Oxidative damage in alveolar macrophages exposed to cigarette smoke extract and participation of nitric oxide in redox balance.

Nitric oxide (NO) acts in both pathological and biological processes. We investigated the role of NO in the regulation of cigarette smoke-induced oxidative stress in rat alveolar macrophages (RAM). RAM collected from Wistar rats were cultured in 5% concentration cigarette smoke extract (CSE) for 1h.

Oxidative stress in mouse plasma and lungs induced by cigarette smoke and lipopolysaccharide.

Short-term exposure to cigarette smoke (CS) or lipopolysaccharide (LPS) leads to acute lung inflammation through oxidant-antioxidant imbalance. We studied the response in mice exposed to smoke or LPS during five consecutive days, as measured by superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, as well as lipid peroxidation and nitric oxide levels in bronchoalveolar lavage fluid (BALF), lung homogenates, and plasma. Control mice were exposed to ambient air.

Mate tea reduced acute lung inflammation in mice exposed to cigarette smoke.

Objective: Short-term cigarette smoke exposure has been associated with acute lung inflammation (ALI) and oxidative damage. We studied mate tea (Ilex paraguariensis infusion) as a possible nutritional resource for ALI.

Methods: C57BL/6 mice (n = 30) were administered with mate tea orally (150 mg/kg, CSMO), mate tea intraperitonially (150 mg/kg, CSMIP), or the vehicle (CS) and then exposed to cigarette smoke for 5 d (six cigarettes per day).

Alpha-tocopherol and ascorbic acid supplementation reduced acute lung inflammatory response by cigarette smoke in mouse.

Objective: Short-term cigarette smoke (CS) exposure leads to acute lung inflammation through its influence over oxidants/antioxidants imbalance. Antioxidant vitamins such as ascorbic acid and alpha-tocopherol interact with oxidizing radicals. It is not clear if antioxidant supplementation can reduce inflammatory lung responses.

Light cigarette smoke-induced emphysema and NFkappaB activation in mouse lung.

Light cigarette (LC) exposure is supposed to be less hazardous with a decreased incidence of cancer and tobacco-associated diseases. C57BL/6 mouse groups were subjected to smoke from 3, 6 or 12 LC for 60 days and compared with mice exposed to ambient air (EAA) in order to study lung injury by morphometrical and biochemical methods. Bronchoalveolar lavage (BAL) analysis and histology and stereology were performed.

Design, synthesis and antiinflammatory activity of novel phthalimide derivatives, structurally related to thalidomide.

As part of an ongoing effort to develop new thalidomide analogues as antiinflammatory lead-candidates, this paper describes the synthesis and antiinflammatory activity of novel N-phenyl-phthalimide functionalized derivatives (4a-d, 5a,b, 6a,b). The target compounds were assayed in an acute lung inflammatory model and all compounds were able to inhibit TNF-alpha production and subsequent neutrophil recruitment in the LPS-acute lung inflammatory model.

Inhibition of interleukin-1beta reduces mouse lung inflammation induced by exposure to cigarette smoke.

We examined nuclear factor kappaB activation, release of inflammatory mediators and cellular infiltration in acute cigarette smoke inflammation models. One hour after exposure to one puff of cigarette smoke, alveolar macrophages from bronchoalveolar lavage (BAL) fluid of C57BL/6J mice showed an increased activity of nuclear factor kappaB-DNA binding but similar numbers as compared to that of BAL fluid from mice exposed to ambient air. Exposure to 1 cigarette/day for 1, 4 or 7 days led to an increase in interleukin-1beta and monocyte chemoattractant protein-1 levels and to a progressive influx of nuclear factor kappaB-activated alveolar macrophages into the BAL fluid and lung tissue.

Immunomodulatory and anti-inflammatory effects of Kalanchoe brasiliensis.

The immunomodulatory effect of juice obtained from leaves of Kalanchoe brasiliensis (Kb) on zymosan-induced inflammation was investigated. C57B110 mice received a subcutaneous injection of 150 microg zymosan in the footpad. After 7 days, there was an increase in footpad thickness from 176 +/- 4 to 236 +/- 9 x 10(-2) mm and in blood flow in the footpad area, monitored by 99mTc, from 98 +/- 4 to 694 +/- 59 counts per minute (cpm).