The Effect of 2 Weeks of Naringenin on AQP4, IL-2 and DNA Damage in Brain Ischemia Reperfusion in Rats

M Somuncu, D Dasdelen, S B Baltaci

  • 1Selcuk University, Medical School, Department of Physiology, 42075, Konya, Turkey -

Insights

Naringenin administration for two weeks in rats significantly reduced brain damage markers, including Aquaporin-4 (AQP4), interleukin-2 (IL-2), and 8-Hydroxydeoxyguanosine (8-OhdG), following ischemia-reperfusion injury.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Brain ischemia-reperfusion (I/R) injury is a critical condition leading to significant neurological damage.
  • Biomarkers such as Aquaporin-4 (AQP4), interleukin-2 (IL-2), and 8-Hydroxydeoxyguanosine (8-OhdG) are elevated following I/R injury.
  • Naringenin, a natural flavonoid, has demonstrated potential therapeutic properties.

Purpose of the Study:

  • To investigate the neuroprotective effects of naringenin on brain I/R injury in a rat model.
  • To assess the impact of naringenin on specific biomarkers: AQP4, IL-2, and 8-OhdG levels in the brain.

Main Methods:

  • Rats were divided into control, sham, I/R, and two naringenin treatment groups (50 mg/kg and 100 mg/kg).
  • Naringenin was administered intraperitoneally for two weeks prior to inducing I/R injury (1 hour occlusion, 1 hour reperfusion).
  • Brain frontal cortex tissue was analyzed for AQP4, IL-2, and 8-OhdG levels post-experiment.

Main Results:

  • Ischemia-reperfusion significantly increased AQP4, IL-2, and 8-OhdG levels in the control group.
  • Both 50 mg/kg and 100 mg/kg doses of naringenin significantly reduced these elevated biomarker levels (P < 0.001).

Conclusions:

  • Two-week intraperitoneal administration of naringenin demonstrates significant neuroprotective effects against brain ischemia-reperfusion injury in rats.
  • Naringenin effectively mitigates the increase in AQP4, IL-2, and 8-OhdG associated with I/R.
  • Naringenin shows promise as a therapeutic agent for preventing or treating brain I/R damage.

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