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Related Experiment Video

Updated: May 13, 2026

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
05:45

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing

Published on: October 25, 2019

Serum leptin levels decrease after permanent MCAo in the rat and remain unaffected by delayed hyperbaric oxygen

Jun Mu1, Robert P Ostrowski, Paul R Krafft

  • 1Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. johnzhang3910@yahoo.com.

Medical Gas Research
|March 21, 2013
PubMed
Summary
This summary is machine-generated.

Hyperbaric oxygen therapy (HBOT) did not alter leptin levels in rats after stroke. While HBOT improved stroke outcomes, the neuroprotective effects were not linked to changes in serum leptin concentrations.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Physiology

Background:

  • Hyperbaric oxygen therapy (HBOT) offers neuroprotection post-ischemic stroke through various mechanisms.
  • Leptin, a hormone from adipose tissue, demonstrates neuroprotective properties in experimental stroke models.
  • The impact of HBOT on leptin levels following permanent middle cerebral artery occlusion (pMCAo) remains uninvestigated.

Purpose of the Study:

  • To investigate the effect of delayed HBOT on serum leptin concentrations in rats subjected to pMCAo.
  • To determine if alterations in leptin levels contribute to the neuroprotective effects of HBOT after stroke.

Main Methods:

  • Rats underwent pMCAo and received delayed HBOT (2.5 ATA, 100% O2, 1 hr/day for 10 days) starting 48 hours post-occlusion.
  • Neurobehavioral deficits, body weight, and infarct size were assessed.
  • Serum leptin concentrations were measured using ELISA on days 1 and 16 post-HBOT initiation.

Main Results:

  • Delayed HBOT significantly reduced infarct size and improved neurobehavioral scores in pMCAo rats.
  • Serum leptin levels decreased in both HBOT-treated and untreated pMCAo groups compared to the sham group.
  • No significant difference in leptin levels was observed between the HBOT and air-treated groups.

Conclusions:

  • The neuroprotective effects of delayed HBOT in pMCAo rats are unlikely mediated by changes in serum leptin concentration.
  • Further research is needed to elucidate the precise mechanisms underlying HBOT's neuroprotective actions post-stroke.