Protective effect of PPAR-αagonist on PAN-induced podocyte injury
10.3969/j.issn.1001-1978.2014.10.011
- VernacularTitle:PPAR-α激动剂对PAN诱导肾小球足细胞损伤的保护作用
- Author:
Junming XU
;
Fangyu PAN
;
Yuan LIU
;
Xiaoyang YUE
;
Jun ZOU
- Publication Type:Journal Article
- Keywords:
PAN;
podocyte injury;
PPAR-α;
fenofi-brate;
structural protein in podocyte;
apoptosis path-way
- From:
Chinese Pharmacological Bulletin
2014;(10):1377-1381,1382
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the function of fenofi-brate on PAN ( puromycin aminonucleoside )-induced podocyte injury. Methods SD female rats of 18-week-old were randomly assigned into 3 groups ( n =6 ) . Mice in PAN group and fenofibrate treated group received a single intravenous injection of PAN ( 65 mg ·kg-1 ) , while those in control group received equal volume of saline. Mice in fenofibrate treated group re-ceived 40 mg · kg-1 · d-1 of fenofibrate ( intragastric administration ) on day 1 after PAN injection , while those in PAN group and control group received equal volume of vehicle. 24 hours urine samples from all group were collected on day 0(1 day before PAN injec-tion), day 6, day 10. The 24 hours urine protein was detected by Bradford assay. All the rats were sacrificed 10 days after the induction of podocyte injury, and glo-merulus sample were collected. The expression of podocyte injury marker and transcription level in apop-tosis, podocyte cytoskeleton protein, slit diaphragm protein were evaluated by Western blot and real-time PCR. Results Compared with the control group, 10 days after injection of PAN, 24 hours urine protein was obviously increased, and the expression and transcrip-tion level of podocyte injury marker desmin, apoptosis, podocyte cytoskeleton protein, slit diaphragm protein were upregulated greatly, however, those were signifi-cantly lower in fenofibrate treated group as compared with those in PAN group. Conclusions PPAR-α ago-nist fenofibrate can ameliorate PAN-induced glomerulus podocyte injury, and the mechanism involved may be associated with inhibition of the mitochondria apopto-sis, TGF-β/Smad pathway and p38 pathway.
