SGLT2 inhibition and inflammasome pathway and diabetic nephropathy

This study investigated the effects of sodium glucose cotransport 2 (SGLT2) inhibition on cardiac redox homeostasis and inflammation in an experimental model of DN. Male C57BL/6J mice were fed either standard chow (SC) or high-fat diet (HFD) for 16 weeks, with the HFD animals receiving streptozotocin (40 mg/kg) at week 8. At week 17, mice were divided into four groups: Sham, Sham+SGLT2i, DN, and DN+SGLT2i (empagliflozin 35 mg/kg for 8 weeks), and their cardiac tissues were analyzed for oxidative stress markers and inflammatory mediators.

本研究在糖尿病肾病（Diabetic Nephropathy, DN）实验模型中，探究了钠-葡萄糖协同转运蛋白2（sodium glucose cotransport 2, SGLT2）抑制剂对心脏氧化还原稳态与炎症反应的影响。实验中将雄性C57BL/6J小鼠分为两组，分别饲喂标准饲料（standard chow, SC）与高脂饲料（high-fat diet, HFD），造模周期为16周；其中高脂饲料组小鼠于第8周给予链脲佐菌素（streptozotocin, 40 mg/kg）以构建糖尿病肾病模型。第17周时，将小鼠分为四组：假手术组（Sham）、假手术+SGLT2抑制剂组（Sham+SGLT2i）、糖尿病肾病模型组（DN）以及糖尿病肾病+SGLT2抑制剂组（DN+SGLT2i，给予恩格列净35 mg/kg，连续给药8周），随后对各组小鼠的心脏组织开展氧化应激标志物与炎症介质的检测分析。