Interleukin-Mediated Inflammatory Pathways and Nerve Injury in Lumbar Disc Herniation: A Narrative Review

This is a narrative review aimed to explore the molecular biosciences mechanisms by which interleukin (IL) networks and inflammatory pathways mediate nerve injury in lumbar disc herniation (LDH), providing translational insights for therapy.

We screened PubMed and Embase databases from January 2010 to January 2026 to search for published studies. The search keywords used are as follows: ["lumbar disc herniation" or "LDH"], [" interleukin" or "IL" or "Interleukin Network"], ["Nerve Injury"], ["Inflammatory"]. A total of 196 peer-reviewed studies were included, comprising 152 experimental studies (128 animal models, 24 in vitro cell experiments) and 44 human clinical studies, with a human-to-animal study ratio of approximately 1:2.9.

Preclinical mechanistic studies indicate that pro-inflammatory interleukins such as IL-1β, IL-6 and IL-17 lead to nerve root demyelination, axonal degeneration and neuropathic pain by activating NLRP3, JAK-STAT3 and p38MAPK pathways. Anti-inflammatory interleukins including IL-4 and IL-10 produce neuroprotective effects through inducing M2 macrophage polarization. Clinical evidence shows that interleukin levels are related to the severity of radicular pain and neurological deficits. Targeted biologics, TCM and acupuncture can regulate interleukin signaling to relieve symptoms. This review is structured with a three-part framework that includes interleukin characteristics and inflammatory signaling in LDH, interleukin-mediated mechanisms of nerve injury and translational interventions as well as clinical challenges.

In the future, it can be transformed into clinical practice of LDH through the development of targeted biologics, the combination of standardized traditional Chinese and Western medicine protocols, and the evaluation of biomarkers based on interleukin.