Wuxi Fisheries College, Nanjing Agricultural University, Wuxi, 214081, China.
Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization, Ministry of Agriculture, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, 214081, China.
Fish Shellfish Immunol. 2018 Dec;83:243-248. doi: 10.1016/j.fsi.2018.09.029. Epub 2018 Sep 11.
High glucose levels are known to impair growth and immune function in fish. Here we investigated the role of glucose-6-phosphate dehydrogenase (G6PD) and NADPH oxidase (NOX) in high glucose-associated impairment of leukocyte respiratory burst activity in Megalobrama amblycephala. We cultured peripheral leukocytes isolated from M. amblycephala with media containing no glucose (non-glucose group), 11.1 mmol/L d-glucose (physiologic glucose group), 22.2 mmol/L d-glucose (high-glucose group), or 11.1 mmol/L d-glucose + 100 μmol/L dehydroepiandrosterone (DHEA) (DHEA-treated group). After 24 h, we assayed production of reactive oxygen species (ROS) as a measure of respiratory burst function as well as activity of G6PD and NOX. The high-glucose group and DHEA-treated group showed significantly reduced respiratory burst function, reduced production of ROS, and reduced G6PD and NOX activity at 24 h, compared to the non-glucose and physiologic glucose groups (P < 0.05). The degree of impairment was similar between high-glucose and DHEA-treated groups (P > 0.05). These findings suggest that reduced NADPH availability likely underlies the suppression of respiratory burst function in M. amblycephala leukocytes exposed to high glucose levels.
高糖水平已知会损害鱼类的生长和免疫功能。在这里,我们研究了葡萄糖-6-磷酸脱氢酶(G6PD)和 NADPH 氧化酶(NOX)在高糖相关的鲫鱼白细胞呼吸爆发活性损伤中的作用。我们用含有无葡萄糖(非葡萄糖组)、11.1mmol/L D-葡萄糖(生理葡萄糖组)、22.2mmol/L D-葡萄糖(高葡萄糖组)或 11.1mmol/L D-葡萄糖+100μmol/L 脱氢表雄酮(DHEA)(DHEA 处理组)的培养基培养从鲫鱼分离的外周白细胞。24 小时后,我们测定活性氧(ROS)的产生作为呼吸爆发功能的衡量标准,以及 G6PD 和 NOX 的活性。与非葡萄糖组和生理葡萄糖组相比,高葡萄糖组和 DHEA 处理组在 24 小时时表现出呼吸爆发功能明显降低、ROS 产生减少以及 G6PD 和 NOX 活性降低(P<0.05)。高葡萄糖组和 DHEA 处理组之间的损伤程度相似(P>0.05)。这些发现表明,在暴露于高糖水平的鲫鱼白细胞中,NADPH 可用性的减少可能是呼吸爆发功能抑制的基础。