Ma Xiao-Hong, Zou Yun, Zhang Yue, He Li-Qun
Department of Nephropathy, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Zhejiang Da Xue Xue Bao Yi Xue Ban. 2013 Sep;42(5):567-72.
To investigate the involvement of MAPK p38 pathway in treatment of chronic renal failure with Jianpi Qinghua Decoction in rats.
Forty SPF SD rats were divided into sham group (n=10),model group (n=10), Jianpi Qinghua group (n=10) and losartan group (n=10). Rat chronic renal failure was induced by 5/6 nephrectomy (Platt method) in model, Jianpi Qinghua and losartan groups, and rats in sham group received sham operation. Jianpi Qinghua decoction (3.9 g 200 g(-1)) or losartan (3.3 g 200 g(-1)) daily were administrated by gavage in Jianpi Qinghua and losartan groups for 60 days, respectively, Rats in sham and model groups were orally administered with saline of the same volume. The serum levels of creatinine and urea nitrogen were measured by biochemical method, the expression of MAPK p38 was detected by Western Blot,and renal pathological changes were observed with hematoxylin-eosin staining.
Compared to model group,serum creatinine levels after 60d in Jianpi Qinghua and losartan groups were decreased significantly (42.67 ± 5.98 or 40.90 ± 5.07 compared with 60.90 ± 9.54, both P<0.01), the expression of MAPK p38 was significantly down-regulated (0.555 ± 0.004 or 0.587 ± 0.045 compared with 0.930 ± 0.265,both P<0.01) and serum urea nitrogen was also decreased (8.56 ± 0.75 or 7.97 ± 0.86 compared with 8.62 ± 0.62,both P<0.05). The renal pathology in the model group presented glomerular mesangial proliferation,hyperplasia of glomenrulus mesangial cells and interstitial inflammation. Those pathological changes were attenuated significantly in Jianpi Qinghua and losartan groups.
Jianpi Qinghua Decoctions can improve the renal function and renal pathological changes in a rat with chronic renal failure, which may be associated with down-regulation of MAPK p38 immune inflammatory pathways.
探讨丝裂原活化蛋白激酶p38（MAPK p38）信号通路在健脾清化方治疗大鼠慢性肾衰竭中的作用机制。
将40只SPF级SD大鼠随机分为假手术组（n = 10）、模型组（n = 10）、健脾清化方组（n = 10）和氯沙坦组（n = 10）。模型组、健脾清化方组和氯沙坦组采用5/6肾切除法（Platt法）制备大鼠慢性肾衰竭模型，假手术组大鼠行假手术。健脾清化方组和氯沙坦组大鼠分别给予健脾清化方（3.9 g·200 g-1）或氯沙坦（3.3 g·200 g-1）灌胃，每日1次，连续60 d；假手术组和模型组大鼠给予等体积生理盐水灌胃。采用生化方法检测血清肌酐和尿素氮水平，Western Blot法检测MAPK p38的表达，苏木精-伊红染色观察肾脏病理变化。
与模型组比较，健脾清化方组和氯沙坦组大鼠60 d后血清肌酐水平显著降低（健脾清化方组42.67±5.98、氯沙坦组40.90±5.07比模型组60.90±9.54，P均<0.01），MAPK p38表达显著下调（健脾清化方组0.555±0.004、氯沙坦组0.587±0.045比模型组0.930±0.265，P均<0.01），血清尿素氮水平也降低（健脾清化方组8.56±0.75、氯沙坦组7.97±0.86比模型组8.62±0.62，P均<0.05）。模型组肾脏病理表现为肾小球系膜增生、肾小球系膜细胞增生和间质炎症，健脾清化方组和氯沙坦组上述病理改变明显减轻。
健脾清化方可改善大鼠慢性肾衰竭的肾功能和肾脏病理变化,其机制可能与下调MAPK p38免疫炎症信号通路有关。
