Association Between LncRNA NONRATT021972 and TNF-αin Diabetes

Abstract

Objective to explore potential association between LncRNA NONRATT021972 and TNF-αin diabetic rat models. Methods Streptozocin (STZ) was treated for SD adult male rats to establish diabetes model. 40 STZ-treated rats were randomly into two groups, and siRNA group received NONRATT021972 siRNA treatment, while the rest received saline treatment (D2M). 20 Normal rats were received saline treatment in Control group. Vein blood sampling was performed in 3 groups. Quantitative Real-time PCR was performed to examine expression of LncRNA NONRATT021972 and TNF-α in blood. Mechanical withdrawal threshold and the thermal withdrawal latency test were performed in1w, 2w, 3w, 4w later for 3 groups’ rats. Results Compared with D2M group, blood samples in Control group and siRNA group contained significantly lower concentration of glucose and LncRNA NONRATT021972 (P<0.05) . Compared with D2M group, blood samples of 3 weeks later in Control group and siRNA group contained significantly lower concentration of TNF-α (P<0.05). Moreover, the concentration of TNF-αamong D2M rats was positively associated with LncRNA NONRATT021972. Compared with control group, D2M group showed decreased mechanical withdrawal threshold and the thermal withdrawal latency. Further experiment showed that inhibition of LncRNA NONRATT021972 by siRNA indeed alleviated neuropathic pain, verified by mechanical withdrawal threshold and the thermal withdrawal latency in siRNA group compared with D2M group. Conclusion LncRNA NONRATT021972 was increased in type 2 diabetes rat and was positively associated with TNF-α. LncRNA NONRATT021972 exacerbated neuropathic pain via glucose and TNF-α related pathways. Inhibition the gene was a therapeutic strategy.