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Berberine Improves Neurological Function in Rats
This preprint investigated the neuroprotective effects of Berberine pretreatment in a rat model of Parkinson's disease.
Key Points:
Berberine supplementation displayed therapeutic benefits:
• Improved motor function and coordination
• Reduced oxidative stress and enhanced antioxidant defenses
• Restored mitochondrial function
• Decreased neuroinflammation and apoptosis
• Effects were mediated through the Nrf2 pathway
Berberine Pretreatment Improved Motor Function and Coordination
Berberine treatment significantly reduced impairments in locomotor activity, rotarod performance, and grip strength. It also improved limb movement and motor coordination in the beam-crossing task.
Berberine Improved Markers of Oxidative Stress
Rotenone increased nitrite and lipid peroxidation, markers of oxidative stress, while decreasing glutathione, superoxide dismutase, and catalase, markers of regenerative capacity.
Berberine treatment significantly reversed these changes, indicating reduced oxidative stress and enhanced antioxidant defenses.
Berberine Restored Mitochondrial Function
Mitochondrial dysfunction, a hallmark of Parkinson’s Disease, was evident in rotenone-treated rats, as shown by decreased levels of succinate dehydrogenase, ATPase, and electron transport chain enzymes.
Berberine administration restored mitochondrial function, an effect that was eliminated by the Nrf2 blocker.
These statements have not been evaluated by the Food and Drug Administration.
These products are not intended to diagnose, treat, cure or prevent any disease.
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