Pan Xiaoxia, Wang Jianfu, Pu Yanhua, Yao Jinming, Wang Huanjun
Department of Endocrinology, The Fourth People's Hospital of Ji'nan, Ji'nan, Shandong, China (mainland).
Department of Radiology, The Fourth People's Hospital of Ji'nan, Ji'nan, Shandong, China (mainland).
Med Sci Monit. 2015 Jul 23;21:2134-40. doi: 10.12659/MSM.893714.
As an important factor causing end-stage renal disease, diabetic nephropathy is correlated with low-grade chronic inflammation and immune system activation. This study aimed to investigate the protective function of puerarin on the kidneys of diabetic rats.
A cohort of healthy male SD rats (7 weeks old) were randomly divided into a control group, a model group, and a puerarin treatment group with high (H), moderate (M), and low (L) dosage. After streptozotocin induction, puerarin was applied via intragastric administration for 8 consecutive weeks with dosages of 0.25, 0. 5 and 1.0 mg/(kg·d) for L, M, and H groups, respectively. Fasting blood glucose (BG), creatinine (Scr), urea nitrogen (BUN), and urine albumin excretion rate (UAER) were measured, along with morphological observation of renal cells. The expression of intracellular adhesion molecule 1 (ICAM-1) and tumor necrosis factor α (TNF-α) was determined using immunohistochemical (IHC) staining, while renal cortex cell apoptosis was assayed by in situ end-labeling method.
Model rats had significantly elevated levels of BG, Scr, BUN, and UAER compared to controls (p<0.05). All these increases were partially but significantly suppressed by puerarin (p<0.05), which also caused marked improvement of histopathological damages. Puerarin at each dosage significantly eliminated elevations of ICAM-1 and TNF-α levels in model rats (p<0.05), and decreased apoptotic indexes of renal cortex cells (p<0.05).
Early-stage renal damages can be significantly improved by puerarin, possibly via its suppression of ICAM-1 and TNF-α expression in diabetic rat kidneys.
作为导致终末期肾病的一个重要因素，糖尿病肾病与低度慢性炎症及免疫系统激活相关。本研究旨在探讨葛根素对糖尿病大鼠肾脏的保护作用。
将一组健康雄性SD大鼠（7周龄）随机分为对照组、模型组以及高（H）、中（M）、低（L）剂量葛根素治疗组。经链脲佐菌素诱导后，葛根素分别以0.25、0.5和1.0mg/（kg·d）的剂量连续8周灌胃给药，L、M、H组剂量依次递增。检测空腹血糖（BG）、肌酐（Scr）、尿素氮（BUN）及尿白蛋白排泄率（UAER），并对肾细胞进行形态学观察。采用免疫组化（IHC）染色法检测细胞间黏附分子1（ICAM-1）和肿瘤坏死因子α（TNF-α）的表达水平，采用原位末端标记法检测肾皮质细胞凋亡情况。
与对照组相比，模型大鼠的BG、Scr、BUN和UAER水平显著升高（p<0.05）。葛根素部分但显著地抑制了这些指标的升高（p<0.05），并使组织病理学损伤得到明显改善。各剂量葛根素均显著降低模型大鼠ICAM-1和TNF-α水平的升高（p<0.05），并降低肾皮质细胞凋亡指数（p<0.05）。
葛根素可显著改善糖尿病大鼠早期肾脏损伤，其机制可能是通过抑制ICAM-1和TNF-α在糖尿病大鼠肾脏中的表达实现的。
