PMID- 25420893
OWN - NLM
STAT- MEDLINE
DCOM- 20151222
LR  - 20181202
IS  - 1473-7760 (Electronic)
IS  - 1052-0295 (Linking)
VI  - 90
IP  - 3
DP  - 2015 Apr
TI  - Phosphodiesterase type 5 inhibition attenuates cyclosporine A induced 
      nephrotoxicity in mice.
PG  - 167-78
LID - 10.3109/10520295.2014.976270 [doi]
AB  - We investigated the renal protective effects of phophodiesterase type 5 (PDE5) 
      inhibitors in mice with cyclosporine A (CyA; a calcineurin phosphatase inhibitor) 
      induced nephrotoxicity. Fifty male mice were divided into five groups of 10. 
      Group 1 received no treatment, group 2 received only saline orally, group 3 
      received 30 mg/kg/day CyA by subcutaneous injection, group 4 received only 30 
      mg/kg/day vardenafil orally, and group 5 received 30 mg/kg/day CyA by 
      subcutaneous injection and 30 mg/kg/day vardenafil orally. At 28 days, 
      platelet-derived growth factor A (PDGF-A) and C (PDGF-C), transforming growth 
      factor-beta 1 (TGF-beta1), cyclo-oxygenase 1 and 2 (COX-1 and COX-2), and P 
      glycoprotein (Pgp) expression levels were measured in the renal tissues. In 
      addition, expressions of COX-1 and COX-2 genes were determined using real-time 
      PCR. PDE5 inhibitor administration ameliorated decreased PDGF-A and C, TGF-beta1, 
      COX-1 and -2, and Pgp expression levels by modulation of cyclic guanosine 
      monophosphate (cGMP) activity in kidneys. The relative expressions of COX-1 and 
      COX-2 genes to GAPDH revealed that the maximum increase was obtained in the group 
      treated with CyA and vardenafil for both COX-1 and COX-2 genes. Our study 
      revealed that long term oral treatment with vardenafil protects kidneys from CyA 
      induced nephrotoxicity. We showed that long term oral treatment with PDE5 
      prevents pathological kidney changes caused by CyA induced nephrotoxicity.
FAU - Essiz, D
AU  - Essiz D
AD  - Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, 
      Kirikkale University , 71450, Kirikkale.
FAU - Sozmen, M
AU  - Sozmen M
FAU - Sudagidan, M
AU  - Sudagidan M
FAU - Devrim, A K
AU  - Devrim AK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141125
PL  - England
TA  - Biotech Histochem
JT  - Biotechnic & histochemistry : official publication of the Biological Stain 
      Commission
JID - 9107378
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B, Member 1)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Phosphodiesterase 5 Inhibitors)
RN  - 0 (Platelet-Derived Growth Factor)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 5O8R96XMH7 (Vardenafil Dihydrochloride)
RN  - 83HN0GTJ6D (Cyclosporine)
RN  - EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
RN  - EC 1.2.1.- (Glyceraldehyde-3-Phosphate Dehydrogenases)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily B, Member 1/metabolism
MH  - Animals
MH  - Body Weight/drug effects
MH  - Cyclosporine/*antagonists & inhibitors/*toxicity
MH  - Glyceraldehyde-3-Phosphate Dehydrogenases/metabolism
MH  - Immunohistochemistry
MH  - Immunosuppressive Agents/*toxicity
MH  - Kidney Diseases/*chemically induced/pathology/*prevention & control
MH  - Male
MH  - Mice
MH  - Organ Size/drug effects
MH  - Oxidative Stress/drug effects
MH  - Phosphodiesterase 5 Inhibitors/*pharmacology
MH  - Platelet-Derived Growth Factor/metabolism
MH  - Prostaglandin-Endoperoxide Synthases/metabolism
MH  - Transforming Growth Factor beta1/metabolism
MH  - Vardenafil Dihydrochloride/pharmacology
OTO - NOTNLM
OT  - cyclosporine A
OT  - immunohistochemistry
OT  - nephrotoxicity
OT  - phosphodiesterase type 5
EDAT- 2014/11/26 06:00
MHDA- 2015/12/23 06:00
CRDT- 2014/11/26 06:00
PHST- 2014/11/26 06:00 [entrez]
PHST- 2014/11/26 06:00 [pubmed]
PHST- 2015/12/23 06:00 [medline]
AID - 10.3109/10520295.2014.976270 [doi]
PST - ppublish
SO  - Biotech Histochem. 2015 Apr;90(3):167-78. doi: 10.3109/10520295.2014.976270. Epub 
      2014 Nov 25.