Muramyl Dipeptide Enhances Thermal Injury-Induced Autophagy and Inflammatory Cytokine Response of Lungs via Activation of Nod2/Rick Signaling Pathway in Rats

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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.


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−1 MDP through the left femoral vein. 5.0 mg kg−1 MDP was administered through the left femoral vein at 24 h after thermal injury in the MDP + Scald group.


20% TBSA thermal injury 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 plus 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.


MDP enhances thermal injury-induced autophagy and pro-inflammatory cytokine response of lung injury, which could be achieved via activating the NOD2/RICK signaling pathway in rats.

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