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Published on: January 7, 2019
Salvianolic acid A alleviates lipopolysaccharide-induced disseminated intravascular coagulation by inhibiting
Qi-Yun Zhang1,2, Jing Guo1,2, Lin Xu1,2
1State Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang, 550014, China.
Insights
Salvianolic acid A (SAA) effectively treats disseminated intravascular coagulation (DIC) by inhibiting complement activation. This natural compound shows significant potential for improving survival rates in DIC patients.
Area of Science:
- Pharmacology
- Immunology
- Hematology
Background:
- Disseminated intravascular coagulation (DIC) involves coagulopathy and organ failure, with overactivated complement pathways.
- The complement system's role in lipopolysaccharide (LPS)-induced DIC is significant.
- Salvianolic acid A (SAA) exhibits anti-complement activity, prompting investigation into its therapeutic potential.
Purpose of the Study:
- To investigate the effects of salvianolic acid A (SAA) on lipopolysaccharide (LPS)-induced disseminated intravascular coagulation (DIC) in rats.
- To determine if SAA's anti-complement action can mitigate DIC progression.
- To evaluate SAA's impact on coagulation function, inflammation, and organ damage in a rat model of DIC.
Main Methods:
- In vitro hemolysis assays and molecular docking were used to assess SAA's anti-complement activity and binding sites.
- LPS-induced DIC was established in male Wistar rats.
- Coagulation function, complement activity, inflammation markers, organ function, and survival rates were analyzed post-SAA treatment.
Main Results:
- SAA demonstrated in vitro and in vivo anti-complement activity, inhibiting both classical and alternative pathways.
- LPS-induced DIC in rats led to impaired coagulation, increased inflammation, organ damage, and an 85% mortality rate.
- SAA treatment significantly reduced complement activation, inflammatory cytokines, D-dimer, and organ damage markers, while improving coagulation parameters and increasing survival rates to 46.2% and 78.6%.
Conclusions:
- Salvianolic acid A effectively reduces lipopolysaccharide-induced disseminated intravascular coagulation by inhibiting complement activation.
- SAA demonstrates considerable therapeutic potential for treating DIC.
Introduction:
Disseminated intravascular coagulation (DIC) is a syndrome characterized by coagulopathy, microthrombus, and multiple organ failure. The complement system in DIC is overactivated, and the functions of complement and coagulation pathways are closely related. Our previous screening revealed that salvianolic acid A (SAA) has anti-complement activity. The hyper-activated complement system was involved in the lipopolysaccharide (LPS) induced DIC in rats. The effects of SAA anti-complement action on LPS-induced DIC in rats were investigated.
Methods:
The complement activity of the classical pathway and alternative pathway was detected through an in vitro hemolysis assay. The binding sites of SAA and complement C3b were predicted by molecular docking. LPS-induced disseminated coagulation experiments were performed on male Wistar rats to assess coagulation function, complement activity, inflammation, biochemistry, blood routine, fibrinolysis, and survival.
Results:
SAA had an anti-complement activity in vivo and in vitro and inhibited the complement activation in the classical and alternative pathway of complement. The infusion of LPS into the rats impaired the coagulation function, increased the plasma inflammatory cytokine level, complemented activation, reduced the clotting factor levels, fibrinogen, and platelets, damaged renal, liver, and lung functions, and led to a high mortality rate (85%). SAA treatment of rats inhibited complement activation and attenuated the significant increase in D-dimer, interleukin-6, alanine aminotransferase, and creatinine. It ameliorated the decrease in plasma levels of fibrinogen and platelets and reversed the decline in activity of protein C and antithrombin III. The treatment reduced kidney, liver, and lung damage, and significantly improved the survival rate of rats (46.2 and 78.6% for the low- and high-dose groups, respectively).
Conclusion:
SAA reduced LPS-induced DIC by inhibiting complement activation. It has considerable potential in DIC treatment.
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