Atractylenolide Ⅰ protects against lipopolysaccharide-induced disseminated intravascular coagulation by anti-inflammatory and anticoagulation effect
Journal Title: Asian Pacific Journal of Tropical Medicine - Year 2017, Vol 10, Issue 6
Abstract
Objective: To investigate whether atractylenolide Ⅰ (ATL-Ⅰ) has protective effect on lipopolysaccharide (LPS)-induced disseminated intravascular coagulation (DIC) in vivo and in vitro, and explore whether NF-kB signaling pathway is involved in ATL-Ⅰ treatment. Methods: New Zealand white rabbits were injected with LPS through marginal ear vein over a period of 6 h at a rate of 600 mg/kg (10 mL/h). Similarly, in the treatment groups, 1.0, 2.0, or 5.0 mg/kg ATL-Ⅰ were given. Both survival rate and organ function were tested, including the level of alanine aminotransferase (ALT), blood urine nitrogen (BUN), and TNF-a were examined by ELISA. Also hemostatic and fibrinolytic parameters in serum were measured. RAW 264.7 macrophage cells were administered with control, LPS, LPS + ATL-Ⅰ and ATL-Ⅰ alone, and TNF-a, phosphorylation (P)-IkBa, phosphorylation (P)-NF-kB (P65) and NF-kB (P65) were determined by Western blot. Results: The administration of LPS resulted in 73.3% mortality rate, and the increase of serum TNF-a, BUN and ALT levels. When ATL-Ⅰ treatment significantly increased the survival rate of LPS-induced DIC model, also improved the function of blood coagulation. And protein analysis indicated that ATL-I remarkably protected liver and renal as decreasing TNF-a expression. In vitro, ATL-I obviously decreased LPS-induced TNF-a production and the expression of P-NF-kB (P65), with the decrease of P-IkBa. Conclusions: ATL-Ⅰ has protective effect on LPS-induced DIC, which can elevate the survival rate, reduce organ damage, improve the function of blood coagulation and suppress TNF-a expression by inhibiting the activation of NF-kB signaling pathway.
Authors and Affiliations
Xi Lin, Liang-Cai Wu
Keywords
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- EP ID EP267436
- DOI 10.1016/j.apjtm.2017.06.007
- Views 100
- Downloads 0
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