He Jiawen, Ju Jian, Jiang Qingliang, Zhao Haiyong, Zhang Yingying, Yang Hui
College of Bioscience and Biotechnology, Yangzhou University, 48 Wenhui Road, Yangzhou 225009, China.
College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Animals (Basel). 2025 May 24;15(11):1537. doi: 10.3390/ani15111537.
The hepatopancreas of plays a crucial role in metabolism and immune response, encompassing vital physiological functions. In our study, we established a hepatopancreatic injury model using thioacetamide (TAA) and evaluated the therapeutic potential of a commercial astaxanthin-based product (AST-product) on hepatopancreatic health. The experimental framework included a control group (Con), an injury model group (M), and a treatment group (T), enabling a comprehensive analysis of the effects of treatments on hepatopancreatic biochemical markers, tissue architecture, gene expression, and metabolic pathways. The biochemical results indicated significant oxidative damage and fibrosis in the M group post-TAA treatment, evidenced by increased malondialdehyde (MDA) levels, decreased superoxide dismutase (SOD) activity, and the disruption of tubular structures. Conversely, treatment with the AST-product significantly reduced MDA levels and ameliorated oxidative stress. Histological evaluations using hematoxylin and eosin (HE) and Sirius Red staining confirmed that the AST-product preserved tubular integrity and inhibited fibrosis progression. Metabolomic profiling revealed that the AST-product modulated key metabolic pathways, including arginine and proline metabolism, porphyrin metabolism, and nucleotide metabolism, which are critical for maintaining energy supply and antioxidative capabilities. This modulation mitigated the TAA-induced oxidative damage. Moreover, qPCR analysis demonstrated that the AST-product downregulated the pro-apoptotic gene CASP2, upregulated the energy metabolism-related gene NDUFA7, and enhanced the expression of the immune-related gene lysozyme, thereby boosting pathogen resistance. These findings elucidate the robust protective effects of the AST-product on hepatopancreatic health in , highlighting its potential to reduce oxidative stress, inhibit fibrosis, and enhance immune responses. This study provides a novel strategy for improving health in aquaculture and contributes valuable insights into hepatopancreatic protection and disease prevention in shrimp farming.
[此处原文中“of ”表述不完整，推测是某种生物，暂按“该生物的”翻译]该生物的肝胰腺在新陈代谢和免疫反应中起着至关重要的作用，涵盖重要的生理功能。在我们的研究中，我们使用硫代乙酰胺（TAA）建立了肝胰腺损伤模型，并评估了一种基于虾青素的商业产品（AST产品）对肝胰腺健康的治疗潜力。实验框架包括对照组（Con）、损伤模型组（M）和治疗组（T），能够全面分析治疗对肝胰腺生化标志物、组织结构、基因表达和代谢途径的影响。生化结果表明，TAA处理后M组存在明显的氧化损伤和纤维化，丙二醛（MDA）水平升高、超氧化物歧化酶（SOD）活性降低以及管状结构破坏证明了这一点。相反，AST产品处理显著降低了MDA水平并减轻了氧化应激。使用苏木精和伊红（HE）染色以及天狼星红染色进行的组织学评估证实，AST产品保留了管状完整性并抑制了纤维化进展。代谢组学分析表明，AST产品调节了关键代谢途径，包括精氨酸和脯氨酸代谢、卟啉代谢和核苷酸代谢，这些途径对于维持能量供应和抗氧化能力至关重要。这种调节减轻了TAA诱导的氧化损伤。此外，qPCR分析表明，AST产品下调了促凋亡基因CASP2，上调了能量代谢相关基因NDUFA7，并增强了免疫相关基因溶菌酶的表达，从而提高了对病原体的抵抗力。这些发现阐明了AST产品对该生物肝胰腺健康的强大保护作用，突出了其降低氧化应激、抑制纤维化和增强免疫反应的潜力。本研究为改善水产养殖中该生物的健康提供了一种新策略，并为对虾养殖中的肝胰腺保护和疾病预防提供了有价值的见解。
