Abstract | BACKGROUND: Inflammatory molecular signals are modulated by a variety of intracellular transduction pathways, the activation of which may induce and amplify the spread of inflammatory response. Suppresser of cytokine signaling 3 (SOCS3) is an established negative feedback regulation transcription factor associated with tumor, diabetes mellitus, inflammation and anaphylaxis. Herein, we investigated whether SOCS3 in the paraventricular nucleus (PVN) can attenuate pro-inflammatory responses, and thereby relieve the inflammatory pain. METHODS: Adeno-associated virus (AAV) overexpressing SOCS3 was pre-injected into the PVN. Three weeks later, rat model of chronic inflammatory pain was established via subcutaneous injection of complete Freund's adjuvant (CFA) into the plantar center of hind paws. The therapeutic effect of SOCS3 was tested by the measurement of thermal and mechanical allodynia. In mechanistic study, the protein level of SOCS3 was evaluated by Western blotting, and the expression of c-fos and Iba-1 were assessed by immunofluorescent staining. RESULTS: CONCLUSION: Inhibition of IL-6 signaling attenuated inflammatory hyperalgesia in the acute phase. SOCS3 overexpression in the PVN attenuated inflammatory pain in the chronic phase via suppression of neuronal activation.
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Authors | Na Meng, Ning-Ning Ji, Ziming Zhou, Yicheng Qian, Yu Tang, Kangbo Yang, Binbin Chen, Yong-Mei Zhang |
Journal | Journal of inflammation (London, England)
(J Inflamm (Lond))
Vol. 17
Pg. 12
( 2020)
ISSN: 1476-9255 [Print] England |
PMID | 32127783
(Publication Type: Journal Article)
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Copyright | © The Author(s) 2020. |