Study on Improvement Effect and Mechanism of Icariin on Renal Lesion in Rats with Spontaneous Hyper-tension
10.6039/j.issn.1001-0408.2017.10.08
- VernacularTitle:淫羊藿苷对自发性高血压大鼠肾损伤的改善作用及机制研究
- Author:
Ling ZHU
;
Zhiqiang QIAN
;
Yeli LI
;
Junyi WANG
;
Hua YANG
;
Danli YANG
- Keywords:
Icariin;
Spontaneously hypertension rats;
Renal tissue;
p-NF-κB-p65;
TNF-α
- From:
China Pharmacy
2017;28(10):1326-1328
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To observe the effect of pathological lesion of renal tissue in rats with spontaneous hypertension (SHR),and study its mechanisms based on nuclear factorκB(NF-κB)signaling pathway. METHODS:21 SHR were randomly di-vided into model group and ICA low-dose,high-dose groups(20,40 mg/kg,denoted by ICA-L,ICA-H groups);other 7 homolo-gous Kyoto rats (WKY) were regarded as control group. All rats were intragastrically administrated,twice a day,for 11 weeks, rats in control group and model group received equal volume of double distilled water,ig. Pathological changes in renal tissue in each group were observed;Western blot method was used to detect protein expressions of p-NF-κB-p65,IκB and TNF-α in renal tissue. RESULTS:Compared with control group,model group showed disorder renal structure,narrow and irregular glomerular cysts;the protein expression of IκB was significantly down-regulated,protein expressions of p-NF-κB-p65 and TNF-α were signifi-cantly up-regulated(P<0.01). Compared with model group,the above-mentioned changes of rats showed improvement in ICA-L, ICA-H groups;the protein expression of IκB was significantly up-regulated in ICA-L,ICA-H groups (P<0.05 or P<0.01);the protein expressions of p-NF-κB-p65 and TNF-α were significantly down-regulated(P<0.01)in ICA-H groups;p-NF-κB-p65 pro-tein expression was significantly down-regulated in ICA-L group(P<0.05);while there was no significant difference in TNF-αpro-tein expression in ICA-L group(P>0.05). CONCLUSIONS:ICA plays a role in improving renal pathological lesion in SHR,and the mechanism may be related to inhibiting NF-κB signaling pathway.
