LncRNA SNHG1 alleviated apoptosis and inflammation during ischemic stroke by targeting miR-376a and modulating...

Ischemic stroke (IS) is a major public health issue causing mortality and disability and is more difficult to treat than other cerebral diseases. Previous study reported that miR-376a was upregulated in the serum of stroke patients, indicating that miR-376a played potential role in occurrence and development of stroke.

IS cell model was induced by oxygen-glucose deprivation (OGD) exposed HCMEC/D3 cells. The mRNA level of SNHG1, miR-376a and inflammatory cytokines were detected by q-PCR. Protein level of CBS, apoptotic proteins were examined by Western blot. Apoptosis was analyzed by flow cytometry, and H₂S level was measured by kit. Interaction among lncRNA, miRNA and target gene was validated by luciferase assay.

Our research revealed that mRNA level of SNHG1 and CBS in HCMEC/D3 cells was downregulated while miR-376a was upregulated under OGD conditions. Further results demonstrated that miR-376a overexpression promoted apoptosis and inflammation while SNHG1 overexpressing alleviated such processes. Mechanistically, SNHG1 directly targeted miR-376a, and CBS was a target of miR-376a. Moreover, SNHG1 exert its function via inhibiting miR-376a to regulate CBS expression.

LncRNA SNHG1 depressed apoptosis and inflammation of IS cell model via inhibiting miR-376a and upregulating CBS/H₂S signal. These results show light on underlying mechanisms of IS and provide potential targets for IS therapy.