Relationship between inflammatory responses and autophagy in lung tissues after scald and NOD2 signaling pathway in septic rats

Objective To evaluate the relationship between inflammatory responses and autophagy in lung tissues after scald and nucleotide-binding oligomerization domain-containing protein 2(NOD2)signaling pathway in septic rats. Methods Twenty SPF healthy male Sprague-Dawley rats, weighing 200-250 g, were divided into control group(group C, n=10) and sepsis after scald group(group SS, n=10)using a random number table.The rats were subjected to a third-degree scald burn covering 20% of total body surface area(body surface was shaved and then exposed to 99-100 ℃ water for 12 s), and 24 h later muramyldipeptide 5 mg/kg was intravenously injected to induce sepsis.The rats were only exposed to 20 ℃ water, and 24 h later normal saline 1 ml was given instead in group C. At 6 h after muramyldipeptide injection in group SS and at 6 h after normal saline injection in group C, arterial blood samples were collected for determination of serum tumor necrosis factor-α and interleukin-6 concentrations by enzyme-linked immunosorbent assay.Then rats were sacrificed and lungs were removed for measurement of activity of myeloperoxidase, NOD2 mRNA expression(using real-time polymerase chain reaction)and expression of receptor interacting protein 2, nuclear factor kappa Bp65 and microtubule-associated protein 1 light chain 3Ⅰ(LC3Ⅰ)and LC3Ⅱ in lung tissues(by Western blot). The LC3Ⅱ/Ⅰratio was calculated. Results Compared with group C, the expression of NOD2 mRNA, receptor interacting protein 2 and nuclear factor kappa Bp65 was significantly up-regulated, and the LC3Ⅱ/Ⅰratio and serum tumor necrosis factor-α and interleukin-6 concentrations were increased in group SS(P<0.05). Conclusion The mechanism underlying enhanced inflammatory responses and autophagy in lung tissues during sepsis after scald may be related to activation of NOD2 signaling pathway in rats. Key words: Burns; Sepsis; Nod2 signaling adaptor protein; Autophagy; Inflammation; Lung