Tan Ding, Li Endian, Xiong Shijie, Sun Yue, Cheng Wenbo, Su Yong, Lu Yang
Laboratory of Gastrointestinal Microbiology, Jiangsu Key Laboratory of Gastrointestinal Nutrition and Animal Health, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.
Institute of Animal Husbandry and Veterinary Science, Shanghai Academy of Agricultural Sciences, Shanghai 201106, China.
Animals (Basel). 2024 Oct 5;14(19):2873. doi: 10.3390/ani14192873.
extract (CME) contains many bioactive compounds, mainly cordycepin (CPN). This study aimed to investigate the possible mechanisms underlying the amelioration of LPS-induced acute liver injury in piglets by CME or CPN supplementation using multi-omics analysis. Twenty-four weaned piglets were randomly distributed into 4 groups ( = 6): the control and LPS groups were fed basal diets; the CPN + LPS (CPN-LPS) and CME + LPS (CME-LPS) groups were fed the basal diets supplemented with CME or CPN. The results showed that CPN or CME supplementation significantly decreased the C-reactive protein level ( < 0.05) and improved liver tissue pathology to prevent acute liver injury after LPS treatment. Compared with LPS, the transcriptomic analysis indicated that CPN supplementation significantly downregulated cell adhesion molecules, while CME supplementation significantly downregulated inflammatory mediator regulation of TRP channels, complement and coagulation cascades and cytokine-cytokine receptor interaction. The metabolomic results showed that CPN or CME supplementation significantly reduced disease biomarker of bicyclo-prostaglandin E2, and increased levels of deoxyinosine and 3-hydroxyanthranilic acid ( < 0.05). The combined transcriptome and metabolome helped identify two metabolites PC 34:2 and PC 36:0, which may be associated with the restoration of liver cell morphology. In conclusion, CPN and CME could attenuate LPS-induced acute liver injury by regulating immune-related genes and metabolites. This study elucidates the potential protective mechanism of CPN or CME supplementation against acute liver injury.
蝉花提取物（CME）含有许多生物活性化合物，主要是虫草素（CPN）。本研究旨在通过多组学分析，探讨补充CME或CPN改善脂多糖（LPS）诱导的仔猪急性肝损伤的潜在机制。24只断奶仔猪随机分为4组（每组n = 6）：对照组和LPS组饲喂基础日粮；CPN + LPS组（CPN-LPS）和CME + LPS组（CME-LPS）饲喂添加了CME或CPN的基础日粮。结果表明，补充CPN或CME可显著降低C反应蛋白水平（P < 0.05），并改善肝组织病理学，以预防LPS处理后的急性肝损伤。与LPS组相比，转录组分析表明，补充CPN可显著下调细胞粘附分子，而补充CME可显著下调TRP通道、补体和凝血级联反应以及细胞因子-细胞因子受体相互作用的炎症介质调节。代谢组学结果表明，补充CPN或CME可显著降低双环前列腺素E2的疾病生物标志物，并增加脱氧肌苷和3-羟基邻氨基苯甲酸的水平（P < 0.05）。转录组和代谢组的联合分析有助于鉴定两种代谢物PC 34:2和PC 36:0，它们可能与肝细胞形态的恢复有关。总之，CPN和CME可通过调节免疫相关基因和代谢物来减轻LPS诱导的急性肝损伤。本研究阐明了补充CPN或CME对急性肝损伤的潜在保护机制。
