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黄芩苷铜配合物通过靶向AKT/NF-κB信号通路减轻禽致病性大肠杆菌感染雏鸡的肠道损伤。

Baicalin-copper complex alleviates intestinal damage in avian pathogenic -infected chicks by targeting the AKT/NF-κB pathway.

作者信息

Cao Panpan, Wei Jiazhen, Cheng Xinyi, Zhuang Yu, Luo Junrong, Cao Huabin, Zhang Caiying, Guo Xiaoquan, Hu Guoliang

机构信息

Jiangxi Provincial Key Laboratory for Animal Health, College of Animal Science and Technology, Institute of Animal Population Health, Jiangxi Agricultural University, Nanchang, China.

School of Jiangxi Biological Vocational College, Nanchang, China.

出版信息

Front Vet Sci. 2025 Aug 26;12:1648736. doi: 10.3389/fvets.2025.1648736. eCollection 2025.

DOI:10.3389/fvets.2025.1648736
PMID:40933528
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12418448/
Abstract

BACKGROUND

Avian pathogenic (APEC), a primary bacterial pathogen in poultry, induces substantial economic losses to the global poultry industry. The baicalin-copper complex (BCU) demonstrates markedly potentiated anti-inflammatory, anti-oxidant, and anti-tumor efficacy relative to either baicalin or copper in their isolated forms. The present study aimed to evaluate the protective effects of BCU against APEC-induced intestinal damage in chicks.

METHODS

Seventy-five one-day-old chicks were randomly assigned to five groups: control group (basic diet), group (basic diet), and BCU treatment groups (10, 20, and 40mg/kg BCU). After a 15-day feeding period, APEC infection was induced via pectoralis injection to ensure consistent systemic infection. Two days later, the chicks were weighed, and blood samples from the pterygoid vein and ileum tissue were collected for subsequent experiments.

RESULTS

The results showed that compared with the group, BCU reduced both diarrhea and mortality rates, with reductions in the BCU40 group to 27% and 7%, respectively. It also significantly up-regulated the mRNA expression of key intestinal physical barrier proteins (ZO-1, ZO-2, Claudin-1, Claudin-3, and Occludin) and chemical barrier components (Mucin 2 (MUC2) and avian β-defensins (AvBD2, AvBD4) ( < 0.05). Compared with the group, as shown by BCU markedly increased activities of antioxidant enzymes GSH-Px, CAT, SOD and reduced MDA level, which along with increased mRNA expression of the Nrf2-antioxidant signaling pathway ( < 0.05). Furthermore, BCU significantly down-regulated the mRNA expression of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, IL-8, and significantly up-regulated the anti-inflammatory cytokines IL-10 and TGF-β ( < 0.05). Moreover, BCU inhibited the AKT/NF-κB signal pathway, as indicated by markedly reduced the protein expression of p-NF-κB and p-AKT ( < 0.01).

CONCLUSION

Collectively, the findings suggested that BCU effectively alleviates intestinal damage induced by APEC-infection through AKT/NF-κB signal pathway to modulate oxidative stress and inflammatory response.

摘要

背景

禽致病性大肠杆菌(APEC)是家禽中的主要细菌性病原体,给全球家禽业造成了巨大经济损失。黄芩苷铜复合物(BCU)相对于单独的黄芩苷或铜,显示出显著增强的抗炎、抗氧化和抗肿瘤功效。本研究旨在评估BCU对APEC诱导的雏鸡肠道损伤的保护作用。

方法

将75只1日龄雏鸡随机分为五组:对照组(基础日粮)、模型组(基础日粮)和BCU处理组(10、20和40mg/kg BCU)。经过15天的饲养期后,通过胸肌注射诱导APEC感染,以确保一致的全身感染。两天后,对雏鸡称重,并采集翼静脉血样和回肠组织用于后续实验。

结果

结果表明,与模型组相比,BCU降低了腹泻率和死亡率,BCU40组分别降至27%和7%。它还显著上调了关键肠道物理屏障蛋白(ZO-1、ZO-2、Claudin-1、Claudin-3和Occludin)和化学屏障成分(粘蛋白2(MUC2)和禽β-防御素(AvBD2、AvBD4))的mRNA表达(P<0.05)。与模型组相比,BCU显著增加了抗氧化酶GSH-Px、CAT、SOD的活性并降低了MDA水平,同时Nrf2-抗氧化信号通路的mRNA表达增加(P<0.05)。此外,BCU显著下调了促炎细胞因子TNF-α、IL-1β、IL-6、IL-8的mRNA表达,并显著上调了抗炎细胞因子IL-10和TGF-β(P<0.05)。此外,BCU抑制了AKT/NF-κB信号通路,表现为p-NF-κB和p-AKT的蛋白表达显著降低(P<0.01)。

结论

总体而言,研究结果表明,BCU通过AKT/NF-κB信号通路有效减轻APEC感染诱导的肠道损伤,以调节氧化应激和炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/5bceec59324e/fvets-12-1648736-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/a59c90c61f69/fvets-12-1648736-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/34712c7ec634/fvets-12-1648736-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/b26efaa8501b/fvets-12-1648736-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/0d8b46641da3/fvets-12-1648736-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/67df8ab55362/fvets-12-1648736-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/7c53f812fa4e/fvets-12-1648736-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/5bceec59324e/fvets-12-1648736-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/a59c90c61f69/fvets-12-1648736-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/34712c7ec634/fvets-12-1648736-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/b26efaa8501b/fvets-12-1648736-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/0d8b46641da3/fvets-12-1648736-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/67df8ab55362/fvets-12-1648736-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/7c53f812fa4e/fvets-12-1648736-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c968/12418448/5bceec59324e/fvets-12-1648736-g007.jpg

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