LDHB from grass carp (Ctenopharyngodon idella) mitigates salinity-induced injury in kidney cells

Salinity fluctuation is a major environmental stressor that affects the physiological functions of freshwater fish. Lactate dehydrogenase B (LDHB), a key enzyme involved in lactate/pyruvate interconversion and redox homeostasis, has been implicated in stress adaptation in mammals; however, its role in fish salinity stress responses remains unclear. In this study, we characterized the grass carp (Ctenopharyngodon idella) LDHB homolog and investigated its potential role in alleviating kidney cell injury induced by salinity stress. Sequence analysis showed that grass carp LDHB encodes a 334-amino-acid protein containing the conserved Ldh_1_N and Ldh_1_C domains. Tissue distribution analysis revealed relatively high LDHB expression in the gill, heart, and kidney. Recombinant LDHB protein was successfully expressed in a prokaryotic system and purified for subsequent functional assays. In CIK cells, salinity stress significantly reduced cell viability and increased intracellular lactate levels. Meanwhile, the mRNA expression levels of inflammation-related genes (MyD88, NF-κB p65, IL-1β, and TNF-α) and antioxidant-related genes (SOD, GPX1, Nrf2, and HO-1) were significantly upregulated, accompanied by increased ROS accumulation. Exogenous recombinant LDHB treatment significantly reversed salinity-induced abnormalities, including accumulated intracellular lactate, elevated ROS levels, and the abnormal upregulation of inflammation- and antioxidant-related genes. Taken together, these findings indicate that LDHB participates in modulating salinity-induced metabolic alterations and exerts a protective effect against cellular injury in grass carp. This study lays a theoretical foundation for unraveling the molecular mechanisms underlying salinity adaptation in fish.