LncRNA SNHG1 alleviated apoptosis and inflammation during ischemic stroke by targeting miR-376a and modulating CBS/H2S pathway

• Published in: International journal of neuroscience 2021-12, Vol.131 (12), p.1162-1172
• Main Authors: Lv, Li, Xi, Hai-Peng, Huang, Jian-Chao, Zhou, Xiang-Yang
• Format: Article
• Language: English
• Subjects: CBS; H2S; ischemic stroke; miR-376a; SNHG1
• ISSN: 0020-7454; 1543-5245; 1563-5279
• DOI: 10.1080/00207454.2020.1782904

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 H 2 S 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/H 2 S signal. These results show light on underlying mechanisms of IS and provide potential targets for IS therapy.