Inhibition of long noncoding RNA MALAT1 suppresses high glucose-induced apoptosis and inflammation in human umbilical vein endothelial cells by suppressing the NF-κB signaling pathway.

The study aimed to investigate the expression of long noncoding RNA (lncRNA) MALAT1 in high glucose (HG)-induced human vascular endothelial cells (HUVECs) and the role of MALAT1 in the apoptosis of HG-induced HUVECs. HUVECs were cultured and induced via 25 mmol/L HG. After that, HUVECs were transfected with MALAT1 siRNA. MALAT1 expression was detected by qPCR, while expression of Bax, Bcl-2, cleaved-caspase-3, cleaved-caspase-9, p-65 and p-p65was detected by Western blot analysis. Besides, the regulatory role of MALAT1 in cell activity and apoptosis was detected by observed by CCK-8 assay, TUNEL staining and flow cytometry. Furthermore, the expression of inflammatory factors (TNF-α and IL-6) was detected by ELISA. The expression of MALAT1, TNF-α and IL-6 in HUVECs were increased in HG environment. After HG induced-HUVECs were treated with silencing MALAT1, it was found that cell proliferation was increased significantly, the expression of TNF-α, IL-6, Bax, cleaved-caspase-3 and cleaved-caspase-9 was decreased, and apoptosis was decreased. MALAT1 silencing inhibited the expression of p-p65 in HG-induced HUVECs. In conclusion, our study demonstrated that MALAT1 was upregulated in HG-induced HUVECs, and inhibition of MALAT1 could inhibit HG-induced apoptosis and inflammation in HUVECs by suppression of the NF-κB signaling pathway.