Background: LKB1/AMPK signaling pathway, as a metabolic checkpoint, is
involved in the pathogenesis of cerebral ischemia injury. Minocycline, a tetracycline
derivative, protects against cerebral ischemia via reducing inflammation, oxidative
stress, and apoptosis. The aim of the study was to evaluate the influence of minocycline
on oxidative biomarkers and LKB1/AMPK signaling pathway in Wistar rats with focal
cerebral ischemia injury and to clarify the neuroprotective mechanism of minocycline
against focal cerebral ischemia injury.
Methods: The focal cerebral ischemia injury of Wistar rats was established by inserting
a thread into the left middle cerebral artery. 2,3,5-Triphenyltetrazolium chloride (TTC)
staining was used to label infarct volume. The levels of MDA and LPO were measured
with a biochemical assay. All other items were determined by Western blotting.
Results: Minocycline decreased cerebral infarct volume, but had no effects on
neurological scores. Minocycline improved the biological activity of GPx-1/2, GSS and
GR, while limited the GGT1 activity in the hippocampus of cerebral ischemia-reperfusion
rats. Minocycline also elevated the biological activity of SOD and counteracted lipid
peroxidation. Minocycline enhanced the activity of both LKB1 and the levels of the three
AMPK subunits in the hippocampus of cerebral ischemia-reperfusion rats.
Conclusion: Minocycline effectively inhibits oxidative stress via modulating antioxidative
enzymes and activating the LKB1/AMPK signaling pathway in the process of
acute cerebral infarct.