Changes in pain behavior induced by formalin, substance P, glutamate and pro-inflammatory cytokines in immobilization-induced stress mouse model

Seo, Young-Jun; Kwon, Min-Soo; Shim, Eon-Jeong; Park, Soo-Hyun; Choi, Ok-Sun; Suh, Hong‐Won

doi:10.1016/j.brainresbull.2006.09.012

Cited by 32 publications

(26 citation statements)

References 54 publications

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“…We also reported pro-inflammatory cytokines induce different pain behaviors than formalin injection or writhing responses (Seo et al, 2006;Shim et al, 2007). Spinal pro-inflammatory cytokines control central sensitization and neuropathic pain development (Watkins et al, 1994;Tadano et al, 1999;Reeve et al, 2000;Robertson et al, 1997;Martucci et al, 2007;Kim et al, 2007).…”

Section: Discussionmentioning

confidence: 91%

Intracerebroventricular gisenosides are antinociceptive in proinflammatory cytokine-induced pain behaviors of mice

et al. 2008

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Several ginsenosides (Rb1, Rb2, Rc, Rd, Re, Rf, Rg1 and Rg3) are neuroprotective and antinociceptive agents. In this study, we assessed the effects of these ginsenosides following intracerebroventricular (i.c.v.) administration on the nociceptive behaviors induced by intrathecal injection of pro-inflammatory cytokines (tumor necrosis factor-a (TNF-alpha), interleukin-1 beta (IL-1 beta), and interferon-gamma (IFN-gamma)). The ginsenosides, Rb1, Rb2, Rc, Rd, Re, Rf and Rg1, significantly attenuated the nociceptive behavior induced by TNF-alpha, IL-1 beta, and IFN-gamma injection, but ginsenoside-Rg3 did not. These results suggest that several ginsenosides may regulate the nociceptive processing induced by pro-inflammatory cytokines.

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Section: Discussionmentioning

confidence: 91%

Intracerebroventricular gisenosides are antinociceptive in proinflammatory cytokine-induced pain behaviors of mice

et al. 2008

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“…The emotional aspect is encoded by the limbic system and encapsulates the relationship between pain and mood (Blackburn and Blackburn 2003). The recent studies have suggested that pain response induced by the activation of nociceptors belongs to stress-induced behavior (Seo et al 2006). One of the responses to stress is the elevation of the blood glucose level (Yamada et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Various pain stimulations cause an increase of the blood glucose level

Sim

Park

Kang

et al. 2012

Animal Cells and Systems

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The relationship between pain stimulation and the blood glucose level was studied in ICR mice. We examined the possible change of the blood glucose level after the pain stimulation induced by acetic acid injected intraperitoneally (i.p.),, formalin injected subcutaneously (s.c.) into the hind paw, or substance P (SP), glutamate, and proinflammatory cytokines (TNF-a and IFN-g) injected intrathecally (i.t.). We found in the present study that acetic acid, formalin, SP, TNF-a, and IFN-g increased the blood glucose level. The blood glucose level reached at maximal state 30 min and returned to normal level 2 h after the pain stimulation in a fasting group. Furthermore, acetic acid, formalin, SP, TNF-a, and IFN-g caused the elevation of the blood glucose level in D-glucose-fed group only in an additive manner. However, i.t. injection of glutamate did not alter the blood glucose level in a fasting group. In contrast, i.t. injection of glutamate enhanced the blood glucose level in the D-glucose-fed group. Our results suggest that the blood glucose level appears to be differentially regulated by various pain stimulation induced by acetic acid, formalin, SP, glutamate, and pro-inflammatory cytokines.

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“…Pain stimulation and its transmission can be processed differently in the spinal and supraspinal regions Choi et al 2001;Hunt & Mantyh 2001). We have previously demonstrated the modality of pain behaviors and mechanisms induced by pro-inflammatory cytokines appear to be different from those induced by subcutaneous injection of formalin into the plantar of the hindpaw or intraperitoneal injection with acetic acid, which induces writhing responses (Seo et al 2006;Shim et al 2007). Spinally administered pro-inflammatory cytokines appear to be involved in the production of central sensitization and neuropathic pain (Watkins et al 1994;Robertson et al 1997;Tadano et al 1999;Reeve et al 2000;Kim et al 2007;Martucci et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Intrathecal treatments with ginsenosides produce antinociceptive effect on proinflammatory cytokines-induced pain behavior in mice

Park

Sim

Kim

et al. 2013

Animal Cells and Systems

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Proinflammatory cytokines have been implicated in the production of neuropathic pain. We have previously reported that several ginsenosides produce antinoception. Especially, we have previously demonstrated that ginsenosides administered supraspinally reduce pain behaviors induced by proinflmmatory cytokines administered spinally. However, spinal action of ginsenosides in the regulation of proinflammtory cytokine-induced pain behavior has not been characterized yet. In the present study, we investigated the effects of ginsenosides following intrathecal treatment on pain behaviors induced by pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-a), interleukin-1b (IL-1b), and interferon-g (IFN-g) injected intrathecally. The ginsenosides such as R b1 , R b2 , R c , R f , R g1 , and R g3 pretreated intrathecally reduced the pain behavior induced by TNF-a, IL-1b, and IFN-g injection. However, ginsenoside R d and R e treated intrathecally did not affect the pain behavior induced by proinflammatory cytokines injected spinally. Our findings suggest that some ginsenosides may exert the antinociceptive effects in proinflammatory cytokine-induced pain model, when they are administered spinally.

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Changes in pain behavior induced by formalin, substance P, glutamate and pro-inflammatory cytokines in immobilization-induced stress mouse model

Cited by 32 publications

References 54 publications

Intracerebroventricular gisenosides are antinociceptive in proinflammatory cytokine-induced pain behaviors of mice

Intracerebroventricular gisenosides are antinociceptive in proinflammatory cytokine-induced pain behaviors of mice

Various pain stimulations cause an increase of the blood glucose level

Intrathecal treatments with ginsenosides produce antinociceptive effect on proinflammatory cytokines-induced pain behavior in mice

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