Objective: This study aimed to explore the effects of lncRNA ANRIL on vascular endothelial growth factor (VEGF) and angiogenesis in diabetes mellitus (DM) combined with cerebral infarction (CI) through NF-kappa B signaling pathway.
Methods: Adult male Wistar rats were randomly divided into control group and DM + CI group, and the DM + CI group were subdivided into Vector, shANRIL, PDTC, pcDNA-ANRIL, and pcDNA-ANRIL + PDTC groups. VEGF and FMS-like tyrosine kinase (FLT-1) expressions were measured by immunohistochemistry and endothelium dependent microvessel density (MVD) was detected by differentiation 31 (CD31) and para-amiuosalicylic acid (PAS) double staining. The qRT-PCR was applied to measure mRNA expressions of VEGF, FLT-1, Kinase insert domain protein receptor (FLK-1) and NF-kappa B, and Western blotting was conducted to detected expressions of VEGF, NF-kappa B and p-I kappa B/I kappa B.
Results: Compared with the control group, protein expressions of VEGF, NF-kappa B, p-I kappa B/I kappa B, expression of ANRIL, and mRNA expressions of VEGF, FLT-1 and NF kappa B were increased in the DM + CI group. Compared with the Vector group, protein expressions of VEGF, NF-kappa B, p-I kappa B/I kappa B, expression of ANRIL, mRNA expressions of VEGF, FLT-1 and NF-kappa B, and endothelium dependent MVD were increased in the pcDNA-ANRIL group, while decreased in the shANRIL group and PDTC group. Compared with the pcDNA-ANRIL group, protein expressions of VEGF, NF-kappa B, p-I kappa B/I kappa B, expression of ANRIL, mRNA expressions of VEGF, FLT-1 and NF-kappa B, and endothelium dependent MVD were decreased in the pcDNA-ANRIL + PDTC group.
Conclusion: Overexpressed lncRNA ANRIL upregulates VEGF and promotes angiogenesis by activating NF-kappa B signaling pathway in DM + CI rats.