Abstract Title:

Ginkgolide A inhibits lipopolysaccharide-induced inflammatory response in human coronary artery endothelial cells via downregulation of TLR4-NF-κB signaling through PI3K/Akt pathway.

Abstract Source:

Pharmazie. 2016 Oct 1 ;71(10):588-591. PMID: 29441927

Abstract Author(s):

Jian Zhaocheng, Long Jinfeng, Yin Luchang, Sun Yequan, Liu Feng, Wang Kai

Article Affiliation:

Jian Zhaocheng


Ginkgolide A (GA) is a one of the active components of Ginkgo biloba. We aimed to detect the effects GA on the lipopolysaccharide (LPS)-induced inflammatory response in human coronary artery endothelial cells (HCAECs) and whether the effects are associated with the inhibition of toll-like receptor 4 (TLR4)-NF-κB signaling through PI3K/Akt pathway. HCAECs were stimulated with LPS and treated with GA or TLR4 inhibitor CLI-095. A PI3K/Akt inhibitor LY294002 was used to block the PI3K/Akt pathway. The toxic effects of GA, LPS and LY294002 on HCAEC were evaluated using MTT assay. Levels inflammatory mediators, TLR4 mRNA, NF-κB signaling activity were valuated. We found LPS stimulation significantly increased the release of IL-6, IL-8, MCP-1 and TNF-αfrom HCAECs, elevated the TLR4 mRNA expression and activated the NF-κB signaling. GA and CLI-095 abolished the LPS-induced inflammatory mediator release and NF-κB signaling activation, and GA reduced the TLR4 mRNA expression without affecting cell viability. However, PI3K/Akt blocking abolished the effects of GA on HCAECs. We conclude that GA could attenuate the LPS-induced inflammatory response in HCAECs and the anti-inflammatory activity might be associated with the inhibition of TLR4-NF-κB signaling through PI3K/AKT pathway. These findings suggest a therapeutic potential of GA in endothelial inflammation.

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Sayer Ji
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