PMID- 34017372
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231111
IS  - 1943-8141 (Print)
IS  - 1943-8141 (Electronic)
IS  - 1943-8141 (Linking)
VI  - 13
IP  - 4
DP  - 2021
TI  - Protective mechanism of apigenin in diabetic nephropathy is related to its 
      regulation of miR-423-5P-USF2 axis.
PG  - 2006-2020
AB  - Apigenin (APG), a natural flavonoid with anti-inflammatory and anti-fibrosis 
      properties, has been shown to play a protective role in diabetic nephropathy 
      (DN), but their molecular protection mechanism for miRNA has not been elucidated 
      in detail. This study was designed to focus on exploring its protective role in 
      DN and whether miR-423-5p-upstream stimulating factor 2 (USF2) axis was involved 
      in its protective mechanism. The in vivo model of rat was induced by 
      streptozotocin (STZ) and the in vitro model of renal tubular epithelial cell 
      (RTEC) was induced by high glucose (HG). Our in vivo study revealed that APG had 
      different protective effects on inflammation, renal fibrosis and epithelial 
      mesenchymal transition (EMT) in DN rats, which is mainly reflected in that the 
      inflammatory factors (IL-6, IFN-gamma, TNF-alpha) were obviously down-regulated, the 
      renal fibrosis markers (IV-C, FN, Col I) were significantly inhibited, the 
      E-cadherin (EMT factors) was significantly up-regulated, while the vimentin and 
      alpha-SMA (EMT factors) were significantly down-regulated, and the renal function 
      indexes (serum Cr, BUN) were significantly improved. In terms of mechanism, the 
      protective effect of APG was related to the regulation of the expression of 
      miR-423-5p-USF2 axis, and there was a targeted relationship between miR-423-5p 
      and USF2. Down-regulating miR-423-5p or up-regulating USF2 could significantly 
      aggravate the disease progression of in vitro model and eliminate DN resistance 
      under APG intervention. The above results revealed that the protective role of 
      APG on DN was mediated by miR-423-5p-USF2 axis.
CI  - AJTR Copyright (c) 2021.
FAU - Hou, Yi
AU  - Hou Y
AD  - Department of Urology, China-Japan Union Hospital of Jilin University Changchun 
      130033, Jilin, P. R. China.
FAU - Zhang, Yan
AU  - Zhang Y
AD  - Department of Endocrinology, China-Japan Union Hospital of Jilin University 
      Changchun 130033, Jilin, P. R. China.
FAU - Lin, Sitong
AU  - Lin S
AD  - Department of Endocrinology, China-Japan Union Hospital of Jilin University 
      Changchun 130033, Jilin, P. R. China.
FAU - Yu, Yue
AU  - Yu Y
AD  - Department of Endocrinology, China-Japan Union Hospital of Jilin University 
      Changchun 130033, Jilin, P. R. China.
FAU - Yang, Liu
AU  - Yang L
AD  - Department of Endocrinology, China-Japan Union Hospital of Jilin University 
      Changchun 130033, Jilin, P. R. China.
FAU - Li, Lei
AU  - Li L
AD  - Department of Urology, China-Japan Union Hospital of Jilin University Changchun 
      130033, Jilin, P. R. China.
FAU - Wang, Wenxiang
AU  - Wang W
AD  - Department of Urology, China-Japan Union Hospital of Jilin University Changchun 
      130033, Jilin, P. R. China.
LA  - eng
PT  - Journal Article
DEP - 20210415
PL  - United States
TA  - Am J Transl Res
JT  - American journal of translational research
JID - 101493030
PMC - PMC8129299
OTO - NOTNLM
OT  - Diabetic nephropathy
OT  - USF2
OT  - apigenin
OT  - inflammation/renal fibrosis/epithelial mesenchymal transition
OT  - miR-423-5p
COIS- None.
EDAT- 2021/05/22 06:00
MHDA- 2021/05/22 06:01
PMCR- 2021/04/15
CRDT- 2021/05/21 06:31
PHST- 2020/11/09 00:00 [received]
PHST- 2021/01/04 00:00 [accepted]
PHST- 2021/05/21 06:31 [entrez]
PHST- 2021/05/22 06:00 [pubmed]
PHST- 2021/05/22 06:01 [medline]
PHST- 2021/04/15 00:00 [pmc-release]
PST - epublish
SO  - Am J Transl Res. 2021 Apr 15;13(4):2006-2020. eCollection 2021.