Study on protective effects of canthaxanthin on immuno-function of acute lung injury mouse model induced by lipopolysaccharide
Pei Ling-peng, Jian Cui
Abstract
Pei Ling-peng, Jian Cui
Abstract
Objective: To study the protective effects of canthaxanthin against decreasing of i mmuno-function of the acute lung injury induced by lipopolysaccharide in mice and research its possible mechanism for offering scientific basis of its health function. Methods: Randomly distribute 60 male Kunming mices into control group, lipopolysaccharide-induced acute lung injury model group(ALI), dexamethasone (DXM) group (5 mg/kg) and low, middle, high dose groups of canthaxanthin (10 mg/kg, 15 mg/kg, 20 mg/kg). After 30 d feed by different dosage canthaxanthin, control group were given physiological saline, ALI model group, canthaxanthin administrated groups and DXM group were injected with lipopolysaccharide (LPS) (6.0 mg/kg) to induce ALI. Six hours after LPS or physiological saline challenged, abdominal aorta blood for measuring lymphocyte subpopulations(CD3+, CD4+, CD8+), tumour factor-α(TNF-α), leckocyte interpose-8(IL-8), malondialdehyde (MDA) content, superoxide dismutase (SOD), glutathione perioxidase (GSH-Px) activities, and lung wet weight/dry weight ratio, neutrophil MPO activity of lung, tumour factor-α(TNF-α), leckocyte interpose-10 (IL-10) content of lung. Results: Treatment with different dosage canthaxanthin could significantly decrease serum TNF-α, IL-8, MPO, MDA content and lung wet weight/dry weight ratio, while inhibit the reduction of IL-10 in lung and SOD, GSH-Px activities, improve the percent of lymphocyte subpopulations. Conclusion: Canthaxanthin showed protective effects on immuno-function of the acute lung injury induced by LPS in mice.
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Objective: To study the protective effects of canthaxanthin against decreasing of i mmuno-function of the acute lung injury induced by lipopolysaccharide in mice and research its possible mechanism for offering scientific basis of its health function. Methods: Randomly distribute 60 male Kunming mices into control group, lipopolysaccharide-induced acute lung injury model group(ALI), dexamethasone (DXM) group (5 mg/kg) and low, middle, high dose groups of canthaxanthin (10 mg/kg, 15 mg/kg, 20 mg/kg). After 30 d feed by different dosage canthaxanthin, control group were given physiological saline, ALI model group, canthaxanthin administrated groups and DXM group were injected with lipopolysaccharide (LPS) (6.0 mg/kg) to induce ALI. Six hours after LPS or physiological saline challenged, abdominal aorta blood for measuring lymphocyte subpopulations(CD3+, CD4+, CD8+), tumour factor-α(TNF-α), leckocyte interpose-8(IL-8), malondialdehyde (MDA) content, superoxide dismutase (SOD), glutathione perioxidase (GSH-Px) activities, and lung wet weight/dry weight ratio, neutrophil MPO activity of lung, tumour factor-α(TNF-α), leckocyte interpose-10 (IL-10) content of lung. Results: Treatment with different dosage canthaxanthin could significantly decrease serum TNF-α, IL-8, MPO, MDA content and lung wet weight/dry weight ratio, while inhibit the reduction of IL-10 in lung and SOD, GSH-Px activities, improve the percent of lymphocyte subpopulations. Conclusion: Canthaxanthin showed protective effects on immuno-function of the acute lung injury induced by LPS in mice.
Key concepts: Malondialdehyde, Lipopolysaccharide, Lung, Superoxide dismutase, Pharmacology, Canthaxanthin, Medicine, Saline