本文采用的英格恩产品: RNA-Entranster-invivo
Long Non-coding RNA BC168687 is Involved in TRPV1-mediated Diabetic Neuropathic Pain in Rats
Chenglong Liu 1 , Congcong Li 2 , Zeyu Deng 1 , Errong Du 1 , Changshui Xu 3
Affiliations
- 1 Department of Physiology, Basic Medical College of Nanchang University, Nanchang 330006, PR China.
- 2 The Second Clinical Medical College of Nanchang University, Nanchang 330006, PR China.
- 3 Department of Physiology, Basic Medical College of Nanchang University, Nanchang 330006, PR China; Jiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang 330006, PR China. Electronic address: xuchangshui@ncu.edu.cn.
Abstract
Long noncoding RNAs (lncRNAs) participate in a diverse range of molecular and biological processes, and dysregulation of lncRNAs has been observed in the pathogenesis of various human diseases. We observed alterations in mechanical withdrawal thresholds (MWT) and thermal withdrawal latencies (TWL) in streptozotocin (STZ)-induced diabetic rats treated with small interfering RNA (siRNA) of lncRNA BC168687. We detected expression of transient receptor potential vanilloid type 1 (TRPV1) in rat dorsal root ganglia (DRG) by a series of molecular experiments. We determined relative levels of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in rat serum by enzyme-linked immunosorbent assay (ELISA). In addition, we examined extracellular regulated protein kinases (ERK) and p38 mitogen-activated protein kinase (MAPK) signaling pathways by Western blot (WB). We showed that the MWT and TWL of diabetic rats increased significantly compared with control. Expression of TRPV1 receptors in DRG substantially decreased. Relative levels of TNF-α and IL-1β in the serum of lncRNA BC168687 siRNA-treated rats were reduced. Phosphorylation (p)-ERK and p-p38 signaling pathways in DRG were also decreased. Taken together, we concluded lncRNA BC168687 siRNA may alleviate TRPV1-mediated diabetic neuropathic pain.
Keywords: DRG; TRPV1; diabetic neuropathic pain; long non-coding RNAs.