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Highlights • LncRNA SNHG1 and miR-338 expression are both up-regulated in OGD treated BMECs. • SNHG1 silence aggravates OGD-induced injury in BMEC. • SNHG1 acts as a degradable sponge for miR-338. • MiR-338 overexpression aggravates OGD-induced injury in BMEC while miR-338 inhibition alleviates OGD-induced injury in BMEC. • HIF-1α is a direct target of miR-338. Abstract Background Brain microvascular endothelial cell (BMEC) is an important therapeutic target for the inhibition of brain vascular dysfunction in ischemic stroke. Expression of long non-coding RNA SNHG1 is reportedly upregulated in BMEC after OGD. The present study aims to investigate the potential roles of SNHG1 in OGD-induced injury in BMEC. Methods Mice primary brain microvascular endothelial cells (BMEC) were cultured under "normal" or "oxygen/glucose-deprived" (OGD) conditions. The expression of SNHG1 and miR-338 after OGD were examined by qPCR. shRNA against SNHG1 was used to knockdown SNHG1 in BMEC. MiR-338-3p mimic and inhibitor were used to change the expression of miR-338 in BMEC. The relationship between SNHG1 and miR-338, and the relationship between miR-338 and HIF-1α were clarified using RNA pull-down and luciferase reporter gene assays, respectively. Results SNHG1 and miR-338 were upregulated in OGD induced BMEC. SNHG1 silence aggravated OGD-induced cell apoptosis by down-regulating Bcl-2, HIF-1α and VEGF-A, and upregulating caspase 3 activity and Bax. MiR-338 was upregulated in SNHG1-silenced BMEC. RNA pull-down assays showed that SNHG1 could be directly bound by miR-338. In addition, miR-338 overexpression reduced cell viability in OGD while miR-338 inhibition protected BMEC against OGD-induced injury. Furthermore, luciferase reporter assay showed that HIF-1α was a direct target of miR-338. Conclusions SNHG1 exerted protective effects against OGD induced injury via sponging miR-338, thus upregulating HIF-1α/VEGF-A in BMEC. [ABSTRACT FROM AUTHOR]