Substance P and beta-endorphin mediate electro-acupuncture induced analgesia in mouse cancer pain model

Lee, Hyo‐Jeong; Lee, Jae Ho; Lee, Eun Ok; Kim, Kwan Hyun; Kim, Sun Hyung; Lee, Keun Sung; Jung, Hyun-Joo; Kim, Sung Hoon

doi:10.1186/1756-9966-28-102

Cited by 27 publications

(27 citation statements)

References 22 publications

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“…A tumor-induced temperature sensitivity model was adapted to our laboratory from earlier studies (28–30) to investigate whether TLR 9 antagonist (Sup ODN) could decrease temperature sensitivity, which is mediated by TRPV1. This model is considered a neuropathic pain model since the tumor-bearing mice experience temperature hypersensitivity.…”

Section: Methodsmentioning

confidence: 99%

Painful Pathways Induced by TLR Stimulation of Dorsal Root Ganglion Neurons

Jia

Buzás

Fan

et al. 2011

The Journal of Immunology

148

124

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We hypothesize that innate immune signals from infectious organisms and/or injured tissues may activate peripheral neuronal pain signals. In this study, we demonstrated that toll-like receptors 3/7/9 (TLRs) are expressed by human dorsal root ganglion neurons (DRGNs) and in cultures of primary mouse DRGNs. Stimulation of murine DRGNs with TLR ligands induced expression and production of proinflammatory chemokines and cytokines CCL5 (RANTES), CXCL10 (IP10), interleukin-1alpha, interleukin-1beta, and prostaglandin E2 (PGE2), which have previously been shown to augment pain. Further, TLR ligands up-regulated the expression of a nociceptive receptor transient receptor potential vanilloid type 1 (TRPV1), and enhanced calcium flux by TRPV1 expressing DRGNs. Using a tumor-induced temperature sensitivity model, we showed that in vivo administration of a TLR9 antagonist, known as a suppressive ODN, blocked tumor-induced temperature sensitivity. Taken together, these data indicate that stimulation of peripheral neurons by TLR ligands can induce nerve pain.

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Section: Methodsmentioning

confidence: 99%

Painful Pathways Induced by TLR Stimulation of Dorsal Root Ganglion Neurons

Jia

Buzás

Fan

et al. 2011

The Journal of Immunology

148

124

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“…Animals of the sham group received only 25 μl of lactated Ringer's solution. This methodology was adapted from Kamioka et al (1999) and Lee et al(2009).…”

Section: Tumor Cell and Implantationmentioning

confidence: 99%

Evidence for the involvement of descending pain-inhibitory mechanisms in the attenuation of cancer pain by carvacrol aided through a docking study

et al. 2014

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“…Since endorphins play a pivotal role in pain modulation and analgesia (41)(42)(43), sex difference to noxious thermal stimulation can be attributed to different brain endorphins content of males compared with females (44).…”

Section: Discussionmentioning

confidence: 99%

sex difference and effects of gonadal hormones on thermal pain thershold in rat

Ahmadi¹

2009

Acta Endo (Buc)

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Various clinical and experimental studies indicate that gonadal hormones exert modulatory effects on nociception and analgesia.The aim of the present study was to investigate the role of gonadal hormones in the response by male and female rats to thermal nociceptive stimulation.Materials and Methods. 7 week old albino (Wistar) rats were used in our study. Animals were randomly divided into control, sham and ovariectomised or orchidectomised groups. Thermal pain threshold was measured through tail immersion test before and 10, 20 or 40 days after gonadectomy. The pain threshold was measured as the time required to elicit a flick of the tail called analgesia time. Serum testosterone, estradiol, progesterone or prolactin levels were measured simultaneously.The results showed that analgesia time was higher in female (5.11 min) than in male (4.93 min) intact animals (p<0.05) indicating sex difference in response to thermal nociception. Serum testosterone, estradiol or progesterone level as well as analgesia time were not significantly reduced 10 days after gondectomy. In male animals, analgesia time was significantly decreased (p<0.01) 20 or 40 days after orchidectomy (2.25 or 2.14 min, respectively) compared with control rats (4.93 min). Serum testosterone concentration was significantly reduced (p<0.05) 20 or 40 days after orchidectomy (0.08 or 0.09 ng/mL, respectively) compared with control serum testosterone level (2.14 ng/mL). In female rats, analgesia time was significantly decreased (p<0.001) 20 or 40 days after ovariectomy (2.87 or 2.66 min, respectively) compared with control rats (5.11 min). Serum estradiol concentration was significantly reduced (p<0.001) 20 or 40 days after ovariectomy (3.17 or 0.87 ng/mL, respectively) compared with control serum estradiol level (19.95 ng/ml). Serum progesterone level was also decreased (p<0.001) 20 or 40 days after orchidectomy (5.27 or 0.55 ng/mL, respectively) compared with control serum estradiol level (17.66 ng/mL). Serum prolactin level was not significantly enhanced during experiment indicating that there was not heat stress influencing the procedure.Conclusively, our findings clearly indicate that depletion of gonadal hormones 20 or 40 days after gonadectomy modulates the pain-induced behavioral responses related to thermal nociception.

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Substance P and beta-endorphin mediate electro-acupuncture induced analgesia in mouse cancer pain model

Cited by 27 publications

References 22 publications

Painful Pathways Induced by TLR Stimulation of Dorsal Root Ganglion Neurons

Painful Pathways Induced by TLR Stimulation of Dorsal Root Ganglion Neurons

Evidence for the involvement of descending pain-inhibitory mechanisms in the attenuation of cancer pain by carvacrol aided through a docking study

sex difference and effects of gonadal hormones on thermal pain thershold in rat

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