Luteolin attenuates the pulmonary inflammatory response involves abilities of antioxidation and inhibition of MAPK and NFκB pathways in mice with endotoxin-induced acute lung injury.

Acute lung injury (ALI) in critically ill patients remains the leading cause of mortality and morbidity. Lipopolysaccharide (LPS) is a key mediator of lung injury. This study investigates the protective effects and mechanisms of luteolin in intratracheal instillation of LPS (100μg)-induced ALI in mice.

Protective effects of luteolin against lipopolysaccharide-induced acute lung injury involves inhibition of MEK/ERK and PI3K/Akt pathways in neutrophils.

Aim: To investigate whether luteolin, the major polyphenolic components of Lonicera japonica, has beneficial effects against lipopolysaccharide (LPS)-induced acute lung injury (ALI) and to determine whether the protective mechanism involves anti-inflammatory effects on neutrophils.

Methods: ALI was induced with intratracheal instillation of LPS in mice. The level of ALI was determined by measuring the cell count and protein content in bronchoalveolar lavage (BAL) fluid.

The short-/intermediate-term changes in novel vascular inflammatory markers after angioplasty plus stenting in patients with symptomatic advanced systemic arterial diseases.

Studies on cell adhesion molecules and high-sensitivity C-reactive protein (hs-CRP) in systemic arterial diseases are limited in numbers and some results not consistent. It also remains undefined whether, for how long and to what extent these markers are perturbed after angioplasty. Patients with systemic arterial diseases admitted for percutaneous transluminal angioplasty (PTA) by standard procedures and techniques were prospectively studied.