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What is the molecular mechanism behind BPC157's neuroprotective effects? 


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BPC157 exerts neuroprotective effects through various mechanisms. It modulates the regional synthesis of 5-HT in the brain , promotes angiogenesis by upregulating VEGFR2 expression and activating the VEGFR2-Akt-eNOS signaling pathway , and regulates cytosolic and mitochondrial Ca2+ dynamics to prevent excitotoxicity and neuronal cell death . Additionally, BPC157 can rescue cancer cachexia by targeting anorexia, hypoanabolism, and hypercatabolism, offering a potential therapeutic approach for this condition . Furthermore, BPC157, when modified by CD157, enhances the transfer of extracellular mitochondrial particles from BMSCs to injured neurons, promoting axon regeneration and reducing cell apoptosis in spinal cord injury models . These multifaceted actions collectively contribute to BPC157's neuroprotective properties.

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CGP37157 protects neurons by inhibiting mitochondrial Na+/Ca2+ exchanger, reducing Ca2+ overload via voltage-gated Ca2+ channel blockage, thus preventing excitotoxicity-induced mitochondrial dysfunction and cell death.
CD157 upregulation in BMSCs enhances extracellular mitochondrial transfer to neurons, reducing apoptosis and promoting functional recovery after spinal cord injury, suggesting a novel neuroprotective mechanism involving mitochondrial transfer.
BPC157's neuroprotective effects in cancer cachexia may involve central nervous system modulation, anorexia alleviation, and anti-inflammatory properties, potentially rescuing patients from muscle wasting and weight loss.
The molecular mechanism behind BPC157's neuroprotective effects involves increasing survival of enteric neurons and promoting proliferation of enteric glial cells, aiding in healing damaged structures in the gastrointestinal tract.
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