Abstract
Intracerebral hemorrhage (ICH) can usually cause severe neuroinflammation and blood-brain barrier (BBB) damage. Previous studies supported the important role of long non-coding RNAs (lncRNAs) in ICH treatment. This study aimed to explore the effect of lncRNA FGD5 antisense RNA 1 (FGD5-AS1) on ICH and its potential molecular mechanisms. C57BL/6 mice were injected with collagenase VII to establish an ICH mice model. In addition, brain cerebral microvascular endothelial cells (BMVECs) were treated by oxygen-glucose deprivation (OGD)/hemin to simulate ICH. RT-qPCR revealed that FGD5-AS1 was upregulated in serum of ICH patients and mice and in OGD/hemin-treated BMVECs. Luciferase reporter gene and pull-down assays predicted and verified that FGD5-AS1 bound to miR-6838-5p, and VEGFA was a target of miR-6838-5p. FGD5-AS1 knockdown decreased the inflammatory factor contents in brain tissues and BMVECs. FGD5-AS1 overexpression inhibited cell proliferation, invasion and tight junction protein levels, and promoted apoptosis, increased the permeability of BBB and secretion of pro-inflammatory factors. In addition, miR-6838-5p knockdown reversed the inhibitory effect of FGD5-AS1 knockdown on the PI3K/Akt signaling pathway. In conclusion, FGD5-AS1 may act as an important regulator to promote apoptosis, cell permeability and inflammatory response of BMVECs via the miR-6838-5p/VEGFA axis in ICH mice.
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