PMID- 36210587
OWN - NLM
STAT- MEDLINE
DCOM- 20221011
LR  - 20221215
IS  - 2174-2030 (Electronic)
IS  - 0870-2551 (Linking)
VI  - 41
IP  - 10
DP  - 2022 Oct
TI  - Pirfenidone alleviates vascular intima injury caused by hyperhomocysteinemia.
PG  - 813-819
LID - S0870-2551(22)00254-2 [pii]
LID - 10.1016/j.repc.2021.12.011 [doi]
AB  - OBJECTIVES: Hyperhomocysteinemia (HHcy) can induce vascular inflammatory and 
      oxidative damage and accelerate intimal hyperplasia. This study investigated the 
      protective effect of pirfenidone (PFD) on the recovery process of injured 
      endothelial arteries during HHcy. MATERIALS AND METHODS: Thirty rabbits were 
      randomly separated into three groups: A control group (n=10, standard rabbit 
      chow), a model group (n=10, control diet plus 30 g methionine/kg food), and a PFD 
      group (n=10, model diet plus oral administration of 90 mg/day of PFD). After 14 
      weeks of arterial injury, histopathological changes were determined. Plasma 
      homocysteine (Hcy) concentrations, lipid profiles and oxidant and antioxidant 
      status were evaluated. Macrophage infiltration was assessed using 
      immunohistochemical staining. RESULTS: PFD supplementation decreased macrophage 
      infiltration of iliac artery significantly without changes in blood lipids and 
      Hcy concentrations. Compared with the model group, PFD restored superoxide 
      dismutase and glutathione peroxidase activities and reduced malondialdehyde and 
      reactive oxygen species levels. A high-methionine diet significantly increased 
      neointimal area and the ratio between neointimal and media area. Systemic 
      administration of PFD inhibited neointimal formation. CONCLUSIONS: PFD can partly 
      alleviate intimal hyperplasia by inhibiting inflammatory and oxidative stress 
      response induced by HHcy during endothelial injury. It may be a potential 
      therapeutic agent for the prevention and treatment of endothelial 
      injury-associated diseases such as atherosclerosis.
CI  - Copyright (c) 2022 Sociedade Portuguesa de Cardiologia. Publicado por Elsevier 
      Espana, S.L.U. All rights reserved.
FAU - Kong, Junying
AU  - Kong J
AD  - Department of Emergency, Second Affiliated Hospital of Harbin Medical University, 
      Harbin, Hei Long Jiang, China.
FAU - Deng, Ying
AU  - Deng Y
AD  - Department of Emergency, Second Affiliated Hospital of Harbin Medical University, 
      Harbin, Hei Long Jiang, China. Electronic address: tougaoshiyong@163.com.
LA  - eng
LA  - por
PT  - Journal Article
PT  - Randomized Controlled Trial, Veterinary
DEP - 20220716
PL  - Portugal
TA  - Rev Port Cardiol
JT  - Revista portuguesa de cardiologia : orgao oficial da Sociedade Portuguesa de 
      Cardiologia = Portuguese journal of cardiology : an official journal of the 
      Portuguese Society of Cardiology
JID - 8710716
RN  - 0 (Antioxidants)
RN  - 0 (Lipids)
RN  - 0 (Oxidants)
RN  - 0 (Pyridones)
RN  - 0 (Reactive Oxygen Species)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - AE28F7PNPL (Methionine)
RN  - D7NLD2JX7U (pirfenidone)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
CIN - Rev Port Cardiol. 2022 Oct;41(10):821-822. PMID: 36210588
MH  - Animals
MH  - Antioxidants/pharmacology/therapeutic use
MH  - Glutathione Peroxidase/pharmacology/therapeutic use
MH  - Homocysteine/pharmacology/therapeutic use
MH  - *Hyperhomocysteinemia/complications/drug therapy/pathology
MH  - Hyperplasia/pathology
MH  - Lipids
MH  - Malondialdehyde/pharmacology
MH  - Methionine/pharmacology/therapeutic use
MH  - Oxidants/pharmacology/therapeutic use
MH  - Pyridones
MH  - Rabbits
MH  - Reactive Oxygen Species/pharmacology/therapeutic use
MH  - Superoxide Dismutase/pharmacology/therapeutic use
MH  - Tunica Intima/pathology
OTO - NOTNLM
OT  - Aterosclerose
OT  - Atherosclerosis
OT  - Hiperhomocisteinemia
OT  - Hiperplasia da neointima
OT  - Hyperhomocysteinemia
OT  - Inflammatory response
OT  - Lesao vascular
OT  - Neointimal hyperplasia
OT  - Oxidative stress
OT  - Resposta inflamatoria
OT  - Stress oxidativo
OT  - Vascular damage
EDAT- 2022/10/11 06:00
MHDA- 2022/10/12 06:00
CRDT- 2022/10/10 02:07
PHST- 2021/09/29 00:00 [received]
PHST- 2021/12/15 00:00 [revised]
PHST- 2021/12/18 00:00 [accepted]
PHST- 2022/10/10 02:07 [entrez]
PHST- 2022/10/11 06:00 [pubmed]
PHST- 2022/10/12 06:00 [medline]
AID - S0870-2551(22)00254-2 [pii]
AID - 10.1016/j.repc.2021.12.011 [doi]
PST - ppublish
SO  - Rev Port Cardiol. 2022 Oct;41(10):813-819. doi: 10.1016/j.repc.2021.12.011. Epub 
      2022 Jul 16.