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2000
Volume 1, Issue 1
  • ISSN: 2210-299X
  • E-ISSN: 2210-3007

Abstract

Background

Glucose regulation and energy homeostasis mitigate energy crises milieu in reperfusion injury. We investigated Banaba for its outcomes on cerebral ischemia reperfusion (IR) injury using artery occlusion in rats. The pleiotropic activity of Banaba on various debilitating mechanisms inducing reperfusion injury was evaluated.

Aim

This study aimed to evaluate the pharmacological activity of Banaba () extract on reperfusion injury and investigate the effect of Banaba on vascular permeability, oxidative stress and cellular damage in ischemia reperfusion injury in rats.

Methods

Transient ischemia and reperfusion through occlusion of the middle cerebral artery (MCAO) lead to Cerebral IR injury in Wistar rats; it was treated with oral administration of Banaba extract (100mg/kg and 200mg/kg). The injury outcomes were evaluated after 22 hours of reperfusion by determining cellular injury, its impact on musculoskeletal coordination, multiple free radical scavenging measures (SOD, GSH, LPO) and vascular permeability of the blood-brain barrier.

Results

Banaba treatment led to a marked improvement in neurological outcomes by enhanced coordination and reduced cerebral infarct in comparison to vehicle control ischemic group. Free radical scavenging activity (SOD and GSH) was significantly better, and lipid peroxidation was reduced by Banaba treatment; it also reduced the vascular permeability of the blood-brain barrier. We observed that a lower dose of Banaba (100 mg/kg) was more effective than the higher (200 mg/kg) in ischemic rats. The anti-inflammatory and anti-oxidant activity could drive the neuroprotective outcomes of Banaba in cerebral IR injury. The critical factor of the beneficial effect of Banaba in cerebral injury is the optimization of dose in this experimental setup of reperfusion injury using rats.

Conclusion

The recovery of injury could be attributed to Banaba’s multi-factorial effect targeting free radicals, inflammation, and necrosis during ischemia-reperfusion injury.

This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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2023-11-07
2025-09-16
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