Xu Hao-Liang, Li Hui, Bao Rong-Kun, Tang Yi-Xi, Elsherbeni Ahmed Ibrahim Ahmed, Gharib Hassan Bayoumi Ali, Li Jin-Long
College of Veterinary Medicine, Northeast Agricultural University, Harbin, China.
Laboratory of Sport Physiology and Biochemistry, Harbin Sport University, Harbin, China.
Front Vet Sci. 2022 Jun 10;9:938826. doi: 10.3389/fvets.2022.938826. eCollection 2022.
With the development of the intensive poultry industry, the health problems of chickens caused by transportation have attracted more and more attention. Transport stress reduces performance, immune function, and meat quality in chicks, which has become one of the most important factors that endanger the development of the poultry industry. Currently, studies on the effects of transport stress have mainly focused on the performance of livestock and poultry to be slaughtered. However, the effects of transport stress on heart damage and oxidative stress in newborn chicks have not been reported. In this study, we selected newborn chicks as the object. This study was intended to explore the effects of transport stress on the heart damage of newly hatched chicks. The findings suggested that transport stress could cause oxidative stress in the hearts of newly hatched chicks by increasing the levels of malondialdehyde (MDA), hydrogen peroxide (HO) and decreasing the contents of Total antioxidant capacity (T-AOC), and the activities of antioxidant enzymes (SOD), together with increasing the activities of antioxidant enzymes (Catalase (CAT) and Glutathione S-transferase (GST)). Transport stress disrupted the balance between oxidation and antioxidant systems. The Nrf2 signaling pathway was activated by transport stress and triggered the transcription of antioxidant signaling. In short, transport stress-induced nitric oxide (NO)-nitric oxide synthases (NOS) system metabolic disorders and cardiac oxidative stress are mitigated by activating the nuclear factor-erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1)/NAD(P)H quinone oxidoreductase-1 (NQO1) antioxidant defense response in newly hatched chicks.
随着集约化家禽业的发展，运输引起的鸡的健康问题越来越受到关注。运输应激会降低雏鸡的生产性能、免疫功能和肉质，这已成为危及家禽业发展的最重要因素之一。目前，关于运输应激影响的研究主要集中在待屠宰畜禽的生产性能上。然而，运输应激对新生雏鸡心脏损伤和氧化应激的影响尚未见报道。在本研究中，我们选择新生雏鸡作为研究对象。本研究旨在探讨运输应激对新孵化雏鸡心脏损伤的影响。研究结果表明，运输应激可通过增加丙二醛（MDA）、过氧化氢（HO）水平，降低总抗氧化能力（T-AOC）、抗氧化酶（SOD）活性，同时增加抗氧化酶（过氧化氢酶（CAT）和谷胱甘肽S-转移酶（GST））活性，导致新孵化雏鸡心脏氧化应激。运输应激破坏了氧化与抗氧化系统之间的平衡。运输应激激活了Nrf2信号通路并触发了抗氧化信号的转录。简而言之，运输应激诱导的一氧化氮（NO）-一氧化氮合酶（NOS）系统代谢紊乱和心脏氧化应激可通过激活新生雏鸡的核因子红细胞2相关因子2（Nrf2）/血红素加氧酶-1（HO-1）/烟酰胺腺嘌呤二核苷酸磷酸（NAD(P)H）醌氧化还原酶-1（NQO1）抗氧化防御反应得到缓解。
