2012
DOI: 10.1002/j.1532-2149.2012.00114.x
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The indirect antinociceptive mechanism of 15dPGJ2 on rheumatoid arthritis‐induced TMJ inflammatory pain in rats

Abstract: In the present study, we demonstrated that 15d-PGJ2 was able to reduce the RA-induced TMJ inflammatory hypernociception by an indirect mechanism. This antinociceptive effect is in part due to decrease of TNF-α, IL-1β and KC levels and PKA/PKCε expression in the TMJ.

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Cited by 26 publications
(43 citation statements)
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References 46 publications
(62 reference statements)
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“…The arthritic rats showed no visible signs of evoked or spontaneous pain prior to formalin TMJ stimulation. However, low-dose formalin (0.5%), known not to induce pain-related behaviors in normal animals [ 27 ], induced a significant increase of facial grimacing, head flinching, facial rubbing, and bilateral mechanical allodynia ( Figure 2 and Figure 3 ), in accordance with previous studies [ 8 , 28 ]. This suggests that the mBSA-induced monoarthritis is nonpainful per se; however, it induces a profound chemical hypersensitivity to normally nonpainful concentrations of inflammatory substances such as formalin [ 12 ].…”
Section: Discussionsupporting
confidence: 89%
“…The arthritic rats showed no visible signs of evoked or spontaneous pain prior to formalin TMJ stimulation. However, low-dose formalin (0.5%), known not to induce pain-related behaviors in normal animals [ 27 ], induced a significant increase of facial grimacing, head flinching, facial rubbing, and bilateral mechanical allodynia ( Figure 2 and Figure 3 ), in accordance with previous studies [ 8 , 28 ]. This suggests that the mBSA-induced monoarthritis is nonpainful per se; however, it induces a profound chemical hypersensitivity to normally nonpainful concentrations of inflammatory substances such as formalin [ 12 ].…”
Section: Discussionsupporting
confidence: 89%
“…Clinical and experimental research on the pathogenesis and mediators involved in the pain process has been widely developed in the last 20 years. Although some mechanisms involved in this process have already been thoroughly described, others remain to be elucidated [ 16 19 ]. In this context, despite being considered of great relevance in the modulation of inflammatory events and studied in a considerable variety of human diseases [ 20 ], oxidative stress has not yet been investigated in clinical models of preemptive analgesia related to third molars surgery.…”
Section: Introductionmentioning
confidence: 99%
“…Certain mechanisms have been proposed to explain the inflammation that occurs as a result of surgical procedures, but a complete understanding of how these events are fully triggered remains unclear. Proinflammatory cytokines such as TNF-a and interleukin 1 beta (IL-1b) have often been described as important mediators in this process [10][11][12][13] . Experimental studies involving acute pain models suggest that IL-1b sensitizes nociceptors and causes hyperalgesia, therefore working actively in the pathophysiology of this type of pain [14][15][16] .…”
mentioning
confidence: 99%