Atractylenolide protects against lipopolysaccharide-induced disseminated intravascular coagulation by anti-inflammatory and anticoagulation effect
10.1016/j.apjtm.2017.06.007
- Author:
Xiao-Mei TANG
1
;
Zhi-Kai LIAO
2
;
You-Wei HUANG
2
;
Xi LIN
2
;
Liang-Cai WU
3
Author Information
1. Department of Obstetrics and Gynecology, The First Affiliated Hospital of Jinan University
2. Department of Pharmacology, Medical College, Jinan University
3. Department of Dermatology, The 6th Affiliated Hospital, Sun Yat-sen University
- Publication Type:Journal Article
- Keywords:
Anti-inflammatory;
Anticoagulation;
Atractylenolide;
Disseminated intravascular coagulation;
Macrophage
- From:
Asian Pacific Journal of Tropical Medicine
2017;10(6):582-587
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate whether atractylenolide (ATL-) has protective effect on lipopolysaccharide (LPS)-induced disseminated intravascular coagulation (DIC) in vivo and in vitro, and explore whether NF-κB signaling pathway is involved in ATL- 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 μg/kg (10 mL/h). Similarly, in the treatment groups, 1.0, 2.0, or 5.0 mg/kg ATL- were given. Both survival rate and organ function were tested, including the level of alanine aminotransferase (ALT), blood urine nitrogen (BUN), and TNF-α 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- and ATL- alone, and TNF-α, phosphorylation (P)-IκBα, phosphorylation (P)-NF-κB (P65) and NF-κB (P65) were determined by Western blot. Results The administration of LPS resulted in 73.3% mortality rate, and the increase of serum TNF-α, BUN and ALT levels. When ATL- 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-α expression. In vitro, ATL-I obviously decreased LPS-induced TNF-α production and the expression of P-NF-κB (P65), with the decrease of P-IκBα. Conclusions ATL- 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-α expression by inhibiting the activation of NF-κB signaling pathway.
