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茴香脑通过激活亚临床坏死性肠炎诱导肉鸡的Nrf2信号通路改善肠道损伤。

-anethole Ameliorates Intestinal Injury Through Activation of Nrf2 Signaling Pathway in Subclinical Necrotic Enteritis-Induced Broilers.

作者信息

Yu Caiyun, Tong Yichun, Li Qiming, Wang Tian, Yang Zaibin

机构信息

College of Animal Sciences and Technology, Nanjing Agricultural University, Nanjing, China.

College of Animal Sciences and Technology, Shandong Agricultural University, Tai'an, China.

出版信息

Front Vet Sci. 2022 Apr 18;9:877066. doi: 10.3389/fvets.2022.877066. eCollection 2022.

Abstract

This study was conducted to investigate the alleviative effects of -anethole (TA) on intestinal oxidative stress by enhancing the activities of intestinal antioxidant enzymes and activating the Nrf2 signaling pathway in subclinical necrotic enteritis (NE) infected broilers. A total of 192 1-day-old male Arbor Acres broilers were randomly allocated into three treatment groups: (1) control (CON); (2) subclinical NE challenge (NE); (3) NE challenge + 600 mg/kg TA (NE+TA600). Subclinical NE was induced by oral administration of live coccidiosis vaccine containing 2 × 10 oocysts at 10 days of age and 2 ml of type A solution (3 × 10 CFU/ml) daily from days 14 to 19. The results showed that NE infection led to a severe decline ( < 0.05) in the final body weight (BW) and average daily gain (ADG), but an increase ( < 0.05) in feed/gain (F/G) of broilers at day 10-21 and day 1-21 compared with the control group. TA administration improved ( < 0.05) the growth performance of NE birds. The intestinal villus height (VH) and villus height/crypt depth (VH/CD) were reduced ( < 0.05) by NE challenge as compared with those of the control group, which was elevated by TA administration. Subclinical NE infection decreased ( < 0.05) serum activities of total superoxide dismutase (T-SOD), total antioxidant capacity (T-AOC), and jejunal and ileal glutathione peroxidase (GSH-PX), and T-SOD activity as well as T-AOC in the jejunum, while TA interventions positively elevated that ( < 0.05). Administration of TA protected the intestine against oxidative stress through up-regulation of intestinal nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway as compared with the NE group ( < 0.05). In addition, dietary inclusion of TA elevated ( < 0.05) mRNA abundance of c-mesenchymal-epithelial transition factor (c-Met), jejunal epidermal growth factor receptor (EGFR), and transforming growth factor-beta 1 (TGF-β1) in the jejunum and ileum of birds after subclinical NE challenge. In conclusion, 600 mg/kg of TA may be a promising tool to prevent and control subclinical NE by increasing intestinal antioxidant status in broilers.

摘要

本研究旨在通过增强肠道抗氧化酶活性和激活亚临床坏死性肠炎(NE)感染肉鸡的Nrf2信号通路,探讨茴香脑(TA)对肠道氧化应激的缓解作用。将192只1日龄雄性艾维茵肉鸡随机分为三个处理组:(1)对照组(CON);(2)亚临床NE攻毒组(NE);(3)NE攻毒+600 mg/kg TA组(NE+TA600)。10日龄时口服含2×10个卵囊的活球虫疫苗,14至19日龄每天口服2 ml A型溶液(3×10 CFU/ml),诱导亚临床NE。结果表明,与对照组相比,NE感染导致肉鸡在10 - 21日龄和1 - 21日龄时终末体重(BW)和平均日增重(ADG)显著下降(P<0.05),但料重比(F/G)升高(P<0.05)。TA给药改善了(P<0.05)NE感染肉鸡的生长性能。与对照组相比,NE攻毒降低了(P<0.05)肠道绒毛高度(VH)和绒毛高度/隐窝深度(VH/CD),而TA给药使其升高。亚临床NE感染降低了(P<0.05)血清总超氧化物歧化酶(T-SOD)、总抗氧化能力(T-AOC)以及空肠和回肠谷胱甘肽过氧化物酶(GSH-PX)的活性,以及空肠中的T-SOD活性和T-AOC,而TA干预使其显著升高(P<0.05)。与NE组相比,TA给药通过上调肠道核因子红细胞2相关因子2(Nrf2)信号通路保护肠道免受氧化应激(P<0.05)。此外,在亚临床NE攻毒后,日粮中添加TA提高了(P<0.05)鸡空肠和回肠中c-间充质-上皮转化因子(c-Met)、空肠表皮生长因子受体(EGFR)和转化生长因子-β1(TGF-β1)的mRNA丰度。总之,600 mg/kg的TA可能是通过提高肉鸡肠道抗氧化状态来预防和控制亚临床NE的一种有前景的手段。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/526c/9062583/6bba9d0f51c1/fvets-09-877066-g0001.jpg

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