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Effects of caveolin-1 scaffolding domain peptide on LPS-induced acute lung injury in mice / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 1475-1480, 2017.
Article Dans Chinois | WPRIM | ID: wpr-608877
ABSTRACT

AIM:

To investigate the effects of caveolin-1 (Cav-1) scaffolding domain peptide, cavtratin, on lipopolysaccharide (LPS)-induced mouse acute lung injury and heme oxygenase-1 (HO-1) activity.

METHODS:

Adult male BALB/c mice were randomly divided into 6 groups (n=8 to 10) control, Antennapedia internalization sequence (AP), LPS, LPS+hemin, LPS+ hemin+cavtratin and LPS+hemin+cavtratin+zinc protoporphyrin IX (ZnPP) groups.After LPS administration for 24 h, the lung pathological changes, the wet/dry weight (W/D) ratio of lung tissues, total cell number in bronchoalveolar lavage fluid and serum lactate dehydrogenase activity were measured.The co-localization of HO-1 and Cav-1 was displayed by immunofluorescence, and the HO-1 activity were detected.The mRNA expression of pro-inflammatory cytokines IL-1β, IL-6, TNF-α, MCP-1 and iNOS was detected by real-time PCR.

RESULTS:

The mice in LPS+hemin+cavtratin group had the decreased interaction between HO-1 and Cav-1, and the increased HO-1 activity compare with LPS group (P<0.05).Compared with LPS group, the pulmonary damage was attenuated in LPS+hemin+cavtratin group, and the injury indexes, including W/D ratio, total cell number in bronchoalveolar lavage fluid and lactate dehydrogenase activity in the serum, and the mRNA expression of inflammatory cytokines all decreased (P<0.05).HO-1 activity inhibitor ZnPP abolished the above protective effect of cavtratin on the lung tissues with LPS-induced acute lung injury.

CONCLUSION:

Cavtratin has beneficial effects on the lung with LPS-induced acute injury by restoring the HO-1 activity.

Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) langue: Chinois Texte intégral: Chinese Journal of Pathophysiology Année: 2017 Type: Article

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Texte intégral: Disponible Indice: WPRIM (Pacifique occidental) langue: Chinois Texte intégral: Chinese Journal of Pathophysiology Année: 2017 Type: Article