Interference of ALOX5 alleviates inflammation and fibrosis in high glucose‑induced renal mesangial cells.

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease (ESRD), seriously threatening the health of individuals. The 5-lipoxygenase (ALOX5) gene has been reported to be associated with diabetes, but whether it is involved in DN remains unclear. The present study aimed to explore the role of ALOX5 in DN and to clarify the potential mechanism. Mouse renal mesangial cells (SV40 MES-13) were treated with high glucose (HG) to mimic a DN model . The expression level of ALOX5 was assessed using reverse transcription-quantitative PCR and western blotting. Cell Counting Kit-8 and flow cytometric assays were performed to determine cell proliferation, the cell cycle and apoptosis. Immunofluorescence was carried out to detect the expression of Ki67 and proliferating cell nuclear antigen (PCNA). The inflammatory cytokines were assessed using ELISA. The expression of fibrosis- and NF-κB-related proteins was determined using western blotting. The results revealed that ALOX5 was significantly upregulated in HG-induced SV40 MES-13 cells. Interference of ALOX5 greatly hindered HG-induced cell viability loss, as well as increasing the expression of Ki67 and PCNA. In addition, HG induced cell cycle arrest in the G1 phase and cell apoptosis, which were then partly abolished by interference of ALOX5. Moreover, the elevated production of inflammatory cytokines and upregulated fibrosis-related proteins induced by HG were weakened by interference of ALOX5. Eventually, interference of ALOX5 was found to reduce the activity of NF-κB signaling in HG-induced SV40 MES-13 cells. Collectively, interference of ALOX5 serves as a protective role in HG-induced kidney cell injury, providing a potential therapeutic strategy of DN treatment.