Liu Yu, Yuan Junmeng, Xi Wenshuo, Wang Zhisheng, Liu Huawei, Zhang Kai, Zhao Jinshan, Wang Yang
College of Animal Science and Technology, Qingdao Agricultural University, Qingdao 266109, China.
Animals (Basel). 2024 Nov 20;14(22):3335. doi: 10.3390/ani14223335.
Oxidative stress induces apoptosis and ferroptosis, leading to intestinal injury of piglets. P8 (P8) has antioxidant capacity, but its roles in intestinal apoptosis and ferroptosis remain unclear. Here, 24 weaned piglets were assigned to three treatments: control (Con), diquat injection (DQ), and P8 supplementation + DQ injection (DQ + P8). The results showed that the increased jejunal oxidative stress, jejunal morphology impairment, and barrier dysfunction in the DQ-treated piglets were decreased by P8 supplementation. TUNEL and apoptosis-related gene expressions showed increased jejunal apoptosis of DQ-treated piglets; however, reduced apoptosis was observed in the DQ + P8 group. In addition, the mitochondrial morphology and ferroptosis-related gene expressions indicated elevated jejunal ferroptosis in the DQ-treated piglets, and the DQ + P8 treatment attenuated the ferroptosis. Transcriptome identified various differentially expressed genes (DEGs) between different treatments. KEGG analysis indicated that the DEGs were enriched in the PI3K-AKT, NF-κB, and apoptosis pathways. The expressions of key DEGs and key proteins in the PI3K-AKT and NF-κB pathways were further verified. In summary, our results indicate that P8 supplementation ameliorated jejunal oxidative stress, morphological damage, barrier dysfunction, apoptosis, and ferroptosis in the DQ-treated piglets. Moreover, the beneficial effect of P8 may be related to the regulation of PI3K/AKT and NF-κB pathways.
氧化应激诱导细胞凋亡和铁死亡，导致仔猪肠道损伤。P8具有抗氧化能力，但其在肠道细胞凋亡和铁死亡中的作用尚不清楚。在此，将24只断奶仔猪分为三组处理：对照组（Con）、百草枯注射组（DQ）和P8补充+百草枯注射组（DQ + P8）。结果表明，补充P8可降低DQ处理仔猪空肠氧化应激增加、空肠形态损伤和屏障功能障碍。TUNEL和凋亡相关基因表达显示DQ处理仔猪空肠细胞凋亡增加；然而，在DQ + P8组中观察到细胞凋亡减少。此外，线粒体形态和铁死亡相关基因表达表明DQ处理仔猪空肠铁死亡增加，而DQ + P8处理减轻了铁死亡。转录组鉴定了不同处理之间的各种差异表达基因（DEG）。KEGG分析表明，DEG在PI3K-AKT、NF-κB和凋亡途径中富集。进一步验证了PI3K-AKT和NF-κB途径中关键DEG和关键蛋白的表达。总之，我们的结果表明，补充P8可改善DQ处理仔猪的空肠氧化应激、形态损伤、屏障功能障碍、细胞凋亡和铁死亡。此外，P8的有益作用可能与PI3K/AKT和NF-κB途径的调节有关。
