Pirfenidone alleviates lung ischemia-reperfusion injury in a rat model

Masao Saito, Toyofumi F. Chen-Yoshikawa, Kimitaka Suetsugu, Ryo Okabe, Akihiro Takahagi, Satohiro Masuda, Hiroshi Date

研究成果: ジャーナルへの寄稿記事

3 引用 (Scopus)

抄録

Objective: Lung ischemia-reperfusion injury is among the complications seen after lung transplantation, resulting in morbidity and mortality. Pirfenidone, an antifibrotic agent for the treatment of idiopathic pulmonary fibrosis, is reported to have cytoprotective properties in various disease models. The purpose of this study was to investigate the effect of pirfenidone on lung ischemia-reperfusion injury. Methods: Male Lewis rats (260-290 g) were divided into 3 groups: sham group (n = 5), warm ischemia (WI) group (n = 10), and WI plus pirfenidone (WI+PFD) group (n = 10). The sham group underwent 210 minutes of perfusion without ischemia. The WI and WI+PFD groups underwent 90 minutes of warm ischemia and 120 minutes of reperfusion. In the WI+PFD group, pirfenidone (300 mg/kg) was administered orally by gavage 30 minutes before ischemia. After reperfusion, arterial blood gas analysis, lung mechanics, lung wet-to-dry weight ratio, and histologic findings were obtained. The gene expressions of proinflammatory cytokines in lung tissue were measured by quantitative reverse transcription polymerase chain reaction. Results: Compared with the WI group, the WI+PFD group had significantly better dynamic pulmonary compliance (P <.01) and oxygenation levels (P <.05). The wet-to-dry ratio was lower in the WI+PFD group (P <.05). Histologic analysis showed that the WI+PFD group had reduced perivascular edema and neutrophil infiltration. The expression of tumor necrosis factor-α messenger RNA was decreased in the WI+PFD group (P <.05). Conclusions: Our results revealed that in a rat hilar clamp model, pirfenidone alleviated lung ischemia-reperfusion through anti-inflammatory effects.

元の言語英語
ページ(範囲)289-296
ページ数8
ジャーナルJournal of Thoracic and Cardiovascular Surgery
158
発行部数1
DOI
出版物ステータス出版済み - 7 2019

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Warm Ischemia
Reperfusion Injury
Lung
Reperfusion
Ischemia
pirfenidone
Lung Compliance
Idiopathic Pulmonary Fibrosis
Blood Gas Analysis
Lung Transplantation
Neutrophil Infiltration
Pulmonary Edema
Mechanics
Reverse Transcription
Edema
Anti-Inflammatory Agents

All Science Journal Classification (ASJC) codes

  • Surgery
  • Pulmonary and Respiratory Medicine
  • Cardiology and Cardiovascular Medicine

これを引用

Saito, M., Chen-Yoshikawa, T. F., Suetsugu, K., Okabe, R., Takahagi, A., Masuda, S., & Date, H. (2019). Pirfenidone alleviates lung ischemia-reperfusion injury in a rat model. Journal of Thoracic and Cardiovascular Surgery, 158(1), 289-296. https://doi.org/10.1016/j.jtcvs.2018.08.098

Pirfenidone alleviates lung ischemia-reperfusion injury in a rat model. / Saito, Masao; Chen-Yoshikawa, Toyofumi F.; Suetsugu, Kimitaka; Okabe, Ryo; Takahagi, Akihiro; Masuda, Satohiro; Date, Hiroshi.

:: Journal of Thoracic and Cardiovascular Surgery, 巻 158, 番号 1, 07.2019, p. 289-296.

研究成果: ジャーナルへの寄稿記事

Saito, M, Chen-Yoshikawa, TF, Suetsugu, K, Okabe, R, Takahagi, A, Masuda, S & Date, H 2019, 'Pirfenidone alleviates lung ischemia-reperfusion injury in a rat model', Journal of Thoracic and Cardiovascular Surgery, 巻. 158, 番号 1, pp. 289-296. https://doi.org/10.1016/j.jtcvs.2018.08.098
Saito M, Chen-Yoshikawa TF, Suetsugu K, Okabe R, Takahagi A, Masuda S その他. Pirfenidone alleviates lung ischemia-reperfusion injury in a rat model. Journal of Thoracic and Cardiovascular Surgery. 2019 7;158(1):289-296. https://doi.org/10.1016/j.jtcvs.2018.08.098
Saito, Masao ; Chen-Yoshikawa, Toyofumi F. ; Suetsugu, Kimitaka ; Okabe, Ryo ; Takahagi, Akihiro ; Masuda, Satohiro ; Date, Hiroshi. / Pirfenidone alleviates lung ischemia-reperfusion injury in a rat model. :: Journal of Thoracic and Cardiovascular Surgery. 2019 ; 巻 158, 番号 1. pp. 289-296.
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abstract = "Objective: Lung ischemia-reperfusion injury is among the complications seen after lung transplantation, resulting in morbidity and mortality. Pirfenidone, an antifibrotic agent for the treatment of idiopathic pulmonary fibrosis, is reported to have cytoprotective properties in various disease models. The purpose of this study was to investigate the effect of pirfenidone on lung ischemia-reperfusion injury. Methods: Male Lewis rats (260-290 g) were divided into 3 groups: sham group (n = 5), warm ischemia (WI) group (n = 10), and WI plus pirfenidone (WI+PFD) group (n = 10). The sham group underwent 210 minutes of perfusion without ischemia. The WI and WI+PFD groups underwent 90 minutes of warm ischemia and 120 minutes of reperfusion. In the WI+PFD group, pirfenidone (300 mg/kg) was administered orally by gavage 30 minutes before ischemia. After reperfusion, arterial blood gas analysis, lung mechanics, lung wet-to-dry weight ratio, and histologic findings were obtained. The gene expressions of proinflammatory cytokines in lung tissue were measured by quantitative reverse transcription polymerase chain reaction. Results: Compared with the WI group, the WI+PFD group had significantly better dynamic pulmonary compliance (P <.01) and oxygenation levels (P <.05). The wet-to-dry ratio was lower in the WI+PFD group (P <.05). Histologic analysis showed that the WI+PFD group had reduced perivascular edema and neutrophil infiltration. The expression of tumor necrosis factor-α messenger RNA was decreased in the WI+PFD group (P <.05). Conclusions: Our results revealed that in a rat hilar clamp model, pirfenidone alleviated lung ischemia-reperfusion through anti-inflammatory effects.",
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AU - Takahagi, Akihiro

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N2 - Objective: Lung ischemia-reperfusion injury is among the complications seen after lung transplantation, resulting in morbidity and mortality. Pirfenidone, an antifibrotic agent for the treatment of idiopathic pulmonary fibrosis, is reported to have cytoprotective properties in various disease models. The purpose of this study was to investigate the effect of pirfenidone on lung ischemia-reperfusion injury. Methods: Male Lewis rats (260-290 g) were divided into 3 groups: sham group (n = 5), warm ischemia (WI) group (n = 10), and WI plus pirfenidone (WI+PFD) group (n = 10). The sham group underwent 210 minutes of perfusion without ischemia. The WI and WI+PFD groups underwent 90 minutes of warm ischemia and 120 minutes of reperfusion. In the WI+PFD group, pirfenidone (300 mg/kg) was administered orally by gavage 30 minutes before ischemia. After reperfusion, arterial blood gas analysis, lung mechanics, lung wet-to-dry weight ratio, and histologic findings were obtained. The gene expressions of proinflammatory cytokines in lung tissue were measured by quantitative reverse transcription polymerase chain reaction. Results: Compared with the WI group, the WI+PFD group had significantly better dynamic pulmonary compliance (P <.01) and oxygenation levels (P <.05). The wet-to-dry ratio was lower in the WI+PFD group (P <.05). Histologic analysis showed that the WI+PFD group had reduced perivascular edema and neutrophil infiltration. The expression of tumor necrosis factor-α messenger RNA was decreased in the WI+PFD group (P <.05). Conclusions: Our results revealed that in a rat hilar clamp model, pirfenidone alleviated lung ischemia-reperfusion through anti-inflammatory effects.

AB - Objective: Lung ischemia-reperfusion injury is among the complications seen after lung transplantation, resulting in morbidity and mortality. Pirfenidone, an antifibrotic agent for the treatment of idiopathic pulmonary fibrosis, is reported to have cytoprotective properties in various disease models. The purpose of this study was to investigate the effect of pirfenidone on lung ischemia-reperfusion injury. Methods: Male Lewis rats (260-290 g) were divided into 3 groups: sham group (n = 5), warm ischemia (WI) group (n = 10), and WI plus pirfenidone (WI+PFD) group (n = 10). The sham group underwent 210 minutes of perfusion without ischemia. The WI and WI+PFD groups underwent 90 minutes of warm ischemia and 120 minutes of reperfusion. In the WI+PFD group, pirfenidone (300 mg/kg) was administered orally by gavage 30 minutes before ischemia. After reperfusion, arterial blood gas analysis, lung mechanics, lung wet-to-dry weight ratio, and histologic findings were obtained. The gene expressions of proinflammatory cytokines in lung tissue were measured by quantitative reverse transcription polymerase chain reaction. Results: Compared with the WI group, the WI+PFD group had significantly better dynamic pulmonary compliance (P <.01) and oxygenation levels (P <.05). The wet-to-dry ratio was lower in the WI+PFD group (P <.05). Histologic analysis showed that the WI+PFD group had reduced perivascular edema and neutrophil infiltration. The expression of tumor necrosis factor-α messenger RNA was decreased in the WI+PFD group (P <.05). Conclusions: Our results revealed that in a rat hilar clamp model, pirfenidone alleviated lung ischemia-reperfusion through anti-inflammatory effects.

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