Downregulation of lncRNA SNHG14 Alleviates Neuropathic Pain and Inflammation in CCI Rats by Targeting miR-182-5p/BDNF

Inflammatory processes hold significant importance for the initiation and long-term maintenance of neuropathic pain (NP). This study aimed to investigate the function of long non-coding RNA SNHG14 in NP and the regulatory mechanism underlying its action via the miR-182-5p/ brain-derived neurotrophic factor (BDNF) axis. 80 serum samples were collected from NP patients and 80 from healthy controls, followed by the detection of SNHG14 expression. A chronic constriction injury (CCI) rat model of the sciatic nerve was established, and animals were assigned to experimental groups for behavioral, molecular, and biochemical analyses, including assessment of mechanical and thermal pain thresholds, quantitative reverse transcription polymerase chain reaction (RT-qPCR), and enzyme-linked immunosorbent assay (ELISA). RNA immunoprecipitation (RIP), and dual-luciferase assays were used to verify the targeted relationship. In both NP patients and CCI rats, SNHG14 expression was significantly upregulated and showed preliminary diagnostic potential, warranting further validation in larger cohorts. Silencing SNHG14 effectively alleviated pain-related behaviors and concurrently reduced the levels of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β). Mechanistic investigations revealed that SNHG14 exerted its regulatory effects by directly binding to and negatively modulating miR-182-5p, which in turn targeted and suppressed BDNF expression. Functional rescue experiments indicated that antagomir-miR-182-5p partially reversed the analgesic and anti-inflammatory effects achieved through SNHG14 knockdown. Conversely, BDNF silencing partially counteracted the hyperalgesia and enhanced inflammatory responses induced by antagomir-miR-182-5p. SNHG14 upregulated BDNF expression by sequestering miR-182-5p, thereby enhancing the hyperalgesic response and neuroinflammatory processes in NP and CCI rats.