Evidence has come to light eliciting the neuroprotective function of SNHG16 in [[cerebrovascular disease]]s. A study sought to analyze the regulatory mechanism of long non-coding RNA small nucleolar RNA host gene16 (SNHG16) in [[oxidative stress]] (OS) injury and cell inflammation. Firstly, models of oxygen-glucose deprivation and reoxygenation (OGD/R) were established in SK-N-SH cells. [[Cell proliferation]] and [[apoptosis]] were appraised using cell counting kit-8 and flow cytometry. Additionally, SNHG16, X-linked inhibitor of apoptosis protein ([[XIAP]]), [[microRNA]] ([[miR 421]]), [[reactive oxygen species]] (ROS), [[lactate dehydrogenase]] (LDH), malondialdehyde (MDA), [[superoxide dismutase]] (SOD), [[tumor necrosis factor]] -α, [[interleukin]] (IL)-1β, and IL-10 expression patterns were determined. In addition, determined and validated the subcellular localization of SNHG16 and the binding relationships between SNHG16 and miR-421, and miR-421 and XIAP. It was found that SNHG16 was poorly-expressed in OGD/R-treated cells. On the other hand, SNHG16 over-expression enhanced cell proliferation, inhibited apoptosis, and alleviated OS and cell inflammation. Furthermore, SNHG16 is bound to miR-421 to facilitate the expression of XIAP. Up-regulation of miR-421 or down-regulation of XIAP could reverse the suppressive effects of SNHG16 on OS and cell inflammation. Collectively, these findings indicated that SNHG16 bound to miR-421 to facilitate XIAP expression, thus alleviating OS injury and inflammation in OGD/R-induced SK-N-SH cells
((Cao X, Ma J, Li S. Mechanism of lncRNA SNHG16 in oxidative stress and inflammation in oxygen-glucose deprivation and reoxygenation-induced SK-N-SH cells. Bioengineered. 2022 Mar;13(3):5021-5034. doi: 10.1080/21655979.2022.2026861. PMID: 35170375.))