a potential role of lipids in inflammatory pain.

13 ole of PAR2 as a mediator of protease-driven inflammatory pain.

14 y neuronal hyperexcitability associated with inflammatory pain.

15 the primary sensory cortex (S1) in rats with inflammatory pain.

16 t mice have enhanced thermal sensitivity and inflammatory pain.

17 increased sensitivity to acute and sub-acute inflammatory pain.

18 a therapeutic target for relief from chronic inflammatory pain.

19 re likely responsible for the maintenance of inflammatory pain.

20 eceptors may be a unique approach to reverse inflammatory pain.

21 periodontitis, neurogenic inflammation, and inflammatory pain.

22 ficacy in the same analgesic model of rodent inflammatory pain.

23 d is thus responsible for the genesis of the inflammatory pain.

24 way contribute to the development of chronic inflammatory pain.

25 ing in SGCs may serve as a target to control inflammatory pain.

26 vel therapeutic targets for the treatment of inflammatory pain.

27 ation in these conditions as well as chronic inflammatory pain.

28 , MGE transplants were not effective against inflammatory pain.

29 served in inflammation and may contribute to inflammatory pain.

30 dontal disease, neurogenic inflammation, and inflammatory pain.

31 ntify NPD1 as a novel analgesic for treating inflammatory pain.

32 ent endogenous inhibitor for TRPV1/TRPA1 and inflammatory pain.

33 anisms underlying mechanical hyperalgesia in inflammatory pain.

34 A may be used as complementary treatment for inflammatory pain.

35 ns may represent new analgesics for treating inflammatory pain.

36 ily targeted for psychiatric indications and inflammatory pain.

37 ereas was ineffective in acute (carrageenan) inflammatory pain.

38 se to target those nociceptors important for inflammatory pain.

39 gesia to N2O in response to formalin-induced inflammatory pain.

40 ls and in the development of neuropathic and inflammatory pain.

41 old more potent than 4 in an animal model of inflammatory pain.

42 ing oral administration in a rodent model of inflammatory pain.

43 t nociceptive hypersensitivity in persistent inflammatory pain.

44 st-carrageenan thermal hyperalgesia model of inflammatory pain.

45 ot efficacious in rodent models of acute and inflammatory pain.

46 odulator and a potential target for treating inflammatory pain.

47 iception in animal models of neuropathic and inflammatory pain.

48 tion channel that plays an important role in inflammatory pain.

49 od pressure readout and an efficacy model of inflammatory pain.

50 autoinflammatory diseases or amelioration of inflammatory pain.

51 ckdown of TrkB by RNA interference attenuate inflammatory pain.

52 key modulator of peripheral neuropathic and inflammatory pain.

53 vate primary afferent nociceptors to produce inflammatory pain.

54 ing thermal (cold) nociception, hearing, and inflammatory pain.

55 , which mediate central sensitization during inflammatory pain.

56 esic agents depolarize nociceptors to elicit inflammatory pain.

57 cancer therapy) as well as acute and chronic inflammatory pain.

58 mal models of acute thermal pain and chronic inflammatory pain.

59 vo activity in animal models of visceral and inflammatory pain.

60 ice also exhibit hyperalgesia in response to inflammatory pain.

61 yperalgesia in an animal model of persistent inflammatory pain.

62 ct from ERK by regulating the early onset of inflammatory pain.

63 ) family of ion channels, may play a role in inflammatory pain.

64 clinical acupuncture research on persistent inflammatory pain.

65 y provide an improved treatment strategy for inflammatory pain.

66 s and the contribution of PI3K activation to inflammatory pain.

67 nds, namely, 8d, to reduce the perception of inflammatory pain.

68 s thought to be distinct from neuropathic or inflammatory pain.

69 o descending control in acute and persistent inflammatory pain.

70 ete Freund's adjuvant, a model of peripheral inflammatory pain.

71 r in the Complete Freund's adjuvant model of inflammatory pain.

72 d nociception and alleviated neuropathic and inflammatory pain.

73 erized as novel targets in acute and chronic inflammatory pain.

74 nd tolerance in models of neuropathic and/or inflammatory pain.

75 e analgesic effects of acetaminophen against inflammatory pain.

76 i-G-CSFR mAb also suppressed zymosan-induced inflammatory pain.

77 agonists as useful therapeutics for chronic inflammatory pain.

78 orolac in this prototypic condition of acute inflammatory pain.

79 edominant temporomandibular disorders (TMDs) inflammatory pain.

80 ts may be useful for treatment of persistent inflammatory pain.

81 for the thermal hyperalgesia associated with inflammatory pain.

82 anti-inflammatory drug (NSAID) for relief of inflammatory pain.

83 smission controls the affective component of inflammatory pain.

84 has potential as a treatment for persistent inflammatory pain.

85 us mice provide a new genetic model to study inflammatory pain.

86 a back pain model and a model of peripheral inflammatory pain.

87 ap1 signaling, thereby inhibiting persistent inflammatory pain.

88 and promotes analgesia in an animal model of inflammatory pain.

89 this mouse model can be used to study dental inflammatory pain.

90 ransmission and have enhanced sensitivity to inflammatory pain.

91 in two different mouse models of persistent inflammatory pain.

92 he complete Freund's adjuvant (CFA) model of inflammatory pain (1.3-1.4-fold improvement over wild-ty

93 In murine models of inflammatory pain, 2,6-DTBP reduced inflammatory hyperal

94 ptors that mediate both sharp acute pain and inflammatory pain; (2) sanshool inhibits action potentia

95 lete Freund's adjuvant (CFA) induced chronic inflammatory pain after oral administration.

96 rovides critical new insights that show that inflammatory pain alters heroin intake through a desensi

97 ings identify a key role of Epac1 in chronic inflammatory pain and a molecular mechanism for controll

98 both CCL17-dependent and unique CCL17-driven inflammatory pain and arthritis models, the latter permi

99 s a factor in the modulation of responses to inflammatory pain and body weight homeostasis.

100 sory neurons is necessary for development of inflammatory pain and for postnatal maintenance of pepti

101 inophen analgesia in mice of either sex with inflammatory pain and found that acetaminophen exerted a

102 of immune-related genes in the PFCTX during inflammatory pain and highlight an exciting role of neut

103 n pain receptor reported as an integrator of inflammatory pain and hyperalgesia and a prime therapeut

104 , in the complete Freund's adjuvant model of inflammatory pain and in the spared nerve injury model o

105 taken to test whether activin contributes to inflammatory pain and increased CGRP and to learn which

106 athecal) administration of IFN-alpha reduced inflammatory pain and increased pain threshold in naive

107 further show that DHCB is effective against inflammatory pain and injury-induced neuropathic pain an

108 signaling molecules that can strongly affect inflammatory pain and ischemia-reperfusion injury respon

109 lete Freund's adjuvant (CFA)-induced chronic inflammatory pain and L5 spinal nerve ligation (SNL)-ind

110 these results identify a connection between inflammatory pain and loss of MOR function in the mesoli

111 nsitive channels that play a pivotal role in inflammatory pain and mechanical hyperalgesia.

112 oss of Arrb2 also results in prolongation of inflammatory pain and neuropathic pain and enhancement o

113 The causes of inflammatory pain and neuropathic pain are fundamentally

114 Recognition of mechanisms common to both inflammatory pain and neuropathic pain might shed light

115 lial signaling inhibitors effectively reduce inflammatory pain and neuropathic pain, arguing against

116 nd our knowledge of the interactions between inflammatory pain and opioid abuse liability, and should

117 of complete Freund's adjuvant (CFA)-induced inflammatory pain and opioid medication on spatial memor

118 sist in uncovering mechanisms for tooth pulp inflammatory pain and other forms of trigeminal pain.

119 gesic effects in the formalin test for acute inflammatory pain and paclitaxel-induced neuropathic pai

120 Finally, using a model of persistent inflammatory pain and pharmacological manipulation of TL

121 synthesis in rats attenuated neuropathic and inflammatory pain and prevented nerve injury-evoked exce

122 i-1 attenuated thermal nociception and acute inflammatory pain and produced deficits in Na(V)1.8 prot

123 e an effective strategy to alleviate chronic inflammatory pain and promote opioid antinociception, es

124 sing Advillin-Cre abolishes mechanical pain, inflammatory pain and reflex withdrawal responses to hea

125 X(2/3) receptor in the signalling of chronic inflammatory pain and some features of neuropathic pain.

126 tion is a promising strategy against chronic inflammatory pain and that, to our knowledge, 2,6-DTBP h

127 horylation occurred during acute and chronic inflammatory pain and under behavioral stress.

128 al ED50 of 0.1 mg/kg in the rat FCA model of inflammatory pain and was selected as a clinical candida

129 e Freund's adjuvant (CFA) was used to induce inflammatory pain, and mechanical sensitivity and therma

130 ical pain, heat pain, capsaicin-evoked pain, inflammatory pain, and neuropathic pain.

131 uron MOR upregulation and antinociception in inflammatory pain, and provides intriguing evidence that

132 nalgesia against acute pain but also against inflammatory pain, and suggest that the relevant CB1 rec

133 essed by microglial cells in neuropathic and inflammatory pain; and the complex actions mediated by P

134 Mechanisms of inflammatory pain are not fully understood.

135 tal manifestations such as arthritis and non-inflammatory pain as well as with metabolic diseases, su

136 populations, is implicated in the control of inflammatory pain, as well as arthritic pain and disease

137 In contrast to their role in inflammatory pain aversion, EP3 receptors on serotonergi

138 (NGF) has been implicated as an effector of inflammatory pain because it sensitizes primary afferent

139 ion of RvE1 or RvD1 in mice potently reduces inflammatory pain behaviors induced by intraplantar inje

140 rons are essential for mechanical, cold, and inflammatory pain but not for neuropathic pain or heat s

141 in animal models of osteoarthritis and acute inflammatory pain, but has not been studied in humans.

142 , mTOR and S6K1 are activated during chronic inflammatory pain, but not during neuropathic pain.

143 c pain, and determined their role in colonic inflammatory pain by gene deletion.

144 AKAP79/150 has been implicated in inflammatory pain by targeting protein kinase A (PKA) an

145 ribute to the development of neuropathic and inflammatory pain by TNFalpha.

146 In models of inflammatory pain, CCR2 knockout mice showed a 70% reduc

147 p.o.) and was antihyperalgesic in a model of inflammatory pain (CFA-induced thermal hyperalgesia, MED

148 mmatory insult, using the lambda-carrageenan inflammatory pain (CIP) model, induced alterations in th

149 to mechanical stimuli and exhibited enhanced inflammatory pain compared with their littermate control

150 orts of central neurochemical changes during inflammatory pain conditions and show that the combinati

151 Central sensitization in inflammatory pain conditions results in behavioral mecha

152 he Zanthoxylum genus have been used to treat inflammatory pain conditions, such as toothache and rheu

153 entral sensitization associated with chronic inflammatory pain conditions.

154 been explored, nor whether ADS is altered in inflammatory pain conditions.

155 ng gray rami might be useful in some chronic inflammatory pain conditions.

156 athway, and its activation during persistent inflammatory pain, could account for sex-based differenc

157 We found that place aversion induced by inflammatory pain depends on prostaglandin E2 that is sy

158 +) non-bone marrow-derived cells, and 3) for inflammatory pain development in which a GM-CSF->CCL17 p

159 demonstrated that lambda-carrageenan-induced inflammatory pain enhanced the in vivo antinociceptive p

160 However, the late phase inflammatory pain following complete Freund's adjuvant i

161 dynia is a common symptom of neuropathic and inflammatory pain following peripheral nerve injury.

162 ndorphin, which produces itch and attenuates inflammatory pain, GRP only elicits itch without affecti

163 In the presence of inflammatory pain, heroin intake under an FR schedule wa

164 modeling the inherent mechanisms underlying inflammatory pain hypersensitivity and painful chemother

165 vels of these receptors has consequences for inflammatory pain hypersensitivity but not acute pain pr

166 it aids in developing a central component of inflammatory pain hypersensitivity by increasing neurona

167 iven the significant roles of VR1 and PKA in inflammatory pain hypersensitivity, VR1 phosphorylation

168 ntribute to various forms of neuropathic and inflammatory pain hypersensitivity.

169 ntribution of peripheral and central COX2 to inflammatory pain hypersensitivity.

170 H neurons is critical for the development of inflammatory pain hypersensitivity.

171 on in the spinal cord and in contributing to inflammatory pain hypersensitivity.

172 nse in two widely used preclinical models of inflammatory pain: (i) intraplantar injection of complet

173 sia of electroacupuncture (EA) on persistent inflammatory pain in an unrestrained, unsedated, and con

174 al and mechanical nociception and persistent inflammatory pain in control mice but had little effect

175 y markers associated with neuropathic and/or inflammatory pain in dorsal root ganglia (DRGs) and spin

176 27 dose-dependently reduced neuropathic and inflammatory pain in experimental rodent models.

177 um channel NaV 1.7 is required for acute and inflammatory pain in mice and humans but its significanc

178 in the formalin test of acute peripheral and inflammatory pain in mice, in which compounds 10a and 11

179 IL4-10 dose-dependently inhibited persistent inflammatory pain in mice: three IL4-10 injections induc

180 rphine antinociception in standard assays of inflammatory pain in rats and synergistically augmented

181 PSD-95) can reduce ischemic brain damage and inflammatory pain in rodents.

182 uncovering molecular mechanisms that govern inflammatory pain in the tooth.

183 IL4-10 injections induced full resolution of inflammatory pain in two different mouse models of persi

184 rotein induces full resolution of persistent inflammatory pain in two different mouse models.

185 1) and TNF-alpha, two critical mediators for inflammatory pain, in regulating spinal cord synaptic tr

186 RVM circuit and its activation by persistent inflammatory pain induced by intraplantar injection of c

187 Cat-S deletion attenuated colonic inflammatory pain induced with trinitrobenzene sulfonic

188 in SDH neurons and is necessary in a form of inflammatory pain-induced plasticity, which involves an

189 esia in mouse models of incisional wound and inflammatory pain, inhibited release of the neuropeptide

190 Inflammatory pain (IP) is a condition underlying several

191 ioid analgesics for the treatment of chronic inflammatory pain is a result of opioid-induced release

192 Inflammatory pain is generally treated with opioids and

193 edominant role of the central 5-HT system in inflammatory pain is inhibitory, its role in acute mecha

194 Inflammatory pain is thought to arise from increased tra

195 The most common way of managing inflammatory pain is to use nonsteroidal antiinflammator

196 While inflammatory pain is well described in skeletal muscle,

197 Here, we tested the hypothesis that inflammatory pain leads to increased heroin self-adminis

198 vement of AMPAR in the mechanisms underlying inflammatory pain led us to hypothesize a role for spina

199 periodontitis, neurogenic inflammation, and inflammatory pain likely via the activation of MRGPRX2.

200 matory pain, suggesting that the presence of inflammatory pain may be an important consideration in t

201 mal, but the increased input associated with inflammatory pain measured using c-Fos staining was dimi

202 echanical stimuli in vivo and did not affect inflammatory pain measured with the formalin test.

203 These data indicate that HDAC4 is a novel inflammatory pain mediator and may be a good therapeutic

204 ted EA-produced anti-hyperalgesia in the CFA inflammatory pain model but did not affect either baseli

205 t in females than males and is reduced in an inflammatory pain model in females only.

206 otent inhibitor of flinching behavior in the inflammatory pain model induced by formalin injection.

207 receptors affect EA anti-hyperalgesia in an inflammatory pain model, these data show that EA inhibit

208 re obtained in the formalin-induced chemical-inflammatory pain model.

209 eshold using the in vivo carrageenan induced inflammatory pain model.

210 in a mouse complete Freund's adjuvant (CFA) inflammatory pain model.

211 exhibited good analgesic potency in the CFA inflammatory-pain model with longer duration of action o

212 efficacy in veratridine and formalin-induced inflammatory pain models in mice.

213 OC3 inhibitors provoked analgesic effects in inflammatory pain models in vivo, suggesting potential t

214 AM1241) exert peripheral antihyperalgesia in inflammatory pain models, the mechanism for cannabinoid-

215 in the induction of thermal hyperalgesia in inflammatory pain models, we evaluated whether the canna

216 portant roles in controlling hyperalgesia in inflammatory pain models, we investigated their modulati

217 at fraction has an antinociceptive effect on inflammatory pain models.

218 ) displayed anti-hyperalgesic effect in both inflammatory pain models.

219 gesia both in neuropathic and in acute/tonic inflammatory pain models.

220 both phase 1 (neurogenic pain) and phase 2 (inflammatory pain) of the formalin test, whereas indomet

221 ation of TRPV1, possibly contributing to the inflammatory pain often observed in bacterial infections

222 l implications of lambda-carrageenan-induced inflammatory pain on brain uptake of a commonly used ana

223 rochemical and functional changes induced by inflammatory pain on MOR-mediated mesolimbic DA transmis

224 downstream of metabotropic receptors elicits inflammatory pain or itch, making it an attractive targe

225 esia was not affected by carrageenan-induced inflammatory pain or the early phase of oxaliplatin neur

226 lete Freund's adjuvant (CFA)-induced chronic inflammatory pain, oral administration of either compoun

227 Activators of neuropathic and inflammatory pain (p38 mitogen-activated protein kinase,

228 nstrate that KCC3 plays an essential role in inflammatory pain pathways.

229 e in which pain is important, as well as for inflammatory pain per se.

230 ioral studies showed greatly reduced thermal inflammatory pain perception in AQP1(-/-) mice evoked by

231 tracellular PAF binding sites, mediate tonic inflammatory pain processing in rats.

232 CFA-induced inflammatory pain produced thermal hyperalgesia in both

233 Neuropathic and inflammatory pain promote a large number of persisting a

234 6G(-) myeloid cells contribute to mechanical inflammatory pain provides a potential cellular target f

235 n a complete Freund's adjuvant (CFA)-induced inflammatory pain rat model.

236 n in low dose FR heroin self-administration, inflammatory pain reduced motivation for a low dose of h

237 We find that inflammatory pain reduces sexual motivation, measured vi

238 In inflammatory pain, reductions in synaptic inhibition occ

239 Inflammatory pain represents an important unmet clinical

240 Human acute and inflammatory pain requires the expression of voltage-gat

241 tant to centrally acting analgesics, whereas inflammatory pain responds well.

242 mice had normal baseline pain, but impaired inflammatory pain responses.

243 e do not show alterations in neuropathic and inflammatory pain sensitivity.

244 taglandin E2 (PGE2) is a crucial mediator of inflammatory pain sensitization.

245 d receptor phosphorylation underlies central inflammatory pain sensitization.

246 ese genes, resulting in amplification of the inflammatory pain signal transduction cascade.

247 , we reported previously that Cdk5 regulates inflammatory pain signaling, partly through phosphorylat

248 he TGF-beta and Cdk5 pathways contributes to inflammatory pain signaling.

249 ivation of TPRA1, an ion channel involved in inflammatory pain signaling.

250 TRPV1 by cationic strength may contribute to inflammatory pain signaling.

251 tor, TRPV1, is a key ion channel involved in inflammatory pain signalling.

252 d in the activation of the PAG by persistent inflammatory pain, significantly more PAG-RVM cells were

253 epression, anxiety, substance abuse, emesis, inflammatory pain, spinal nociception, gastrointestinal

254 ccompanies development and maintenance of an inflammatory pain state.

255 glial signaling in some neuropathic pain and inflammatory pain states, although both sexes show ident

256 mpared with understanding of neuropathic and inflammatory pain states.

257 e peripheral pain mediators, particularly in inflammatory pain states.

258 ze to NGF and has important implications for inflammatory pain states.

259 decreased extracellular pH are hallmarks of inflammatory pain states.

260 induction and maintenance of neuropathic and inflammatory pain states.

261 a peripheral pain mediator, particularly in inflammatory pain states.

262 e (FAAH) is analgesic in models of acute and inflammatory pain states.

263 ical assessment of prospective analgesics in inflammatory pain states.

264 Inflammatory pain such as arthritic pain is typically tr

265 Inflammatory pain, such as arthritis pain, is a growing

266 increased during lambda-carrageenan-induced inflammatory pain, suggesting that the presence of infla

267 iated behavioral alterations in the formalin inflammatory pain test, we administered CRH or the CRH r

268 CGRP) is a sensory neuropeptide important in inflammatory pain that conveys pain information centrall

269 targets, and here we describe two models of inflammatory pain that involve ultraviolet B (UVB) irrad

270 /-) mice exhibit sustained, mGluR5-dependent inflammatory pain that is linked to enhanced mGluR signa

271 nnabinoid system to antihyperalgesia against inflammatory pain, the main indication of acetaminophen,

272 st that P2X receptors are useful targets for inflammatory pain therapy.

273 system and nociceptive neurons is central to inflammatory pain; therefore, new therapies might target

274 havioral level, BomoTx elicits nonneurogenic inflammatory pain, thermal hyperalgesia, and mechanical

275 in plasma PGE metabolites and an increase in inflammatory pain threshold compared with wild-type mice

276 vestigate whether sigma-1 antagonism reduces inflammatory pain through the disinhibition of the endog

277 microbe-derived antigens, can reduce somatic inflammatory pain through the local release of opioids.

278 r neurons express an ion channel involved in inflammatory pain, transient receptor potential ankyrin

279 ation offering therapy for acute and chronic inflammatory pain treatment by scavenging OxPAPC.

280 ncy was evaluated in the Hargreaves model of inflammatory pain using the BBB-impermeable neuropeptide

281 ed a parallel investigation of two models of inflammatory pain, using ultraviolet B (UVB) irradiation

282 A1) contribute importantly to the genesis of inflammatory pain via both peripheral mechanisms (periph

283 Behavioral studies showed that inflammatory pain was attenuated or abolished.

284 Inflammatory pain was induced by injecting complete Freu

285 Using the CFA model of chronic inflammatory pain, we found that increasing GRK2 or decr

286 h the established link between TNF-alpha and inflammatory pain, we identified its increased expressio

287 formalin test as a mouse model of persistent inflammatory pain, we show that activation of ERK in the

288 baseline pain and the formalin induced acute inflammatory pain were intact in CKO mice.

289 These mechanisms may underlie inflammatory pain, where multiple proteases are generate

290 analgesic effects in a rodent model of acute inflammatory pain, which was antagonized by CB1 and CB2

291 reversed thermal hyperalgesia in a model of inflammatory pain, which was induced by complete Freund'

292 effects in rodent models of nociceptive and inflammatory pain, which were mediated by CB(1) cannabin

293 ly in TRPA1-dependent paradigms of acute and inflammatory pain, while heat and mechanical sensitivity

294 d the patients, and a translational model of inflammatory pain will ideally induce both peripheral an

295 promising strategy to treat neuropathic and inflammatory pain with minimal or no cannabimimetic side

296 ynaptic NMDAR responses in a rodent model of inflammatory pain, with an associated downregulation of

297 rathecal RvD2 also reversed adjuvant-induced inflammatory pain without altering baseline pain and mot

298 locks spinal LTP and reduces TRPV1-dependent inflammatory pain, without affecting baseline pain.

299 rated fatty acids, are potent inhibitors for inflammatory pain, without noticeable side effects.

300 ght represent one potential way to attenuate inflammatory pain, yet spare basal sensitivity and produ