Effects of lncRNA gm4419 on rats with hypertensive cerebral atherosclerosis through NF-κB pathway.

OBJECTIVE: To explore the effects of long non-coding ribonucleic acid (lncRNA) Gm4419 on rats with hypertensive cerebral atherosclerosis through the nuclear factor-kappa B (NF-kappaB) pathway. MATERIALS AND METHODS: Healthy male rats were selected and randomly divided into control group, model group (hypertensive cerebral atherosclerosis model), and lncRNA group (hypertensive cerebral atherosclerosis model + lncRNA injection). Neurological deficit scoring criteria, flow cytometry, Western blotting, and staining method were adopted to measure the differences in the neurological function score, NF-kappaB activity, and chemerin level of rats in the three groups. RESULTS: The neurological scores revealed that the neurological function of rats was not damaged in control group, while it was severely damaged in model group. However, the neurological function of rats was more severely damaged in lncRNA group than that in control group and model group, while the neurological function deficits were slighter in model group. In terms of NF-kappaB expression activity in mononuclear cells, the serum activity of NF-kappaB in control group appeared the lowest among the three groups and was significantly higher in lncRNA group than in model group. The serum chemerin level was evidently increased in model group compared with control group, while it was significantly decreased in lncRNA group compared with model group and control group. Moreover, the levels of NF-kappaB and chemerin were most evidently influenced in lncRNA group. CONCLUSIONS: Activating the NF-kappaB signal, lncRNA Gm4419 promotes the expression of chemerin signal, accelerates the apoptosis of nerve cells, and motivates the deterioration of hypertensive cerebral arteriosclerosis.