کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2540848 1122613 2014 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Protective effect of taraxasterol on acute lung injury induced by lipopolysaccharide in mice
ترجمه فارسی عنوان
اثر محافظتی تاراکساسترول بر آسیب ریه حاد ناشی از لیپوپلی ساکارید در موش
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
چکیده انگلیسی


• Taraxasterol attenuated lung histopathologic changes; MPO activity in LPS-induced ALI models.
• Taraxasterol inhibited the LPS-induced TNF-α, IL-6 and IL-1β production in BALF.
• Taraxasterol blocked the phosphorylation of IkBα, p65, p38, ERK and JNK.
• Taraxasterol has a protective effect against the LPS-induced ALI.

Taraxasterol, a pentacyclic-triterpene isolated from Taraxacum officinale, has been reported to have potent anti-inflammatory properties. However, the effect of taraxasterol on lipopolysaccharide (LPS)-induced mice acute lung injury has not been investigated. The aims of this study were to investigate whether taraxasterol could ameliorate the inflammation response in LPS-induced acute lung injury and to clarify the possible mechanism. Male BALB/c mice were pretreated with taraxasterol 1 h before intranasal instillation of LPS. 7 h after LPS administration, the myeloperoxidase (MPO) in lung tissues, lung wet/dry ratio and inflammatory cells in the bronchoalveolar lavage fluid (BALF) were detected. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β) in the BALF were measured by ELISA. The extent of phosphorylation of IκB-α, p65 NF-κB, p46–p54 JNK, p42–p44 ERK, and p38 were determined by western blotting. The results showed that taraxasterol attenuated the infiltration of inflammatory cells, the activity of myeloperoxidase (MPO), lung wet/dry ratio, and the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in a dose-dependent manner. Additionally, western blotting results showed that taraxasterol inhibited the phosphorylation of IκB-α, p65 NF-κB, p46–p54 JNK, p42–p44 ERK, and p38 caused by LPS. Our data suggest that anti-inflammatory effects of taraxasterol against the LPS-induced ALI may be due to its ability of inhibition of the NF-κB and MAPK signaling pathways.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 19, Issue 2, April 2014, Pages 342–350
نویسندگان
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