Neuroprotective Effects of Lobeline in Cerebral Ischemia-Reperfusion Injury

Abstract

Objective: To evaluate the neuroprotective potential of Lobeline, a piperidine alkaloid derived from Lobelia inflata, in attenuating the effects of cerebral I/R injury.

Methodology: An experimental model of cerebral ischemia-reperfusion was induced in laboratory animals. The study involved the administration of Lobeline at therapeutic doses prior to and/or after the ischemic insult. Parameters such as infarct volume, neurological deficit scoring, oxidative stress markers (e.g., MDA, SOD, GSH), inflammatory cytokine levels (e.g., TNF-α, IL-1β), and histopathological changes in brain tissue were measured to assess the extent of neuronal damage and the protective effects of Lobeline.

Results: Lobeline-treated groups demonstrated a significant reduction in infarct size compared to controls. There was marked improvement in neurological scores and a decrease in oxidative stress markers, indicating a reduction in lipid peroxidation and enhanced antioxidant defense. Furthermore, histological analysis revealed preserved neuronal architecture, and pro-inflammatory cytokine levels were notably reduced, suggesting an anti-inflammatory effect.

Conclusion: Lobeline exhibits a promising neuroprotective effect in cerebral ischemia-reperfusion injury by modulating oxidative stress and inflammatory responses. These findings support its potential as a therapeutic agent in the management of ischemic stroke and related neurological disorders. Further studies are warranted to elucidate its molecular mechanisms and evaluate its clinical applicability.