慢性热应激通过增强 NF-κB 和 NLRP3 信号通路促进肉鸡肝脏炎症。

BACKGROUND

This study investigated the effects of chronic heat stress on liver inflammatory injury and its potential mechanisms in broilers. Chickens were randomly assigned to the 1-week control group (Control 1), 1-week heat stress group (HS1), 2-week control group (Control 2), and a 2-week heat stress group (HS2) with 15 replicates per group. Broilers in the heat stress groups were exposed to heat stress (35 ± 2 °C) for 8 h/d for 7 or 14 consecutive days, and the rest of 26 hours/day were kept at 23 ± 2 °C like control group broilers. Growth performance and liver inflammatory injury were examined for the analysis of liver injury.

RESULTS

The results showed that heat stress for 2 weeks decreased the growth performance, reduced the liver weight (P < 0.05) and liver index (P < 0.05), induced obvious bleeding and necrosis points. Liver histological changes found that the heat stress induced the liver infiltration of neutrophils and lymphocytes in broilers. Serum levels of AST and SOD were enhanced in HS1 (P < 0.01, P < 0.05) and HS2 (P < 0.01, P < 0.05) group, compared with control 1 and 2 group broilers. The MDA content in HS1 group was higher than that of in control 1 group broilers (P < 0.05). Both the gene and protein expression levels of HSP70, TLR4 and NF-κB in the liver were significantly enhanced by heat stress. Furthermore, heat stress obviously enhanced the expression of IL-6, TNF-α, NF-κB P65, IκB and their phosphorylated proteins in the livers of broilers. In addition, heat stress promoted the activation of NLRP3 with increased NLRP3, caspase-1 and IL-1β levels.

CONCLUSIONS

These results suggested that heat stress can cause liver inflammation via activation of the TLR4-NF-κB and NLRP3 signaling pathways in broilers. With the extension of heat stress time, the effect of heat stress on the increase of NF-κB and NLRP3 signaling pathways tended to slow down.

背景

本研究探讨了慢性热应激对肉鸡肝脏炎症损伤的影响及其潜在机制。将鸡随机分为 1 周对照组（Control 1）、1 周热应激组（HS1）、2 周对照组（Control 2）和 2 周热应激组（HS2），每组 15 个重复。热应激组的鸡连续 7 或 14 天每天暴露于热应激（35±2°C）8 小时，其余 26 小时/天保持在 23±2°C，类似于对照组鸡。为分析肝损伤，检测了生长性能和肝脏炎症损伤。

结果

结果表明，2 周热应激降低了生长性能，降低了肝脏重量（P<0.05）和肝脏指数（P<0.05），引起明显的出血和坏死点。肝脏组织学变化发现，热应激诱导了鸡肝脏中性粒细胞和淋巴细胞的浸润。与对照组 1 和 2 组相比，HS1（P<0.01，P<0.05）和 HS2（P<0.01，P<0.05）组血清 AST 和 SOD 水平升高。HS1 组 MDA 含量高于对照组 1 组鸡（P<0.05）。热应激明显增强了 HSP70、TLR4 和 NF-κB 在肝脏中的基因和蛋白表达水平。此外，热应激明显增强了鸡肝脏中 IL-6、TNF-α、NF-κB P65、IκB 及其磷酸化蛋白的表达。此外，热应激通过激活 TLR4-NF-κB 和 NLRP3 信号通路促进 NLRP3 的激活，增加 NLRP3、caspase-1 和 IL-1β 水平。