IL-35 alleviates inflammation progression in a rat model of diabetic neuropathic pain via inhibition of JNK signaling

Journal of Inflammation
Yinghai JiangLingjie Xia

Abstract

Emerging evidence has demonstrated that inflammation is involved in the occurrence and development of diabetic neuropathic pain (DNP). The anti-inflammatory property of interleukin (IL)-35 makes it a promising candidate to block the pain perception. The present study was undertaken to investigate whether IL-35 could attenuate DNP in streptozotocin (STZ)-induced rat model and its potential mechanism. The rat model of DNP was established by a single STZ injection followed by measurements of fasting blood glucose and insulin. Fourteen days after STZ injection, DNP rats were intrathecally injected with IL-35, c-Jun N-terminal kinase (JNK) inhibitor or activator or dimethylsulfoxide (DMSO) as vehicle control, respectively. The mechanical allodynia was assayed to evaluate the therapeutic effect of IL-35. In mechanism study, the serum and protein levels of inflammatory cytokines using ELISA and western blotting and the activation of JNK signaling were further evaluated by quantitative reverse transcription PCR (qRT-PCR). Histopathologic changes were evaluated by Nissl staining. Apoptosis was examined using TUNEL staining. DNP rats exhibited increased fasting blood glucose and insulin levels and reduced insulin sensitivity index (ISI)....Continue Reading

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Citations

Feb 13, 2020·Frontiers in Immunology·Gilson Gonçalves Dos SantosMaripat Corr
Aug 8, 2020·Journal of Cellular and Molecular Medicine·Shanshan ZhaoGuihua Hou
Mar 13, 2021·Progress in Neurobiology·Rabia Bouali-BenazzouzPascal Fossat
Oct 17, 2020·Neurotherapeutics : the Journal of the American Society for Experimental NeuroTherapeutics·Cosmin I Ciotu, Michael J M Fischer
Jul 8, 2021·Seminars in Liver Disease·Ying TangLanlan Yang

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Methods Mentioned

BETA
ELISA
enzyme-linked immunosorbent assay
electrophoresis
PCR

Software Mentioned

SPSS

Related Concepts

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis