From:  Neuroprotective potential of phycocyanobilin and C-phycocyanin: from molecular targets to translational applications

 Summary of preclinical evidence on PCB and CPC in models of MS, ischemic stroke, and AD.

Model/DiseaseCompoundKey findingsReferences
EAE-MS modelPCBOral PCB reduced clinical scores, suppressed IL-6, IFN-γ, TNF-α; ↓ NOX2 (CYBB); ↑ HO-1, SOD2; improved redox and inflammatory balance.[12, 15, 16]
CPCReduced disease severity, preserved myelin, induced regulatory T cells; ↓ inflammatory cytokines; created a permissive environment for remyelination.[17, 18]
Cerebral ischemia modelsPCB↓ Oxidative stress (malondialdehyde, protein carbonyls); ↑ HO-1, SOD2, CAT; ↓ IL-6, TNF-α; improved neurological outcomes; reduced infarct volume.[19, 20]
CPCPreserved mitochondrial function, reduced reactive oxygen species, improved survival after ischemia/reperfusion.[21]
AD modelsCPCImproved memory in scopolamine and Aβ models; ↓ Aβ aggregation, ↓ glial activation, ↑ BDNF and synaptic markers.[23, 24]

The data include the principal molecular mechanisms and functional outcomes. Aβ: amyloid-beta; AD: Alzheimer’s disease; BDNF: brain-derived neurotrophic factor; CAT: catalase; CPC: C-Phycocyanin; CYBB: cytochrome b-245 beta chain; EAE: experimental autoimmune encephalomyelitis; HO-1: heme oxygenase-1; IFN-γ: interferon-γ; IL-6: interleukin-6; MS: multiple sclerosis; NOX2: nicotinamide adenine dinucleotide phosphate oxidase 2; PCB: phycocyanobilin; SOD2: superoxide dismutase 2; TNF-α: tumor necrosis factor-alpha. The arrow pointing upwards (↑) represents an increase, and the arrow pointing downwards (↓) represents a decrease.