Cyclosporine, an Immunosuppressant, Attenuates Phorbol-Induced Lung Injury in Rats

C. L. Su, C. F. Chen, L. L. Chiang, C. N. Lee, D. Wang, S. L. Lo, S. J. Kao

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Objective: White cell activation in the lung plays a critical role to induce lung injury and lymphocytes in the thoracic duct system may also participate. We evaluated the effect of cyclosporine on phorbol myristate acetate (PMA)-induced lung injury. Materials and Methods: We used an in situ isolated, blood perfused rat lung model to measure pulmonary arterial pressure (PAP) and lung weight gain (LWG; g) for 50 minutes after a bolus injection of PMA (0.05 μg/mL). Oxygen radical release was estimated by an LKB 1251 luminometer and by nitric oxide (NO) release as measured by an ENO-20 NO analyzer. Results: In the group exposed to PMA alone, the mean PAP increased from 16.53 ± 1.28 to 43.33 ± 3.40 mm Hg (P <.001), and lung weight increased by 4.35 ± 0.67 g during the 50-minute perfusion after PMA challenge (P <.001). In vitro measurement showed that PMA induced a significant increase in oxygen radical release (P <.001). PMA attenuated NO release (P <.001) into the perfusion system. Pretreatment with cyclosporine (3 mg/kg) for 3 days prevented the increases in both PAP (P <.01) and LWG (P <.001). NO release was maintained in cyclosporine-pretreated rats. Cyclosporine also showed dose-dependent attenuation of oxygen radical release by PMA-activated white blood cells. Conclusion: The mechanisms responsible for the protective effect of cyclosporine on the lung injury induced by phorbol may be related to an attenuation of oxygen radical production with maintenance of NO release.

Original languageEnglish
Pages (from-to)2709-2711
Number of pages3
JournalTransplantation Proceedings
Volume40
Issue number8
DOIs
Publication statusPublished - Oct 2008

Fingerprint

Lung Injury
Tetradecanoylphorbol Acetate
Immunosuppressive Agents
Cyclosporine
Lung
Nitric Oxide
Reactive Oxygen Species
Arterial Pressure
Perfusion
Thoracic Duct
phorbol
Weight Gain
Leukocytes
Maintenance
Lymphocytes
Weights and Measures
Injections

ASJC Scopus subject areas

  • Surgery
  • Transplantation

Cite this

Cyclosporine, an Immunosuppressant, Attenuates Phorbol-Induced Lung Injury in Rats. / Su, C. L.; Chen, C. F.; Chiang, L. L.; Lee, C. N.; Wang, D.; Lo, S. L.; Kao, S. J.

In: Transplantation Proceedings, Vol. 40, No. 8, 10.2008, p. 2709-2711.

Research output: Contribution to journalArticle

Su, C. L. ; Chen, C. F. ; Chiang, L. L. ; Lee, C. N. ; Wang, D. ; Lo, S. L. ; Kao, S. J. / Cyclosporine, an Immunosuppressant, Attenuates Phorbol-Induced Lung Injury in Rats. In: Transplantation Proceedings. 2008 ; Vol. 40, No. 8. pp. 2709-2711.
@article{700ca8788be24cfab2198e492835e918,
title = "Cyclosporine, an Immunosuppressant, Attenuates Phorbol-Induced Lung Injury in Rats",
abstract = "Objective: White cell activation in the lung plays a critical role to induce lung injury and lymphocytes in the thoracic duct system may also participate. We evaluated the effect of cyclosporine on phorbol myristate acetate (PMA)-induced lung injury. Materials and Methods: We used an in situ isolated, blood perfused rat lung model to measure pulmonary arterial pressure (PAP) and lung weight gain (LWG; g) for 50 minutes after a bolus injection of PMA (0.05 μg/mL). Oxygen radical release was estimated by an LKB 1251 luminometer and by nitric oxide (NO) release as measured by an ENO-20 NO analyzer. Results: In the group exposed to PMA alone, the mean PAP increased from 16.53 ± 1.28 to 43.33 ± 3.40 mm Hg (P <.001), and lung weight increased by 4.35 ± 0.67 g during the 50-minute perfusion after PMA challenge (P <.001). In vitro measurement showed that PMA induced a significant increase in oxygen radical release (P <.001). PMA attenuated NO release (P <.001) into the perfusion system. Pretreatment with cyclosporine (3 mg/kg) for 3 days prevented the increases in both PAP (P <.01) and LWG (P <.001). NO release was maintained in cyclosporine-pretreated rats. Cyclosporine also showed dose-dependent attenuation of oxygen radical release by PMA-activated white blood cells. Conclusion: The mechanisms responsible for the protective effect of cyclosporine on the lung injury induced by phorbol may be related to an attenuation of oxygen radical production with maintenance of NO release.",
author = "Su, {C. L.} and Chen, {C. F.} and Chiang, {L. L.} and Lee, {C. N.} and D. Wang and Lo, {S. L.} and Kao, {S. J.}",
year = "2008",
month = "10",
doi = "10.1016/j.transproceed.2008.07.116",
language = "English",
volume = "40",
pages = "2709--2711",
journal = "Transplantation Proceedings",
issn = "0041-1345",
publisher = "Elsevier USA",
number = "8",

}

TY - JOUR

T1 - Cyclosporine, an Immunosuppressant, Attenuates Phorbol-Induced Lung Injury in Rats

AU - Su, C. L.

AU - Chen, C. F.

AU - Chiang, L. L.

AU - Lee, C. N.

AU - Wang, D.

AU - Lo, S. L.

AU - Kao, S. J.

PY - 2008/10

Y1 - 2008/10

N2 - Objective: White cell activation in the lung plays a critical role to induce lung injury and lymphocytes in the thoracic duct system may also participate. We evaluated the effect of cyclosporine on phorbol myristate acetate (PMA)-induced lung injury. Materials and Methods: We used an in situ isolated, blood perfused rat lung model to measure pulmonary arterial pressure (PAP) and lung weight gain (LWG; g) for 50 minutes after a bolus injection of PMA (0.05 μg/mL). Oxygen radical release was estimated by an LKB 1251 luminometer and by nitric oxide (NO) release as measured by an ENO-20 NO analyzer. Results: In the group exposed to PMA alone, the mean PAP increased from 16.53 ± 1.28 to 43.33 ± 3.40 mm Hg (P <.001), and lung weight increased by 4.35 ± 0.67 g during the 50-minute perfusion after PMA challenge (P <.001). In vitro measurement showed that PMA induced a significant increase in oxygen radical release (P <.001). PMA attenuated NO release (P <.001) into the perfusion system. Pretreatment with cyclosporine (3 mg/kg) for 3 days prevented the increases in both PAP (P <.01) and LWG (P <.001). NO release was maintained in cyclosporine-pretreated rats. Cyclosporine also showed dose-dependent attenuation of oxygen radical release by PMA-activated white blood cells. Conclusion: The mechanisms responsible for the protective effect of cyclosporine on the lung injury induced by phorbol may be related to an attenuation of oxygen radical production with maintenance of NO release.

AB - Objective: White cell activation in the lung plays a critical role to induce lung injury and lymphocytes in the thoracic duct system may also participate. We evaluated the effect of cyclosporine on phorbol myristate acetate (PMA)-induced lung injury. Materials and Methods: We used an in situ isolated, blood perfused rat lung model to measure pulmonary arterial pressure (PAP) and lung weight gain (LWG; g) for 50 minutes after a bolus injection of PMA (0.05 μg/mL). Oxygen radical release was estimated by an LKB 1251 luminometer and by nitric oxide (NO) release as measured by an ENO-20 NO analyzer. Results: In the group exposed to PMA alone, the mean PAP increased from 16.53 ± 1.28 to 43.33 ± 3.40 mm Hg (P <.001), and lung weight increased by 4.35 ± 0.67 g during the 50-minute perfusion after PMA challenge (P <.001). In vitro measurement showed that PMA induced a significant increase in oxygen radical release (P <.001). PMA attenuated NO release (P <.001) into the perfusion system. Pretreatment with cyclosporine (3 mg/kg) for 3 days prevented the increases in both PAP (P <.01) and LWG (P <.001). NO release was maintained in cyclosporine-pretreated rats. Cyclosporine also showed dose-dependent attenuation of oxygen radical release by PMA-activated white blood cells. Conclusion: The mechanisms responsible for the protective effect of cyclosporine on the lung injury induced by phorbol may be related to an attenuation of oxygen radical production with maintenance of NO release.

UR - http://www.scopus.com/inward/record.url?scp=53349107469&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=53349107469&partnerID=8YFLogxK

U2 - 10.1016/j.transproceed.2008.07.116

DO - 10.1016/j.transproceed.2008.07.116

M3 - Article

VL - 40

SP - 2709

EP - 2711

JO - Transplantation Proceedings

JF - Transplantation Proceedings

SN - 0041-1345

IS - 8

ER -