畜牧兽医学报 ›› 2023, Vol. 54 ›› Issue (6): 2641-2652.doi: 10.11843/j.issn.0366-6964.2023.06.040

• 临床兽医 • 上一篇    下一篇

羊骨胶原肽对镉的螯合作用及对镉致鸡肝损伤的干预作用

赵栋皓, 原梦, 马凯腾, 段卓, 祝一鑫, 唐芳, 韩克光, 霍乃蕊*   

  1. 山西农业大学动物医学学院, 太谷 030801
  • 收稿日期:2022-11-02 出版日期:2023-06-23 发布日期:2023-06-16
  • 通讯作者: 霍乃蕊,主要从事骨代谢疾病防治研究,E-mail:tgnrhuo@163.com
  • 作者简介:赵栋皓(1998-),男,山西阳城人,硕士生,主要从事预防兽医学研究,E-mail:1014006053@qq.com
  • 基金资助:
    山西省重点研发计划课题(202102140601019-2);国家自然科学基金(30870434);山西省回国留学人员项目(2014-042)

Chelating Role of Sheep Bone Collagen Peptide to Cadmium and Its Protection Role against Liver Injuries Induced by Cadmium in Chickens

ZHAO Donghao, YUAN Meng, MA Kaiteng, DUAN Zhuo, ZHU Yixin, TANG Fang, HAN Keguang, HUO Nairui*   

  1. College of Veterinary Medicine, Shanxi Agricultural University, Taigu 030801, China
  • Received:2022-11-02 Online:2023-06-23 Published:2023-06-16

摘要: 环境镉(cadmium, Cd)极易在动植物体内富集,不仅危害动物健康,而且影响食品安全,本研究旨在探究羊骨胶原肽(sheep bone collagen peptide, SBCP)对镉的螯合作用及对镉致鸡肝损伤的干预作用。海兰褐雏鸡随机分组(n=10):对照组常规饲养,模型组(Cd组)饲喂氯化镉添加量为140 mg·kg-1的含镉饲料,SBCP组每天灌胃3 g·kg-1的肽,Cd+SBCP组饲喂与Cd组相同的含镉饲料并灌胃与SBCP组相同的等剂量肽;42 d后测定各组的镉残留水平和肝抗氧化水平,评估肝损伤程度,分析线粒体凋亡途径相关基因的mRNA表达水平。电感耦合等离子体质谱检测结果表明,对照组和SBCP组肝和胸肌中镉残留的检测值为0,Cd组的镉残留分别为412.57 μg·kg-1 (肝)和129.47 μg·kg-1 (胸肌),Cd+SBCP组分别为216.06 μg·kg-1 (肝)和49.68 μg·kg-1 (胸肌);与对照组相比:Cd组肝组织T-SOD和GSH-Px活力显著下降,MDA含量显著升高(P<0.05),血清谷丙转氨酶(ALT)、谷草转氨酶(AST),以及IL-2、IL-8、TNF-α、IFN-γ等炎症因子含量显著增加(P<0.05),肝组织切片显示,肝索排列紊乱,核浓缩坏死,间质淋巴细胞浸润,bax、cyt C、caspase-3和caspase-9等促凋亡基因的mRNA表达水平显著升高(P<0.05),而抗凋亡基因bcl-2表达水平则显著下降(P<0.05)。SBCP干预后:Cd+SBCP组抗氧化酶活力显著升高,MDA含量显著下降(P<0.05),ALT和AST水平以及上述4种炎症因子含量显著减少(P<0.05),肝组织结构明显改善,上述各促凋亡基因的表达水平显著下降,抗凋亡基因表达水平显著升高(P<0.05)。红外谱图显示,SBCP与Cd螯合后生成了一种新物质,且对Cd的螯合率达到47%。SBCP可通过对重金属离子的螯合作用来降低镉残留,减轻镉对鸡只造成的氧化应激和炎症反应,并通过线粒体凋亡途径抑制肝细胞坏死,研究结果为预防畜禽重金属中毒,保障动物性食品安全提供了可借鉴思路。

关键词: 羊骨胶原肽, 肝, 镉中毒, 抗氧化, 线粒体凋亡

Abstract: Environmental cadmium (Cd) is easily enriched in animals and plants, and enter various organisms through the food chain, which in turn, endangers the health of human and animals. The aim of this study is to evaluate the chelation effect of sheep bone collagen peptide (SBCP) with cadmium and determine the protective effects of SBCP against Cd-induced liver injury in chickens. All Hy-line brown chicks were randomly assigned into four groups including control group (basal diet, n=10), Cd group (basal diet with 140 mg·kg-1 Cd, n=10), SBCP group (basal diet with 3 g·kg-1 SBCP, n=10) and Cd + SBCP group (basal diet with 140 mg·kg-1 Cd and 3 g·kg-1 SBCP, n=10). After 42 days, the cadmium residue level, oxidative stress status, histological changes and mRNA expression levels of mitochondrial apoptosis-related genes in liver were detected. The results showed that no Cd were detected in liver and chest muscle of control group and SBCP group by inductively coupled plasma-mass spectrometry (ICP-MS). Cd in liver and chest muscle of Cd group were 412.57 and 129.47 μg·kg-1, respectively. Cd in liver and chest muscle of Cd + SBCP group were 216.06 and 49.68 μg·kg-1, respectively. Meanwhile, compared to control group, the significantly reduced T-SOD and GSH-Px activities, and significantly increased levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and inflammatory cytokines such as IL-2, IL-8, TNF-α, IFN-γ were detected in Cd group. The histopathological results demonstrated that Cd exposure caused disordered arrangement of liver cords, nuclei concentrated necrosis and interstitial lymphocytic infiltration. In addition, Cd exposure significantly increased pro-apoptotic genes bax, cyt C, caspase-3 and caspase-9 expression levels, and significantly reduced the mRNA expression of anti-apoptotic gene bcl-2. However, compared to Cd group, SBCP treatment significantly ameliorated Cd-caused liver injury, reflected by the significantly increased T-SOD and GSH-Px activities, and the significantly decreased levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and inflammatory cytokines. In addition, SBCP treatment improved morphological changes of liver and restored the mRNA expression levels of apoptosis-related genes. Importantly, the results of infrared spectroscopy showed that SBCP chelated with Cd, and produced a new substance, the chelation rate of Cd and SBCP reached 47%. SBCP can reduce cadmium residue by its chelation effect and thus alleviated Cd induced oxidative stress, inflammatory injury and hepatocyte apoptosis. All these results provide theoretical basis that SBCP could be a promising candidate for the prevention of animals poisoning caused by heavy metal.

Key words: sheep bone collagen peptide, liver, cadmium, antioxidant, mitochondrial apoptosis

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