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紫菀皂苷B4通过抑制NF-κB和PI3K/Akt/mTOR信号通路减轻由[具体因素未给出]诱导的蛋鸡坏死性肠炎。

Anemoside B4 attenuates necrotic enteritis of laying hens induced by via inhibiting NF-κB and PI3K/Akt/mTOR signalling pathways.

作者信息

Tian Xinyue, Li Jingyang, Liu Siyu, Dong Qiaoli, Fu Yunjian, Luo Ronghui, Sun Yamin, Guo Ling, Lu Qirong, Ye Chun, Liu Jin, Fu Shulin, Qiu Yinsheng

机构信息

Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan, 430023, PR China.

Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety, Wuhan, 430023, PR China.

出版信息

Heliyon. 2024 Jun 15;10(12):e33161. doi: 10.1016/j.heliyon.2024.e33161. eCollection 2024 Jun 30.

DOI:10.1016/j.heliyon.2024.e33161
PMID:39005924
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11239702/
Abstract

Poultry necrotic enteritis is an important enteric disease which might be controlled by antibiotics. However, with the excessive use of antibiotics, the phenomenon of drug resistance of is becoming increasingly prominent. Anemoside B4 exhibits important anti-inflammatory, antioxidant and immunomodulatory effects. This study was performed to estimate the effect of Anemoside B4 on chicken necrotic enteritis induced by and . In the experiment we investigated the efficacy of Anemoside B4 on the growth curve, biofilm formation, haemolytic activity, virulence-related gene expression and NF-κB and PI3K/AKT/mTOR activation in Caco-2 cells induced by . The results showed that 12.5-50 μg/mL Anemoside B4 had no antibacterial activity but could inhibit biofilm formation, attenuate haemolytic activity and virulence-related gene expression of and weaken NF-κB and PI3K/Akt/mTOR activation triggered by in Caco-2 cells. In the experiment, 60 17-day-old healthy White Leghorns were randomly divided into six groups. The growing laying hens of the control group were fed a basic diet, and those of the five challenged groups were fed a basic diet (infection group), added 0.43 g/kg Anemoside B4 (0.43 g/kg Ane group), 0.86 g/kg Anemoside B4 (0.86 g/kg Ane group), 1.72 g/kg Anemoside B4 (1.72 g/kg Ane group) and 40 mg/kg lincomycin (lincomycin group), respectively. All challenged laying hens were infected with 1 × 10 CFU from day 17-20. Blood and intestinal samples were obtained, and the data demonstrated that Anemoside B4 improved the blood biochemical parameters, attenuated jejunum tissue injury, increased the spleen, thymus, bursa of fabricius index, and decreased lesion scores of the jejunum and the ileum. In the jejunum, Anemoside B4 and lincomycin downregulated the expression of , , , -α and at mRNA levels. Moreover, Anemoside B4 significantly enhanced both mRNA and protein levels of tight junctions ZO-1, Claudin-1 and MUC-2 in the jejunum. Anemoside B4 weakened p-P65, p-PI3K, -Akt and -mTOR protein expression in the jejunum infected by . Diets supplemented with Anemoside B4 alleviated -induced necrotic enteritis in laying hens by inhibiting NF-κB and PI3K/Akt/mTOR signalling pathways and improving intestinal barrier functions.

摘要

家禽坏死性肠炎是一种重要的肠道疾病,可用抗生素进行控制。然而,随着抗生素的过度使用,耐药现象日益突出。薯蓣皂苷元B4具有重要的抗炎、抗氧化和免疫调节作用。本研究旨在评估薯蓣皂苷元B4对由[未提及具体细菌名称]和[未提及具体细菌名称]诱导的鸡坏死性肠炎的影响。在体外实验中,我们研究了薯蓣皂苷元B4对[未提及具体细菌名称]诱导的Caco-2细胞生长曲线、生物膜形成、溶血活性、毒力相关基因表达以及NF-κB和PI3K/AKT/mTOR激活的影响。结果表明,12.5 - 50μg/mL的薯蓣皂苷元B4无抗菌活性,但可抑制生物膜形成,减弱[未提及具体细菌名称]的溶血活性和毒力相关基因表达,并削弱[未提及具体细菌名称]在Caco-2细胞中触发的NF-κB和PI3K/Akt/mTOR激活。在体内实验中,将60只17日龄健康白来航鸡随机分为六组。对照组的生长蛋鸡饲喂基础日粮,五个攻毒组的蛋鸡分别饲喂添加0.43g/kg薯蓣皂苷元B4(0.43g/kg Ane组)、0.86g/kg薯蓣皂苷元B4(0.86g/kg Ane组)、1.72g/kg薯蓣皂苷元B4(1.72g/kg Ane组)和40mg/kg林可霉素(林可霉素组)的基础日粮。所有攻毒蛋鸡在第17至20天感染1×10[未提及具体数量单位]CFU[未提及具体细菌名称]。采集血液和肠道样本,数据表明薯蓣皂苷元B4改善了血液生化参数,减轻了空肠组织损伤,增加了脾脏、胸腺、法氏囊指数,并降低了空肠和回肠的病变评分。在空肠中,薯蓣皂苷元B4和林可霉素在mRNA水平下调了[未提及具体基因名称]、[未提及具体基因名称]、[未提及具体基因名称]、[未提及具体基因名称]-α和[未提及具体基因名称]的表达。此外,薯蓣皂苷元B4显著提高了空肠中紧密连接蛋白ZO-1、Claudin-1和MUC-2的mRNA和蛋白水平。薯蓣皂苷元B4减弱了[未提及具体细菌名称]感染的空肠中p-P65、p-PI3K、[未提及具体蛋白名称]-Akt和[未提及具体蛋白名称]-mTOR的蛋白表达。添加薯蓣皂苷元B4的日粮通过抑制NF-κB和PI3K/Akt/mTOR信号通路以及改善肠道屏障功能,减轻了[未提及具体细菌名称]诱导的蛋鸡坏死性肠炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/44a8c8484eca/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/6fd3d8f6cb56/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/91b24e45fd7f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/eb3c00decbac/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/ebc005ef6abf/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/d62f8aa298c0/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/4ecccfbb86a7/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/b1a2619ef982/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/44a8c8484eca/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/6fd3d8f6cb56/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/91b24e45fd7f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/eb3c00decbac/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/ebc005ef6abf/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/d62f8aa298c0/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/4ecccfbb86a7/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/b1a2619ef982/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1591/11239702/44a8c8484eca/mmcfigs1.jpg

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