Effect of Lipopolysaccharide (LPS) on Oxidative Stress and Apoptosis in Immune Tissues from Schizothorax prenanti.

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.