Investigation of Neuropathology after Nerve Release in Chronic Constriction Injury of Rat Sciatic Nerve.
Szu-Han ChenChia-Ching WuSheng-Che LinWan-Ling TsengTzu-Chieh HuangAnjali YadavFu-I LuYa-Hsin LiuShau-Ping LinYuan-Yu HsuehPublished in: International journal of molecular sciences (2021)
Peripheral compressive neuropathy causes significant neuropathic pain, muscle weakness and prolong neuroinflammation. Surgical decompression remains the gold standard of treatment but the outcome is suboptimal with a high recurrence rate. From mechanical compression to chemical propagation of the local inflammatory signals, little is known about the distinct neuropathologic patterns and the genetic signatures after nerve decompression. In this study, controllable mechanical constriction forces over rat sciatic nerve induces irreversible sensorimotor dysfunction with sustained local neuroinflammation, even 4 weeks after nerve release. Significant gene upregulations are found in the dorsal root ganglia, regarding inflammatory, proapoptotic and neuropathic pain signals. Genetic profiling of neuroinflammation at the local injured nerve reveals persistent upregulation of multiple genes involving oxysterol metabolism, neuronal apoptosis, and proliferation after nerve release. Further validation of the independent roles of each signal pathway will contribute to molecular therapies for compressive neuropathy in the future.
Keyphrases
- neuropathic pain
- spinal cord
- spinal cord injury
- oxidative stress
- genome wide
- peripheral nerve
- traumatic brain injury
- lipopolysaccharide induced
- cerebral ischemia
- lps induced
- cognitive impairment
- signaling pathway
- minimally invasive
- cell proliferation
- brain injury
- single cell
- gene expression
- skeletal muscle
- inflammatory response
- current status
- blood brain barrier
- long non coding rna
- preterm birth