Dongying Bai, Wenrui Zhen, Kexin Liu, Xueqing Xiao, Haiqiu Tan, Xiaodi Hu, Xiqiang Ma, Xiaolin Xie, Yi Zhang, Fangshen Guo, Koichi Ito, Bingkun Zhang, Cai Zhang, Yanbo Ma
Our previous research found that when broilers were subjected to LPS-induced immunological stimulation, the Cyclooxygenase-2(COX-2)/Prostaglandin E2 (PGE2)/EP4 pathway was activated in the hypothalamus, leading to decreased production performance. In this study, we investigated the effects of chlorogenic acid (CGA) on the COX-2-related signaling pathway in the hypothalamus of LPS-stressed broilers to explore the mechanism of CGA's improvement in the growth of broilers under immune stress conditions. A total of 336 one-day-old Arbor Acres broilers were randomly assigned to four treatment groups with six replicates of 14 broilers each. The treatment groups were: (i) Saline: broilers injected i.p. with saline and fed with basal diet; (ii) LPS: broilers injected with LPS and fed with basal diet; (iii) 0.1 % CGA: broilers injected with saline and fed basal diet plus 0.1 % CGA; and (iv) 0.1 % CGA+LPS: broilers injected with LPS and fed basal diet plus 0.1 % CGA. Broilers in the four treatment groups were intraperitoneally injected with the same concentration of LPS or saline from 14 days of age for three consecutive days. The lower average daily feed intake (ADFI) and average daily gain (ADG), as well as the increased feed conversion ratio (FCR) in LPS-challenged birds, were alleviated by CGA supplementation (P < 0.05). Dietary CGA mitigated the elevated serum corticosterone (CORT) and TNF-α level (P < 0.05), and the decreased serum IGF-1 concentration (P < 0.05). Further validation by RT-qPCR showed that dietary CGA significantly downregulated the LPS-induced mRNA expression of TLR1B, MyD88, SOCS3, CD40 and STAT1 in the Toll-like receptor signaling pathway (P < 0.05), reducing subsequent COX-2 expression and up-regulating the gene expression of NPY and GHRH (P < 0.05). The results demonstrated that CGA could alleviate LPS-induced immune stress in broilers and that the mechanism was related to inhibition of the hypothalamic COX-2 pathway.