Y F Xia1, J H Zhang2, Z F Xu3, X M Deng4. 1. Department of Anesthesiology, Shanghai International Medical Center Shanghai 201318, China. 2. Department of Anesthesiology, Shanghai First People's Hospital, Medical College, Shanghai Jiaotong University Shanghai 200080, China. 3. Department of Anesthesiology, International Peace Maternal and Child Health Hospital, Shanghai Jiaotong University Shanghai 200030, China. 4. Department of Anesthesiology and Critical Care, Changhai Hospital, Second Military Medical University Shanghai 200433, China.
Abstract
BACKGROUND: During mechanical ventilation, high end-inspiratory lung volume results in a permeability type pulmonary oedema, called ventilator-induced lung injury (VILI). The pathophysiology of ventilator-induced lung injury involves multiple mechanisms, such as excessive inflammation. And pycnogenol is a mixture of flavonoid compounds extracted from pine tree bark that have anti-inflammatory activity. OBJECTIVE: We investigated the effects of pyncogenol on ventilator-induced lung injury in rats. METHODS: Rats were orally administrated with pycnogenol once (30 mg/kg) 2 days before lung injury induction with mechanical ventilation, then the rats were divided into three groups: lung-protective ventilation (LV group, n = 20), injurious ventilation (HV group, n = 20), HV + pycnogenol group (HV + Pyc group, n = 20). Lung specimens and the bronchoalveolar lavage fluid (BALF) were isolated for histopathological examinations and biochemical analyses. RESULTS: Pretreatment with pycnogenol could markedly decrease lung wet/dry ratio, lower myeloperoxidase (MPO) activity and total protein concentration and reduce the production of TNF-α, IL-6, IL-1β and MIP-2 in the BALF in ventilator-induced lung injury rats. Additionally, pycnogenol improved the histology of the lung and significantly inhibited the phosphorylation of NF-κB p65 and the degradation of IκB-α. CONCLUSION: Pycnogenol treatment could attenuate ventilator-induced lung injury in rats, at least in part, through its ability to reduce the production of inflammatory cytokines via inhibiting the activation of NF-κB, indicating it as a potential therapeutic candidate for ventilator-induced lung injury.
BACKGROUND: During mechanical ventilation, high end-inspiratory lung volume results in a permeability type pulmonary oedema, called ventilator-induced lung injury (VILI). The pathophysiology of ventilator-induced lung injury involves multiple mechanisms, such as excessive inflammation. And pycnogenol is a mixture of flavonoid compounds extracted from pine tree bark that have anti-inflammatory activity. OBJECTIVE: We investigated the effects of pyncogenol on ventilator-induced lung injury in rats. METHODS:Rats were orally administrated with pycnogenol once (30 mg/kg) 2 days before lung injury induction with mechanical ventilation, then the rats were divided into three groups: lung-protective ventilation (LV group, n = 20), injurious ventilation (HV group, n = 20), HV + pycnogenol group (HV + Pyc group, n = 20). Lung specimens and the bronchoalveolar lavage fluid (BALF) were isolated for histopathological examinations and biochemical analyses. RESULTS: Pretreatment with pycnogenol could markedly decrease lung wet/dry ratio, lower myeloperoxidase (MPO) activity and total protein concentration and reduce the production of TNF-α, IL-6, IL-1β and MIP-2 in the BALF in ventilator-induced lung injuryrats. Additionally, pycnogenol improved the histology of the lung and significantly inhibited the phosphorylation of NF-κB p65 and the degradation of IκB-α. CONCLUSION:Pycnogenol treatment could attenuate ventilator-induced lung injury in rats, at least in part, through its ability to reduce the production of inflammatory cytokines via inhibiting the activation of NF-κB, indicating it as a potential therapeutic candidate for ventilator-induced lung injury.
Entities:
Keywords:
NF-kB pathway; Pycnogenol; flavonoid; inflammation; ventilator-induced ALI
Authors: M B Amato; C S Barbas; D M Medeiros; R B Magaldi; G P Schettino; G Lorenzi-Filho; R A Kairalla; D Deheinzelin; C Munoz; R Oliveira; T Y Takagaki; C R Carvalho Journal: N Engl J Med Date: 1998-02-05 Impact factor: 91.245
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