Ischemic postconditioning reduces spinal cord ischemia-reperfusion injury through ATP-sensitive potassium channel.

STUDY DESIGN: Animal study. OBJECTIVES: Explore the neuroprotective effect of remote limb ischemic postconditioning (Post C) in spinal cord ischemic reperfusion injury (SCII) and related mechanisms. SETTING: Anesthesiology Laboratory of Southwest Medical University. METHODS: We established a rabbit SCII model and processed it with Post C. To evaluate the neural function, spinal cord tissue was taken 48 h later, normal neurons were evaluated by HE staining, and the expression of ATP-sensitive potassium channel (KATP) marker molecule Kir6.2 was detected by Western blot. Immunofluorescence detection of spinal cord Iba-1 expression, ELISA detection of M1 type microglia marker iNOS and M2 type microglia marker Arg, and Western blot detection of NF-κB and IL-1ß expression. Through these experiments, we will explore the protective effect of Post C in SCII, observe the changes in the protective effect after using KATP blockers, and verify that Post C can play a neuroprotective effect in SCII by activating KATP. RESULTS: We observed that Post C significantly improved exercise ability and the number of spinal motor neurons in the SCII model. Microglia are activated and expression of M1 microglia in the spinal cord was decreased, while M2 was increased. This neuroprotective effect was reversed by the nonspecific KATP inhibitor. CONCLUSION: Post C has a neuroprotective effect on SCII, and maybe a protective effect produced by activating KATP to regulate spinal microglia polarization and improve neuroinflammation.