A research team led by Professor Kiichi Hirota of Kansai Medical University has elucidated the mechanism of neuropathy known as a side effect of local anesthesia and nerve block anesthesia.A paper showing the possibility of risk reduction was published in the English scientific journal "Scientific Reports".The results are based on joint research with Shimane University, Kyoto University, and Life Science Integrated Database Center.

　Although the safety of peripheral nerve block, which blocks the transmission of pain by injecting a local anesthetic into the peripheral nerves separated from the spinal cord, has been established, it causes motor and sensory disorders when the nerves in the spinal cord are damaged. In some cases.Therefore, there is a need for research that elucidates the mechanism of the occurrence of neuropathy and is useful for its prevention and treatment.

　So far, research groups have shown that local anesthetics generate reactive oxygen species in intracellular mitochondria and induce cell death, and that removal of these reactive oxygen species prevents cell death.It was also known that hypoxia-inducible factor 1 (HIF-1) regulates oxygen metabolism in mitochondria.

　This time, HIF-1 was artificially activated to change the expression state of genes involved in intracellular energy and oxygen metabolism, and the dependence on mitochondria in cell energy production was reduced.This indicates that cell death can be avoided by suppressing the generation of active oxygen from mitochondria by local anesthetics.In addition, we were able to present a method for preventing cell damage with a local anesthetic as well as basic medical value by analysis including comprehensive gene expression data.

　This result shows that perioperative medication and treatment may reduce the risk of neuropathy during local anesthesia, and the development of highly safe treatment not only in surgery but also in pain management such as pain clinics. Is expected.

Paper information: [Scientific Reports] HIF-1-mediated suppression of mitochondria electron transport chain 3 function confers resistance to lidocaine-induced cell death