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Dioclea violacea lectin preserves brain mitochondrial function and prevents oxidative damage after

Pedro Lourenzo Oliveira Cunha1, Maria Stella Batista de Freitas Neta1, Ludmila Araújo de Lima1

  • 1Faculdade de Medicina, Universidade Federal Do Cariri, Barbalha, CE, Brazil.

Biochimie
|February 5, 2026
PubMed

Insights

Dioclea violacea lectin (DVL) protects brain tissue from ischemic stroke by preserving mitochondrial function and reducing oxidative stress. This plant lectin shows promise for neuroprotection against stroke-related damage.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Ischemic stroke causes brain damage via mitochondrial dysfunction and oxidative stress.
  • Mitochondrial calcium overload can trigger the mitochondrial permeability transition pore (MPTP) opening, leading to cell death.
  • Dioclea violacea lectin (DVL), a plant lectin, possesses various biological activities.

Purpose of the Study:

  • To investigate the neuroprotective effects of in vivo DVL treatment in a rat model of ischemic stroke.
  • To characterize DVL's impact on mitochondrial function, oxidative stress, and MPTP opening post-ischemia.
  • To explore the potential mechanism of DVL's neuroprotection, including its interaction with glutamate.

Main Methods:

  • Rats received intracerebroventricular DVL injection before inducing global cerebral ischemia via bilateral carotid occlusion.
  • Evaluated locomotor activity, oxidative stress markers (nitrite, TBARS, H2O2, SOD activity), mitochondrial respiration, and MPTP opening.
  • Assessed DVL's binding affinity to glutamate.

Main Results:

  • DVL administration prior to ischemia demonstrated significant neuroprotective effects, restoring exploratory behavior and mitigating depression.
  • DVL treatment improved mitochondrial oxygen consumption and ADP/O ratio, reduced oxidative stress markers, and preserved SOD activity.
  • Mitochondria from DVL-treated rats showed reduced susceptibility to Ca2+-induced MPTP opening, and DVL was found to bind glutamate.

Conclusions:

  • DVL exhibits potent neuroprotective effects against ischemic stroke in rats.
  • DVL's mechanism involves preserving mitochondrial function, reducing oxidative stress, and inhibiting MPTP opening.
  • DVL's ability to bind glutamate suggests a novel therapeutic strategy for ischemic stroke.
Keywords:
Free radicalsIschemia/reperfusionLectinMitochondriaNeuroprotection

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