Division of Nephrology, The Second Xiangya Hospital, Research Institute of Nephrology, Central South University, Changsha, PR China.
Ren Fail. 2012;34(5):600-9. doi: 10.3109/0886022X.2012.660826. Epub 2012 Feb 27.
To investigate the effect of Shenfushu granule (SFSG) and atropine treatment on microvessels of the kidney and intestine after chronic renal failure (CRF) induced by 5/6 nephrectomy.
Sprague Dawley rats were randomly divided into a sham group, a model group, an SFSG group, and an SFSG + atropine group. SFSG was administered daily 1 week after inducing CRF. Rats were sacrificed at the end of the eighth week. Urinary protein and stool and serum urea nitrogen (UN) and creatinine (Cr) levels were assessed. Hematoxylin and eosin and periodic acid-Schiff staining of the kidney and examination of the vascular endothelial growth factor (VEGF) and microvessel density (MVD) levels in kidney and intestine were performed.
The Cr and UN levels were significantly increased in blood and stool of the model group. SFSG significantly improved renal function, and the protective effects were further enhanced with the addition of atropine. Glomerular sclerosis, tubulointerstitial fibrosis, and microvessel loss were observed in CRF rats, and these pathological changes were ameliorated in the two treatment groups (p < 0.05), especially in the SFSG + atropine group. The expression of VEGF and MVD was decreased in the CRF rats compared with the sham group. SFSG treatment increased the expression of these proteins and reversed the degree of microvessel loss, glomerular sclerosis, and tubulointerstitial fibrosis (p < 0.05). Co-treatment with atropine enhanced these effects.
SFSG alleviated renal function, upregulated the expression of VEGF and MVD in the kidney and intestine, and attenuated the degree of microvessel loss, glomerular sclerosis, and tubulointerstitial fibrosis in the early stages of CRF in rats, and addition of atropine enhanced these effects.
探讨肾衰舒颗粒（SFSG）联合阿托品对 5/6 肾切除诱导的慢性肾衰竭（CRF）大鼠肾脏和肠道微血管的影响。
SD 大鼠随机分为假手术组、模型组、SFSG 组和 SFSG+阿托品组。CRF 诱导后 1 周开始每日给予 SFSG 治疗。第 8 周末处死大鼠，检测尿蛋白和粪便及血清尿素氮（UN）和肌酐（Cr）水平，行肾和肠苏木精-伊红（HE）及过碘酸雪夫（PAS）染色，观察血管内皮生长因子（VEGF）和微血管密度（MVD）在肾脏和肠道的表达。
模型组大鼠血、便中 Cr 和 UN 水平显著升高，SFSG 可明显改善肾功能，加用阿托品后保护作用进一步增强。CRF 大鼠肾小球硬化、肾小管间质纤维化和微血管丢失，两治疗组上述病理改变均有改善（p<0.05），尤以 SFSG+阿托品组明显。与假手术组相比，CRF 大鼠 VEGF 和 MVD 表达降低，SFSG 治疗可增加这些蛋白的表达，逆转微血管丢失、肾小球硬化和肾小管间质纤维化程度（p<0.05），加用阿托品可增强这些作用。
SFSG 可改善 CRF 大鼠早期肾功能，上调肾脏和肠道 VEGF 和 MVD 的表达，减轻微血管丢失、肾小球硬化和肾小管间质纤维化程度，加用阿托品可增强这些作用。
