OBJECTIVE To explore the regularity of the change of S-100 protein in degenerative nerve after different pathological brachial plexus injuries. METHODS Eighty SD rats were randomly divided into two groups, right C5, C6 preganglionic injury, and postganglionic injury. The distribution and content of S-100 protein in distal degenerative nerve were detected after 1, 2, 3 and 6 months of injury by immunohistochemical methods. RESULTS The S-100 protein was mainly distributed along the axons. The S-100 protein positive axons of each time interval decreased after operation, with significant difference from normal nerves (P lt; 0.01). There was no statistically significant difference among 1, 2, 3 and 6 months group (P gt; 0.05). The S-100 protein stain of postganglionic group was negative. CONCLUSION In preganglionic injury, the functional expression of Schwann’s cells in the distal stump keeps at a certain level and for a certain period. Since Schwann’s cell has inductive effect on nerve regeneration, it suggests that the distal nerve stump in preganglionic injury can be used as nerve grafts.
Diabetic retinal neurodegeneration (DRN) is a condition in which the normal function of retinal neurovascular units is impaired due to various factors such as oxidative stress, microvascular damage, metabolic disorders, neurotrophic factor imbalance, and immune damage in hyperglycemia environment. The loss of neurons and glial dysfunction is involved in the destruction of the blood-retinal barrier, impaired vascular response and neurovascular coupling, leading to microvascular disease and neurodegeneration. More and more studies have proved that DRN is associated with microangiopathy and diabetic retinopathy pathogenesis. A deeper understanding of the pathogenesis of neurovascular injury may provide new and more effective prevention strategies for diabetic retinopathy.
Diabetic retinal neurodegeneration is a serious complication of diabetes mellitus, manifested by apoptosis and gliosis, and its pathogenesis is closely related to the oxidative stress induced by high glucose levels. The increase in blood glucose in the body leads to excessive production of reactive oxygen species and the downregulation of antioxidant defense signaling pathways, which leads to oxidative stress in the body, which in turn induces apoptosis, mitochondrial damage and autophagy, resulting in diabetic retinal neurodegeneration. Antioxidant stress therapy with gene therapy, flavonoids, recombinant Ad-β-catenin carriers, and autophagy inducers to exert neuroprotective effects. In the future, more clinical trials are needed to explore the effective dosage and side effects of drugs, and to develop new drugs and treatment strategies for oxidative stress to prevent and treat diabetic retinal neurodegeneration and protect retinal nerve function.