4.5 Article

Resveratrol Suppresses Gut-Derived NLRP3 Inflammasome Partly through Stabilizing Mast Cells in a Rat Model

Journal

MEDIATORS OF INFLAMMATION
Volume 2018, Issue -, Pages -

Publisher

HINDAWI LTD
DOI: 10.1155/2018/6158671

Keywords

-

Funding

  1. Shenzhen Science and Technology Innovation Commission (SZSTI) [JCYJ20150402090413031]
  2. Science and Technology Planning Project of Guangdong Province [2014A020212003]
  3. Shenzhen Maternity and Child Healthcare Hospital [FYB2017017]
  4. Natural Science Foundation of China [81501693, 81601724]
  5. Natural Science Foundation of Guangdong Province [2016A030313232]

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Background. Inflammatory responses induced by intestinal ischemia-reperfusion (IIR) lead to serious systemic organ dysfunction and pose a challenge for current treatment. This study aimed at investigating the effects of resveratrol on IIR-induced intestinal injury and its influence on mast cells (MCs) in rats. Methods. Rats subjected to intestinal ischemia for 60 min and 4 h of IIR were investigated. Animals were randomly divided into five groups (n = 8 per group): sham, IIR, resveratrol (RESV, 15mg/kg/day for 5 days before operation)+IIR, cromolyn sodium (CS, MC membrane stabilizer)+IIR, and RESV+compound 48/80 (CP, MC agonist)+IIR. Results. Intestinal injury and increased proinflammatory cytokines including tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-18 were observed in the IIR group. Intestinal MC-related tryptase and beta-hexosaminidase levels were also increased after rats were subjected to IIR accompanied by activation of NLRP3 inflammasomes. Interestingly, pretreatment with resveratrol significantly suppressed the activities of proinflammatory cytokines and attenuated intestinal injury. Resveratrol also reduced MC and NLRP3 inflammasome activation, which was consistent with the effects of cromolyn sodium. However, the protective effects of resveratrol were reversed by the MC agonist compound 48/80. Conclusions. In summary, these findings reveal that resveratrol suppressed IIR injury by stabilizing MCs, preventing them from degranulation, accompanied with intestinal mucosa NLRP3 inflammasome inhibition and intestinal epithelial cell apoptosis reduction.

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