Ma Weiming, Wei Wanqing, Dong Yang, Zhao Yan, Xia Tian, Wang Xitao, Han Conghui
Suzhou Medical College of Soochow University, Suzhou, Jiangsu, China.
Department of Urology, Xuzhou Central Hospital, Xuzhou, Jiangsu, China.
J Cell Mol Med. 2024 Dec;28(24):e70250. doi: 10.1111/jcmm.70250.
High intake of dietary linoleic acid may increase the incidence of many diseases. The aim of this research is to examine the impact of linoleic acid on the damage caused by calcium oxalate kidney stones on renal tubular epithelial cells. Calcium oxalate monohydrate (COM) crystals were prepared and used to treat HK-2 cells, which were further treated with different concentrations of linoleic acid in vitro. Also, a small-interfering RNA lentiviral vector of milk fat globule epidermal growth factor 8 (MFGE8) was constructed and transfected into HK-2 cells. The cell viability, level of intracellular ROS and autophagy were tested. In vivo experiments were also carried out with a rat model for renal urolithiasis treated with linoleic acid. The results indicated that COM crystals promoted crystal deposition and apoptosis, increased levels of intracellular Ca and ROS levels and inhibited the proliferation of HK-2 cells. Linoleic acid exacerbated the damage of COM crystal-treated HK-2 cells and renal tubular epithelial cells of the rat model for renal urolithiasis, which can be partially reversed by downregulation of MFGE8. These results collectively suggest that linoleic acid might enhance the damage of renal tubular epithelial cells caused by COM crystals.
高膳食亚油酸摄入量可能会增加多种疾病的发病率。本研究的目的是探讨亚油酸对草酸钙肾结石对肾小管上皮细胞造成的损伤的影响。制备一水合草酸钙（COM）晶体并用于处理HK-2细胞，这些细胞在体外进一步用不同浓度的亚油酸处理。此外，构建了乳脂肪球表皮生长因子8（MFGE8）的小干扰RNA慢病毒载体并转染到HK-2细胞中。检测细胞活力、细胞内ROS水平和自噬水平。还用亚油酸处理的大鼠肾尿石症模型进行了体内实验。结果表明，COM晶体促进晶体沉积和细胞凋亡，增加细胞内Ca水平和ROS水平，并抑制HK-2细胞的增殖。亚油酸加剧了COM晶体处理的HK-2细胞和大鼠肾尿石症模型肾小管上皮细胞的损伤，下调MFGE8可部分逆转这种损伤。这些结果共同表明，亚油酸可能会增强COM晶体对肾小管上皮细胞的损伤。
