The main causes of lumbar disc herniation leading to low back pain are twofold: mechanical compression of nerves, aseptic inflammation of nerve roots and nutritional disorders of nerve roots and conduction damage of nerve roots. The mechanism of action of intra- and extra-discal injection of medical ozone for lumbar disc herniation is considered to be: ① Oxidation of proteoglycans: this is the main mechanism of medical ozone for lumbar disc herniation. The normal nucleus pulposus is composed of proteoglycans, collagen fibrous network and nucleus pulposus cells. Proteoglycan is one of the most important macromolecular structures of the nucleus pulposus, which can absorb charge into the nucleus pulposus matrix and generate high osmotic pressure in the nucleus pulposus matrix, which is the main factor of up to 85% of water in the nucleus pulposus. Proteoglycans lose the property of fixed charge density when they are disrupted. The decrease in the osmotic pressure of the nucleus pulposus matrix eventually leads to water loss and atrophy and reduction in the volume of the nucleus pulposus, thus reducing the pressure in the intervertebral disc and enabling the elimination of symptoms and achieving the purpose of treatment. In contrast, medical ozone has a weaker effect on the cartilage endplates and the fibrous rings. The pathological results of animal experiments by Zhijian Yu and Xiaofeng He showed that the end result of medical ozone on the normal nucleus pulposus was a decrease in water, which resulted in a decrease in the volume and pressure of the nucleus pulposus; loss of elasticity, color change and drying of the nucleus pulposus could be observed in large specimens, and the nucleus pulposus did not expand when the disc was cut; the large vesicle-like structures within the nucleus pulposus matrix disappeared under electron microscopy. ②Destruction of the nucleus pulposus cells: Iliakis et al. demonstrated that medical ozone injected into the nucleus pulposus tissue caused degeneration of the nucleus pulposus cells at an early stage, followed by necrotic lysis of the cells. Damage to myeloid cells inevitably causes a decrease in proteoglycan synthesis and secretion. (3) Anti-inflammatory effect: the prominent nucleus pulposus and fibrous ring compress the dura mater, nerve roots and surrounding veins, causing impaired reflux, exudation and tissue edema; the nucleus pulposus tissue is strongly irritating and releases a large amount of histamine after contact with nerve roots, causing chemical inflammation of spinal nerve roots; the glycoprotein and beta protein released after fibrous ring fracture act as antigenic substances, causing the body to produce an immune response. Studies have shown that medical ozone causes vasodilation and improves reflux by stimulating the overexpression of antioxidant enzymes to neutralize excess reactive oxygen species in the inflammatory response; stimulating the release of cytokines that antagonize the inflammatory response and/or immunosuppressive cytokines (e.g., IL-10, TGF-β); and stimulating the release of nitric oxide (N0) and platelet-derived growth factor (PDGF) from vascular endothelial cells to reduce edema around nerve roots and promote inflammation absorption. (4) Analgesic effect: When activated by mechanical stimuli such as pressure and traction on small lumbar articular prominences, or by inflammatory factors and chemicals released from the herniated nucleus pulposus (such as substance P or phosphatase A2), the sensitivity increases, causing reflex muscle spasm and resulting in lower back pain or (and) sciatica. Bocci E also hypothesized that the analgesic effect of medical ozone injected with fine needles for the treatment of lumbar disc herniation may be a mechanism of action similar to “chemical puncture”, i.e., inhibition of unmyelinated damage to The analgesic effect of fine needle injection of medical ozone for lumbar disc herniation may be due to a mechanism of action similar to that of chemical puncture, i.e., inhibition of unmyelinated receptor fibers, which stimulates the release of enkephalins from inhibitory interneurons by activating pain perception inhibitory mechanisms.