Herniated nucleus pulposus is the main pathological manifestation of lumbar disc herniation, and it is believed that the nature and degree of back and leg pain in patients with lumbar disc herniation depends on the size and type of herniated nucleus pulposus. The traditional view is that the pain caused by lumbar disc herniation is due to the compression of the nerve roots by the herniated discs, and therefore the main treatment is to solve the mechanical compression problem, such as surgical removal of the herniated discs. However, in many clinical cases, it is difficult to explain by mechanical compression. In some patients, the pressure on the nerve root is not serious, but the pain is very severe; in some patients, the pressure on the nerve is quite heavy, but the pain is not obvious; in some patients, through conservative treatment, although the herniated disc does not change, the clinical symptoms are significantly improved. It indicates that pain caused by lumbar disc herniation is a complex pathophysiological process, and there are other pathophysiological mechanisms involved in addition to mechanical compression mechanism. Phospholipase A2 is an important inflammatory mediator and pain-causing substance in human body, as well as a marker of tissue inflammation. Hou Shuxun led the group to systematically study the pathogenesis of pain in patients with lumbar disc herniation, starting from the relationship between the level of phospholipase A2 activity in lumbar disc tissue and pain. They measured the phospholipase A2 activity levels in blood and disc nuclei obtained during surgery in 20 patients with lumbar disc herniation by micro acid titration, and the results were studied against the patients’ pain level and intraoperative pathological findings. The level of phospholipase A2 activity in the nucleus pulposus of lumbar disc herniation was found to be 35 and 10 times higher than that in the nucleus pulposus of own blood and healthy nucleus pulposus, respectively. . The herniated nucleus pulposus is the main pathological manifestation of lumbar disc herniation, and it has been suggested that the nature and degree of low back and leg pain in patients with lumbar disc herniation depends on the size and type of nucleus pulposus protrusion. The type of herniated nucleus pulposus and its relationship with nerve roots were observed and recorded intraoperatively, and compared with the symptoms and signs of patients before surgery. It was found that among 300 patients, 68 patients had significant congestion, edema, and adhesions in the nerve roots and nearby soft tissues, and these tissues were extremely sensitive to the stimulation of surgery, and all of these patients had severe preoperative back and leg pain. In the remaining 232 patients, the dural sac, epidural fat, ligamentum flavum, posterior longitudinal ligament and fibrous ring, which had no inflammatory reaction, were insensitive to the mechanical irritation of surgery. It indicates that the degree of pain in patients with lumbar disc herniation is independent of the type of nucleus pulposus herniation and that the inflammatory response is an important factor in producing pain. The traditional view is that the pain caused by lumbar disc herniation is due to the compression of the nerve roots by the herniated discs, and therefore the main treatment is to solve the mechanical compression problem, such as surgical removal of the herniated discs. However, in many clinical cases, it is difficult to explain by mechanical compression. In some patients, the nerve root compression is not serious, but the pain is very severe, and in some patients, the nerve compression is quite heavy, but the pain is not obvious, and in some patients, through conservative treatment, although the herniated disc does not change, the clinical symptoms get significantly improved. It indicates that pain caused by lumbar disc herniation is a complex pathophysiological process, and there are other pathophysiological mechanisms involved in addition to mechanical compression mechanism. Phospholipase A2 is an important inflammatory mediator and pain-causing substance in human body, as well as a marker of tissue inflammation. Hou Shuxun led the group to systematically study the pathogenesis of pain in patients with lumbar disc herniation, starting from the relationship between the level of phospholipase A2 activity in lumbar disc tissue and pain. They measured the phospholipase A2 activity levels in blood and disc nuclei obtained during surgery in 20 patients with lumbar disc herniation by micro acid titration, and the results were studied against the patients’ pain level and intraoperative pathological findings. Phospholipase A2 activity levels in the nucleus pulposus of herniated lumbar discs were found to be up to 35-fold and 10-fold higher than in their own blood and healthy nucleus pulposus, respectively, and phospholipase A2 activity levels were significantly correlated with the patient’s pain level. This demonstrates that inflammation of nerve roots induced by inflammatory mediators in the nucleus pulposus is directly related to pain.