This is an early access version, the complete PDF, HTML, and XML versions will be available soon.
Effect of Lipopolysaccharide (LPS) on Oxidative Stress and Apoptosis in Immune Tissues from Schizothorax prenanti
by
,
Jiqin Huang
1,*, 
Wei Jiang
1,
Hongying Ma
1,
Han Zhang
1,
Hu Zhao
1,
Qijun Wang
1 and
Jianlu Zhang
1,2,* 1
Shaanxi Key Laboratory of Qinling Ecological Security, Shaanxi Institute of Zoology, Xi’an 710032, China
2
College of Urban and Environmental Sciences, Northwest University, Xi’an 710127, China
*
Authors to whom correspondence should be addressed.
Animals 2025, 15(9), 1298; https://doi.org/10.3390/ani15091298
Submission received: 4 March 2025
/
Revised: 27 April 2025
/
Accepted: 28 April 2025
/
Published: 30 April 2025
(This article belongs to the Special Issue Oxidative Stress in Aquaculture Organisms: Impact of Environmental Stressors and Nutritional Factors)
Simple Summary
Schizothorax prenanti is a valuable and commercially farmed fish in China. Injecting lipopolysaccharide (LPS) into fish can simulate the reaction of the body after infection. In this study, we found that LPS infection downregulated the catalase and B-cell lymphoma/Leukemia-2 expression levels, and upregulated B-cell lymphoma/Leukemia-2-associated X and cysteine-aspartic-specific protease-3 levels in S. prenanti. Meanwhile, superoxide dismutase and catalase enzymatic activities were inhibited and malondialdehyde content was increased by LPS treatment. Additionally, LPS treatment induced oxidative stress (OS) damage and apoptosis in tissue sections. This study helps us further understand the effects of bacteria or LPS on the OS and apoptosis of immune tissue in fish. Furthermore, we can increase the tolerance of fish to this OS through dietary manipulation in the future.
Abstract
Schizothorax prenanti is an economically important cold-water fish in China. Lipopolysaccharide (LPS) can induce an immune response in S. prenanti; however, little is known about the effects of LPS on oxidative stress (OS) and apoptosis in S. prenanti. In this study, S. prenanti fish were stimulated with LPS at a dose of 10 mg/kg of body weight. After 0 h, 12 h and 24 h, the tissue samples were collected. The OS- and apoptosis-related genes and enzymatic activities in the liver, head kidney (HK), and spleen of S. prenanti were analyzed by a two-way repeated-measures analysis of variance (ANOVA). Hematoxylin and eosin and terminal transferase uridyl nick end labeling staining were also performed. In S. prenanti, LPS administration downregulated the catalase (CAT) and B-cell lymphoma/Leukemia-2 (Bcl-2) expression levels, and upregulated BCL2-associated X (Bax) and cysteine-aspartic-specific protease-3 (caspase-3) expression levels. Meanwhile, superoxide dismutase and CAT enzymatic activities were inhibited and malondialdehyde (MDA) content was increased by LPS treatment. Additionally, LPS treatment induced OS damage and apoptosis in tissue sections. These results indicated that apoptosis in the liver, HK, and spleen of LPS-administered S. prenanti may be mediated by OS via the mitochondrial apoptotic signaling pathway. Our findings are expected to contribute to a better understanding of the responses of different tissues to bacterial challenges. In addition, we can increase the tolerance of fish to the OS through dietary manipulation in the future.
