Department of Pharmacology, School of Pharmacy, Fudan University, Shanghai 201203, China.
Clinical trial institution, Obstetrics and Gynecology Hospital of Fudan University, Shanghai 201203, China.
Chin J Nat Med. 2019 Sep;17(9):641-649. doi: 10.1016/S1875-5364(19)30078-0.
Bupleurum polysaccharides (BPs) is isolated from Bupleurum smithii var. parvifolium, a key traditional Chinese medicine. The study was to investigate the effects of BPs on diabetic kidney injury. After two intraperitoneal injections of streptozotozin (STZ) 100 mg·kg, renal injury in diabetic mice was induced and BPs was orally administrated at dosages of 30 and 60 mg·kg·d. The STZ injected mice developed renal function damage, renal inflammation and fibrosis known as diabetic kidney disease (DKD). BPs significantly reduced serum creatinine level and urinary albumin excretion rate, with the attenuated swelling of kidneys. BPs treatment obviously alleviated the pathological damage of renal tissue. The progression of renal injury in BPs treated mice was inhibited with less expression of type IV collagen (Col IV), fibronectin (FN) and α-smooth muscle actin (α-SMA). The inhibition of inflammation in kidney was associated with the reduced level of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). BPs administration suppressed the over-expression of toll like receptor 4 (TLR4) and high-mobility group box 1 (HMGB1) with lowered activity of nuclear factor kappa B (NF-κB) in renal tissue of diabetic mice. Oral administration of BPs effectively prevented the development ofrenal injury in diabetic mice. This study suggested that the protection provided by BPs might affect through the interruption of HMGB1-TLR4 pathway, leading to the inhibition of renal inflammation and fibrotic process.
柴胡多糖（BPs）从柴胡属植物小柴胡的变种中分离出来，是一种重要的中药。本研究旨在探讨 BPs 对糖尿病肾病损伤的影响。腹腔注射链脲佐菌素（STZ）100mg·kg-1 2 次后，诱导糖尿病小鼠肾损伤，BPs 以 30 和 60mg·kg-1·d-1 的剂量口服给药。注射 STZ 的小鼠发生了肾功能损伤、肾脏炎症和纤维化，即糖尿病肾病（DKD）。BPs 显著降低了血清肌酐水平和尿白蛋白排泄率，同时减轻了肾脏肿胀。BPs 治疗明显减轻了肾脏组织的病理损伤。BPs 治疗小鼠的肾脏损伤进展受到抑制，IV 型胶原（Col IV）、纤维连接蛋白（FN）和α-平滑肌肌动蛋白（α-SMA）的表达减少。肾脏炎症的抑制与肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）水平降低有关。BPs 给药抑制了糖尿病小鼠肾脏组织中 TLR4 和高迁移率族蛋白 B1（HMGB1）的过度表达，核因子 kappa B（NF-κB）活性降低。BPs 口服给药可有效预防糖尿病小鼠肾损伤的发生。本研究表明，BPs 的保护作用可能通过阻断 HMGB1-TLR4 通路来实现，从而抑制肾脏炎症和纤维化过程。
