Department of Nephropathy, the First Affiliated Hospital of Anhui Medical University.
Biosci Trends. 2017 Jan 16;10(6):489-495. doi: 10.5582/bst.2016.01188. Epub 2016 Dec 24.
Recent evidence suggests that the endoplasmic reticulum stress (ERS)-thioredoxin-interacting protein (TXNIP)-inflammation chain contributes to diabetic renal injury. The aim of the current study was to investigate whether total glucosides of peony (TGP) could inhibit ERS and attenuate up-regulation of TXNIP in the kidneys of rats with streptozotocin-induced diabetes. TGP was orally administered daily at a dose of 50, 100, or 200 mg/kg for 8 weeks. The expression of glucose-regulated protein 78 (GRP78), phospho-protein kinase RNA-like ER kinase (p-PERK), phosphor- eukaryotic translation initiation factor 2α (p-eIF2α), C/EBP-homologous protein (CHOP), and TXNIP was assessed. Results indicated that TGP significantly decreased diabetes-induced albuminuria and it acted by down-regulating activation of the ERS-TXNIP-inflammation chain in the kidneys of diabetic rats. These findings indicate that renoprotection from TGP in diabetic rats possibly contributed to inhibition of ERS and decreased expression of TXNIP. These findings also offer a new perspective from which to study the molecular mechanisms of diabetic nephropathy and prevent its progression.
最近的证据表明，内质网应激（ERS）-硫氧还蛋白相互作用蛋白（TXNIP）-炎症链有助于糖尿病肾损伤。本研究旨在探讨芍药总苷（TGP）是否可以抑制 ERS 并减轻链脲佐菌素诱导的糖尿病大鼠肾脏中 TXNIP 的上调。TGP 每天以 50、100 或 200mg/kg 的剂量口服给药 8 周。评估葡萄糖调节蛋白 78（GRP78）、磷酸蛋白激酶 RNA 样内质网激酶（p-PERK）、磷酸化真核翻译起始因子 2α（p-eIF2α）、C/EBP 同源蛋白（CHOP）和 TXNIP 的表达。结果表明，TGP 可显著降低糖尿病诱导的白蛋白尿，其作用机制可能是通过下调糖尿病大鼠肾脏中 ERS-TXNIP-炎症链的激活。这些发现表明，TGP 对糖尿病大鼠的肾脏保护作用可能归因于抑制 ERS 和降低 TXNIP 的表达。这些发现还为研究糖尿病肾病的分子机制并阻止其进展提供了新的视角。
