miR-346 targets SLC38A1 to mediate neuropathic pain following spinal cord injury

We have removed the subheadings and revised the abstract into an unstructured version as required. The revised abstract is shown below: This study aimed to explore the role and underlying mechanism of miR‑346 in neuropathic pain secondary to spinal cord injury, a common complication whose molecular mechanisms remain incompletely elucidated. A rat spinal cord injury model was established, and intrathecal injection of miR‑346 mimic was used for intervention. The BBB score, von Frey test, and hot plate test were applied to assess motor function and pain hypersensitivity. An LPS‑induced BV‑2 microglial inflammation model was adopted for in vitro investigation; qPCR, ELISA, oxidative stress detection, and dual‑luciferase reporter assays were performed to confirm the targeting relationship between miR‑346 and SLC38A1, as well as the regulatory effects of miR‑346 on microglial inflammatory polarization and oxidative stress. The results revealed that miR‑346 was significantly downregulated in the spinal cord tissue of rats after spinal cord injury. Intrathecal administration of miR‑346 mimic restored miR‑346 levels, improved motor function recovery and alleviated neuropathic pain, manifested as increased BBB scores and normalized mechanical and thermal withdrawal thresholds. In vitro experiments showed that miR‑346 promoted M2 microglial polarization, suppressed inflammatory responses and attenuated oxidative stress, and SLC38A1 was identified as its direct target mediating these protective effects. In conclusion, miR‑346 regulates microglial inflammatory polarization and oxidative stress by targeting SLC38A1 in acute‑phase neuropathic pain following spinal cord injury, and it may be a potential therapeutic target.