RESUMO
Objective To observe the changes of NF-κB and inflammatory cytokine expression after CD200 pretreatment in severe heatstroke rats for exploring whether the molecular mechanism of CD200 inhibition of severe heat stroke inflammatory response is related to NF-κB signaling pathway. Methods Forty male Wistar rats were randomly divided into control group (n=8), severe heatstroke model group (HS group, n=16), and CD200 pretreatment group (CD200 group, n=16). The HS group and the CD200 group were injected with physiological saline and CD200 recombinant fusion protein before heat exposure to prepare a classical rat heat stroke model, and the control group was placed at room temperature of 22.0±1.0 ℃. The expression of NF-κB/ p65 mRNA in lung tissue were detected at 60 min after model establishment, and serum high mobility group protein B1 (HMGB1), tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were detected. The pathological changes of the lungs were observed, and the survival time of severe heatstroke rats were recorded. Results CD200 pretreatment could inhibit the expression of NF-κB/p65mRNA. Compared with the control group, the expressions of NF-κB/p65 mRNA in the HS group and CD200 group were significantly increased (P<0.05), and the expression of NF-κB/p65 mRNA in CD200 group was lower than that in HS group (P<0.05). Serum HMGB1, TNF-α and IL-6 in HS group and CD200 group were significantly higher than those in the control group (P<0.05). The HMGB1, TNF-α and IL-6 in the HS group were higher than those in the CD200 group (P<0.05). The median survival time of severe heat stroke were prolonged in the CD200 group compared with the HS group (P<0.05), and the pathomorphological changes showed that inflammation and alveolar exudation were significantly reduced in the CD200 group compared with the HS group. Conclusions CD200 pretreatment can alleviate the inflammatory response in severe heatstroke rats. The possible molecular mechanism of CD200 to relieve severe heatstroke inflammatory response may be involved with NF-κB signaling pathway, which can reduce severe disease by inhibiting the activation of NF-κB and the expression of inflammatory factors.