Hesperidin ameliorates functional and histological outcome and reduces neuroinflammation in experimental stroke

Syed Shadab Raza1, Mohd Moshahid Khan, Ajmal Ahmad

  • 1Neurotoxicology Laboratory, Department of Medical Elementology & Toxicology, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi-110062, India.

Brain Research
|October 1, 2011
PubMed

Insights

Hesperidin treatment protected rats against stroke by reducing brain damage and inflammation. This natural compound improved antioxidant levels and neurological function after middle cerebral artery occlusion (MCAO).

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Stroke is a leading global cause of mortality.
  • Middle cerebral artery occlusion (MCAO) is a common experimental model for studying stroke.
  • Oxidative stress and inflammation play critical roles in stroke-induced brain injury.

Purpose of the Study:

  • To investigate the neuroprotective effects of hesperidin in a rat model of ischemic stroke.
  • To evaluate hesperidin's impact on oxidative stress markers, antioxidant enzyme activity, and inflammatory mediators.
  • To assess hesperidin's efficacy in improving functional and histological outcomes post-stroke.

Main Methods:

  • A middle cerebral artery occlusion (MCAO) model was established in male Wistar rats for 2 hours followed by 22 hours of reperfusion.
  • Rats were administered hesperidin (50 mg/kg body weight) daily for 15 days prior to MCAO.
  • Infarct size, neurological deficits, thiobarbituric acid reactive species (TBARS), antioxidant enzyme activities (GPx, GR, CAT, SOD), glutathione (GSH) content, and inflammatory markers (TNF-α, IL-1β, iNOS, GFAP) were measured.

Main Results:

  • Hesperidin treatment significantly reduced infarct size and neurological deficits in MCAO rats.
  • Hesperidin administration protected against elevated TBARS levels and restored depleted antioxidant enzyme activities and GSH content.
  • Prophylactic hesperidin significantly attenuated the levels of inflammatory mediators (TNF-α, IL-1β) and the expression of iNOS and GFAP.

Conclusions:

  • Prophylactic treatment with hesperidin demonstrates significant neuroprotective effects in an experimental stroke model.
  • Hesperidin ameliorates functional and histological outcomes by enhancing endogenous antioxidant status and reducing inflammation.
  • Hesperidin shows potential as a pharmacological agent to mitigate brain damage by reducing free radicals and associated inflammation following stroke.