Protective effects of glycated Skipjack (Katsuwonus pelamis) peptide on uric acid-induced injury of human kidney cell(HK-2)
[Objective]The protective effects of Skipjack trypsin hydrolysate (STH) and its maillard product (STH-M) and the segmentation of STH-M (STH-M-S) on uric-acid-induced injury in human kidney (HK-2) cells were investigated. [Methods] HK-2 human kidney cells were cultured in vitro and divided into control group, model group, STH-M groups and STH-M-S groups. HK-2 cell viability was determined by CCK-8 method. The apoptosis and cell cycle of HK-2 cells were detected by flow cytometry. The differentially expressed genes (DEGs) in uric-induced damaged cells and after STH-M treatment were obtained by transcriptional sequencing (RNA-Seq). The DEGs were analyzed, GO functional enrichment analysis and KEGG pathway analysis were performed, and mRNA levels of key genes were verified. [Results] Compared with control group, HK-2 cell vitality was significantly decreased, apoptosis rate was significantly increased, and cell S phase was significantly prolonged in model group (P<0.05). Compared with the model group, the HK-2 cell viability and apoptosis rate of STH-M and STH-M-S groups were significantly increased, the S phase of cell in STH-M group was significantly prolonged, and the S phase of cell in STH-M group was significantly shortened (P<0.05). DEGs are mainly concentrated in the extracellular matrix and are mainly involved in biological processes such as signal transduction and transcriptional regulation. The molecular functions they may perform mainly include protein binding, metal ion binding and nucleotide binding. Key genes were mainly concentrated in Wnt and Hippo signaling pathways and Renin secretion. The accuracy of the sequencing results was verified by the model and the expression level of key genes under the action of the active substance. [Conclusion] STH-M and STH- M-S may regulate cell proliferation, apoptosis, cell cycle, oxidative stress and other processes through Wnt and Hippo signaling pathways and Renin secretion to protect renal cells, providing a theoretical basis for the study of the molecular mechanism of glycosylated skipjack peptides to protect kidney.