Black Seed OilvsCordyceps

Thymoquinone is the primary bioactive, providing neuroprotection through multiple mechanisms: it scavenges reactive oxygen species (superoxide, hydroxyl radical, peroxynitrite) and upregulates Nrf2/ARE pathway, increasing glutathione (via GCLC, GSS), superoxide dismutase (SOD1/SOD2), and catalase. It inhibits NF-kB by preventing IkB-alpha degradation and blocking p65 nuclear translocation, reducing neuroinflammation and pro-inflammatory cytokine release. Thymoquinone inhibits acetylcholinesterase (AChE) at the peripheral anionic site, increasing synaptic acetylcholine. It modulates GABA-A receptors (positive allosteric modulation at benzodiazepine site), providing anxiolytic effects. Thymoquinone protects neurons from amyloid-beta toxicity by reducing oxidative stress and inhibiting beta-secretase (BACE1). It reduces tau hyperphosphorylation by inhibiting GSK-3beta and CDK5.

Cordycepin (3'-deoxyadenosine), the primary bioactive compound, increases ATP production by enhancing mitochondrial electron transport chain efficiency — it may act as an alternative substrate or modulator of Complex I and Complex III. Cordycepin activates AMPK (AMP-activated protein kinase) via increased AMP/ATP ratio or direct activation of the alpha subunit, promoting glucose uptake through GLUT4 translocation and fatty acid oxidation via CPT-1 and ACC inhibition. Cordyceps increases erythropoietin (EPO) production, likely through HIF-1alpha stabilization in hypoxic-sensitive tissues, improving oxygen-carrying capacity. Cordycepin has adenosine-like activity, modulating purinergic P1 (A1, A2A, A2B, A3) and P2 receptors. Anti-inflammatory effects occur through inhibition of NF-kB (reducing IKK degradation of IkB and nuclear translocation) and reduction of pro-inflammatory cytokines (IL-1beta, IL-6, TNF-alpha). Adenosine deaminase-resistant cordycepin may also affect RNA polyadenylation.