Wang Huan, Wang Anqi, Wang Xinqiao, Zeng Xiangyin, Xing Houjuan
College of Animal Science and Technology, Northeast Agricultural University, Harbin, 150030, People's Republic of China.
College of Chemical Engineering and Environment, China University of Petroleum, Beijing, 102249, People's Republic of China.
Environ Pollut. 2022 Feb 1;294:118659. doi: 10.1016/j.envpol.2021.118659. Epub 2021 Dec 8.
The experiment was conducted to investigate the effects of Cadmium (Cd) on growth performance, blood biochemical parameters, oxidative stress, hepatocyte apoptosis and autophagy of weaned piglets. A total of 12 healthy weaned piglets were randomly assigned to the control and the Cd group, which were fed with a basal diet and the basal diet supplemented with 15 ± 0.242 mg/kg CdCl for 30 d, respectively. Our results demonstrated that Cd significantly decreased final body weight, average daily feed intake (ADFI), average daily gain (ADG) and increased feed-to-gain (F/G) ratio (P < 0.05). For blood biochemical parameters, Cd treatment significantly decreased the red blood cell (RBC), hemoglobin (HGB), hematocrit (HCT), total protein, albumin, copper content and iron content (P < 0.05). In addition, liver injury was observed in the Cd-exposed group. Our results also demonstrated that Cd exposure contributed to the production of ROS, activated the AMPK/PPAR-γ/NF-κB pathway (increasing the expressions of P-AMPK/AMPK, NF-κB, I-κB-β, COX-2, and iNOS, decreasing the expressions of PPAR-γ and I-κB-α), finally induced autophagy (increasing the expressions of Beclin-1, the ratio of LC3-II/LC3-I and p62), and apoptosis (increasing the expressions of Bax, Bak, Caspase-9, and Caspase-3, decreasing the expression of Bcl-2). Overall, these findings revealed the vital role of AMPK/PPAR-γ/NF-κB pathway in Cd-induced liver apoptosis and autophagy, which provided deeper insights into a better understanding of Cd-induced hepatotoxicity.
本实验旨在研究镉（Cd）对断奶仔猪生长性能、血液生化参数、氧化应激、肝细胞凋亡和自噬的影响。总共12只健康断奶仔猪被随机分为对照组和镉组，分别饲喂基础日粮和添加15±0.242 mg/kg CdCl的基础日粮30天。我们的结果表明，镉显著降低了终末体重、平均日采食量（ADFI）、平均日增重（ADG），并提高了料重比（F/G）（P<0.05）。对于血液生化参数，镉处理显著降低了红细胞（RBC）、血红蛋白（HGB）、血细胞比容（HCT）、总蛋白、白蛋白、铜含量和铁含量（P<0.05）。此外，在镉暴露组中观察到肝损伤。我们的结果还表明，镉暴露促进了活性氧的产生，激活了AMPK/PPAR-γ/NF-κB通路（增加了P-AMPK/AMPK、NF-κB、I-κB-β、COX-2和iNOS的表达，降低了PPAR-γ和I-κB-α的表达），最终诱导了自噬（增加了Beclin-1、LC3-II/LC3-I比值和p62的表达）和凋亡（增加了Bax、Bak、Caspase-9和Caspase-3的表达，降低了Bcl-2的表达）。总体而言，这些发现揭示了AMPK/PPAR-γ/NF-κB通路在镉诱导的肝脏凋亡和自噬中的重要作用，为更好地理解镉诱导的肝毒性提供了更深入的见解。
