Background/Aims:
Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits
after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA-
155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA.
We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of
oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral
inhibition of miR-155.
Methods:
CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western
blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression
of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain
edema were examined to assess neurological functions.
Results:
We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus
of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus.
This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of
miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC
and oxidative stress.
Conclusion:
We showed the significant role of blocking miR-155 signal in improving the neurological function
in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting
that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions
during CA-evoked global cerebral ischemia.
A broad complex tachycardia suggesting global ischemia or repolarization abnormalities
