Neuroprotective Effects of Lobeline in Cerebral Ischemia-Reperfusion Injury

Neuroprotective Effects of Lobeline in Cerebral Ischemia-Reperfusion Injury

Hetvi Shah1*, Dr. Nishkruti Mehta2, Dr. Pragnesh Patani3, Sanjana Chandarana4

1*Department of Pharmacology, Khyati College of Pharmacy, India.

2 Professor, Department of Pharmacology, Khyati College of Pharmacy, Palodia, Ahmedabad

3 Principal and Professor, Department of Pharmacology, Khyati College of Pharmacy, Palodia, Ahmedabad

4 Department of Pharmacology, Khyati College of Pharmacy, India.

*Corresponding Author: Hetvi Shah

*Department of Pharmacology, Khyati College of Pharmacy, India, Email: hetvishah1304@gmail.com

Abstract

Background: Cerebral ischemia-reperfusion (I/R) injury remains a major cause of morbidity and mortality worldwide. It results from the temporary interruption of cerebral blood flow followed by the restoration of circulation, which paradoxically exacerbates neuronal injury through a cascade involving oxidative stress, inflammation, and excitotoxicity. The pathophysiological mechanisms include energy failure, ion imbalance, elevated intracellular calcium levels, generation of reactive oxygen species (ROS), and activation of inflammatory cytokines. These processes lead to cellular damage and death, primarily through necrosis and apoptosis.

Objective: This study aims to evaluate the neuroprotective potential of Lobeline, a piperidine alkaloid derived from Lobelia inflata, in attenuating the effects of cerebral I/R injury. Lobeline is known for its diverse pharmacological effects, including antioxidant and anti-inflammatory properties, which may contribute to neuroprotection.

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 also 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.