Protective Effects of Astaxanthin on Thioacetamide-Induced Hepatopancreatic Damage in Procambarus clarkii: Insights from Biochemical, Histological, and Metabolomic Analyses

The hepatopancreas of <i>Procambarus clarkii</i> 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 <i>P. clarkii</i>, highlighting its potential to reduce oxidative stress, inhibit fibrosis, and enhance immune responses. This study provides a novel strategy for improving <i>P. clarkii</i> health in aquaculture and contributes valuable insights into hepatopancreatic protection and disease prevention in shrimp farming.

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Publication Details

Journal
Animals
Published
2025-05-24
DOI
https://doi.org/10.3390/ani15111537
Citations
3
Primary Topic
Aquaculture disease management and microbiota
Type
article
Field-Weighted Citation Impact
2.39

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article

Protective Effects of Astaxanthin on Thioacetamide-Induced Hepatopancreatic Damage in Procambarus clarkii: Insights from Biochemical, Histological, and Metabolomic Analyses

Jiawen He, Qiyu Jiang, Jian Ju, Yingying Zhang et al.
3 citations
Animals
Aquaculture disease management and microbiota
2.39
article

Protective Effects of Astaxanthin on Thioacetamide-Induced Hepatopancreatic Damage in Procambarus clarkii: Insights from Biochemical, Histological, and Metabolomic Analyses

Jiawen He, Qiyu Jiang, Jian Ju, Yingying Zhang, Haiyong Zhao, Hui Yang
article en
3 citations

Abstract

The hepatopancreas of <i>Procambarus clarkii</i> 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 <i>P. clarkii</i>, highlighting its potential to reduce oxidative stress, inhibit fibrosis, and enhance immune responses. This study provides a novel strategy for improving <i>P. clarkii</i> health in aquaculture and contributes valuable insights into hepatopancreatic protection and disease prevention in shrimp farming.

AnimalsVol. 15(11)
Yangzhou University (CN)
National Natural Science Foundation of China, Yangzhou University
Affordable and clean energy
Openalex Percentile: Top 11%
Aquaculture disease management and microbiota
2.39
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