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

Abstract

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 (K_ATP) 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-1β expression. Through these experiments, we will explore the protective effect of Post C in SCII, observe the changes in the protective effect after using K_ATP blockers, and verify that Post C can play a neuroprotective effect in SCII by activating K_ATP.

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 K_ATP inhibitor.

Conclusion: Post C has a neuroprotective effect on SCII, and maybe a protective effect produced by activating K_ATP to regulate spinal microglia polarization and improve neuroinflammation.