In vitro experiments demonstrated that G1 pretreatment significantly inhibited LPS-mediated increases of TNF-α, IL-6, and MIP2 in a dose-dependent manner.Ĭonclusions: These results demonstrated that GPER activation attenuated lung injury of male and OVX female mice by inhibiting the inflammatory response of alveolar macrophages.Ĭurrent treatments for pneumonia (PNA) are focused on the pathogens.

Results: Activation of GPER by G1 administration significantly ameliorated lung pathological damage, attenuated alveolar capillary barrier destruction, inhibited recruitment of inflammatory cells into alveoli, and decreased concentrations of the pro-inflammatory factors tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) in BALF of LPS-administered male and OVX female mice, but not intact female mice. In vitro experiments were also performed on alveolar macrophages (MH-S cells) to investigate the effect of GPER activation on LPS-induced inflammatory responses. Histological injury and inflammatory cell infiltration in lung tissue, as well as cytokine and protein concentrations in BALF were determined. After 24 h, mice were sacrificed to collect blood, bronchoalveolar lavage fluid (BALF), and lung tissue. The GPER-selective agonist G1 or vehicle were intraperitoneally injected 0.5 h before intratracheal administration of LPS or phosphate-buffered saline in male and female mice. Methods: Female mice were randomly subjected to bilateral ovarectomy (OVX) or sham surgery two weeks before lung injury. This study is aimed to investigate the effect of GPER activation on LPS-induced ARDS in mice.

But the role of another estradiol receptor, G protein-coupled estradiol receptor 1 (GPER1) in ARDS are not undertood.

Moreover, the estradiol receptors α, not β,participated in E2-induced attenuation of ARDS. Estrogen can reportedly alleviate ARDS caused by numerous insults in mice. Background: Acute respiratory distress syndrome (ARDS), a common and critical disease, is clinically characterized by uncontrolled inflammation and alveolar-capillary barrier disruption.

Exces de estrogen