Abstract：Abstract: Based on the mast cell-mediated angiotensin Ⅱ (AngⅡ) pathway, the mechanism of renal injury in uric acid nephropathy was preliminarily explored. SD rats were randomly divided into control and model groups. The model groups were given adenine at a dose of 100 mg/(kg·d) and fed a diet containing 10% yeast powder. The rat model of uric acid nephropathy was established after continuous intervention for 14 days, 21 days and 28 days, respectively. The levels of blood urea nitrogen (BUN), serum creatinine (SCr), cy-statin-C, serum uric acid (SUA) and urinary uric acid (UUA) were detected by an automatic biochemical ana-lyzer. The pathological changes and mast cells in rat kidneys were observed by HE, Masson and toluidine blue staining. The urinary toxin content in rat kidney was detected by UPLC-MS/MS technology. The levels of serum and kidney glutathione (GSH), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were detected by testing kits. Meanwhile, the content of serum AngⅡ in rats was evaluated by ELISA. The re-sults showed that, with the increase of modeling days, the contents of BUN, SCr, cystatin-C and SUA in-creased significantly (P<0.05), and the content of UUA decreased significantly (P<0.05). Renal histopathology revealed a significant increase in renal tubular dilatation, urate crystal deposition, fibrotic lesions, and a sig-nificant increase in the number of mast cells (P<0.05). The contents of urinary toxins represented by indoxyl sulfate and p-cresol sulfate were significantly increased (P<0.05). The contents of GSH, SOD and GSH-Px in sera and kidneys were significantly decreased (P<0.05). Serum AngⅡ content was significantly increased (P<0.05). The experimental results preliminarily showed that, with the increase of modeling days, the accu-mulation of urate and urine toxins in the kidneys increased, and the kidney damage in rats was aggravated. Mast cells were involved in uric acid kidney injury by promoting the production of AngⅡ and oxidative stress, and reducing serum and kidney GSH, SOD and GSH-Px levels.
引用本文:
张明康, 周 燕, 武新安. 肥大细胞通过血管紧张素Ⅱ途径参与尿酸性肾损伤[J]. 生命科学研究, 2022, 26(4): 301-308. ZHANG Ming-kang, ZHOU Yan, WU Xin-an. Mast Cells Participate in Uric Acid Nephropathy Through Angiotensin II Pathway. Life Science Research, 2022, 26(4): 301-308.
