目的:慢性炎症是糖尿病的常见特征,尤其是当血糖水平控制不好时。这种慢性低度炎症可以影响各种器官,包括肾脏.足细胞损伤在糖尿病肾病(DN)的发生发展中起关键作用。该研究的目的是评估BoeravinoneB(BB)对链脲佐菌素(STZ)诱导的大鼠DN的肾保护作用并探讨其潜在机制。
方法:在本实验研究中,大鼠腹腔注射STZ(60mg/kg)诱导DN。口服施用各种剂量的BB(2.5、5和7.5mg/kg)。葡萄糖水平,体重,评估器官重量(肝和肾)。肾,组织形态学,抗氧化剂,肝,和细胞因子水平测定,JAK2和STAT3的mRNA表达水平。在实验研究结束时,处死大鼠,取出肾组织进行组织病理学评估.
结果:BB治疗降低了血糖水平,增加了体重。这种治疗抑制了肝脏重量,肾组织重量增加,还降低了肾脏参数,如尿酸,尿素,胆红素,肌酐(Cr)和,白蛋白。肾肥大指数(KHI)等组织形态参数有下降(P<0.001),平均肾小球体积(MGV),足突融合率(FPFR),用BB治疗后的肾小球基底膜厚度(GBMT)。此外,这种治疗改善了肾podocin的水平,肾CD2相关蛋白(CD2AP)和抑制肝脏参数水平。BB治疗(P<0.001)改变了抗氧化剂参数和细胞因子水平,并抑制JAK2,STAT3,RAGE,KIM-1NAGL,S100A8
结论:给药BB对STZ诱导的DN大鼠具有肾脏保护作用,可能通过减轻氧化应激和炎症反应。
OBJECTIVE: Chronic inflammation is a common feature in diabetes, especially when blood sugar levels are poorly controlled. This chronic low-grade inflammation can affect various organs, including the kidneys. Podocyte damage play a key role in the development of diabetic nephropathy (DN). The aim of the study was to evaluate the nephroprotective effect of Boeravinone B (BB) against streptozotocin (STZ) induced DN in rats and explore the underlying mechanism.
METHODS: In this experimental study, the rats received intraperitoneal injections of STZ (60 mg/kg) to induce DN. Various doses of BB (2.5, 5, and 7.5 mg/kg) were administered orally. Glucose levels, body weights, and organ weights (hepatic and renal) were assessed. Renal, histomorphological, antioxidant, hepatic, and cytokine levels were determined, as were the mRNA expression levels of JAK2 and STAT3. At end of the experimental study, the rats were sacrificed and their renal tissues were removed for histopathological assessment.
RESULTS: BB treatment decreased glucose levels and increased body weights. This treatment suppressed hepatic weights, increased renal tissue weights, and also decreased renal parameters like uric acid, urea, bilirubin, creatinine (Cr) and, albumin. There was a decrease (P<0.001) in histomorphological parameters such as kidney hypertrophy index (KHI), mean glomerular volume (MGV), foot process fusion ratio (FPFR), and glomerular basement membrane thickness (GBMT) after treatment with BB. In addition, this treatment improved the levels of renal podocin, renal CD2- associated protein (CD2AP) and suppressed hepatic parameter levels. BB treatment (P<0.001) altered antioxidant parameters and cytokine levels, and suppressed mRNA expressions of JAK2, STAT3, RAGE, KIM-1, NAGL, and S100A8.
CONCLUSIONS: Administration of BB showed renal protective effects against STZ-induced DN in rats via the reduction of oxidative stress and inflammatory reactions.