Shock (Augusta, Ga.) · 2018
Muramyl Dipeptide Enhances Thermal Injury-Induced Autophagy and Inflammatory Cytokine Response of Lungs via Activation of NOD2/Rick Signaling Pathway in Rats.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Wu Xiao-Jing, Liang Hui, Zhang Ying, Yang Xu-Ming, Wang Hong-Yu, Li Hui, Li Xin-Yi, Chen Kai, Wang Yan-Lin, Li Jian-Guo, Zhang Zong-Ze, Song Xue-Min
Аннотация
OBJECTIVE: Nucleotide-binding oligomerization domain 2 (NOD2) is the innate receptor of muramyl dipeptide (MDP). Our previous study revealed that MDP could enhance thermal injury-induced inflammatory cytokine production and organ function injury in rats. The present study was to determine the effect of MDP on autophagy and NOD2/receptor-interacting serine/threonine protein kinases (RICK) signaling pathway of lung injury after thermal injury.
METHODS: Forty male Sprague-Dawlay rats were randomly divided into four groups: normal control (NC) group, MDP group, Scald group, and MDP + Scald group. Scald group only suffered 20% total body surface area third-degree (TBSA) thermal injury. MDP group was only administered 5.0 mg/kg MDP through the left femoral vein; 5.0 mg/kg MDP was administered through the left femoral vein at 24 h after thermal injury in the MDP + Scald group.
RESULTS: TBSA thermal injury (20%) not only significantly increased the plasma inflammatory cytokines production, but also elevated the expression of LC3-I/II, the accumulation of autophagosome in the lung tissue. Compared with the Scald group, MDP + Scald double hit led to more serious inflammatory responses and higher expression of NOD2 mRNA, RICK, NF-κB p65, LC3-I/II, and the accumulation of more autophagosome in the lung tissue.
CONCLUSIONS: MDP enhances thermal injury-induced autophagy and proinflammatory cytokine response of lung injury, which could be achieved via activating the NOD2/RICK signaling pathway in rats.
METHODS: Forty male Sprague-Dawlay rats were randomly divided into four groups: normal control (NC) group, MDP group, Scald group, and MDP + Scald group. Scald group only suffered 20% total body surface area third-degree (TBSA) thermal injury. MDP group was only administered 5.0 mg/kg MDP through the left femoral vein; 5.0 mg/kg MDP was administered through the left femoral vein at 24 h after thermal injury in the MDP + Scald group.
RESULTS: TBSA thermal injury (20%) not only significantly increased the plasma inflammatory cytokines production, but also elevated the expression of LC3-I/II, the accumulation of autophagosome in the lung tissue. Compared with the Scald group, MDP + Scald double hit led to more serious inflammatory responses and higher expression of NOD2 mRNA, RICK, NF-κB p65, LC3-I/II, and the accumulation of more autophagosome in the lung tissue.
CONCLUSIONS: MDP enhances thermal injury-induced autophagy and proinflammatory cytokine response of lung injury, which could be achieved via activating the NOD2/RICK signaling pathway in rats.