Most studies have focused on the protective effects of
ginkgolide A against
ischemia/reperfusion-induced
cardiomyopathy and injury of the brain, liver, and other organs, but there are few reports about the protection of lung tissues. This study was designed to clarify the protection of
ginkgolide A against
lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial cell (PMVEC) injury. PMVECs were extracted and fell into control, LPS, and
ginkgolide A groups. Next, we delved into the growth activity and apoptosis rate of cells via the
CCK-8 assay and Hoechst staining, independently. Beyond that, western blotting (WB) was implemented for measurement of the expressions of
cyclin D1,
cyclin-dependent kinase 4 (CDK4), and CDK inhibitor (p21) that pertained to the cell cycle. The target sites of
ginkgolide A were confirmed by
miRNA array and real-time quantitative PCR. The relationship between miR-224 and p21 was analyzed using dual-
luciferase reporter gene assay. Compared with the control group, the LPS group and
ginkgolide A group had significantly decreased cell growth activity and relative expressions of
cyclin D1 and CDK4 and elevated apoptosis rate and p21 expression. Pronounced elevations were observable in the cell growth activity and expressions of
cyclin D1, CDK4, and p21, while the
ginkgolide A group presented with a reduced apoptosis rate in comparison with the LPS group (P < 0.05). MiR-224 was the target of
ginkgolide A, which had targeted regulatory effects on p21.
Ginkgolide A can modulate miR-224 expression and regulate p21 expression in a targeted manner to enhance the resistance of PMVECs to LPS-induced cell apoptosis.