Description: <p><b>Ginseng</b> = adaptogenic herbal root from the genus <i>Panax</i>; main species: Asian ginseng (<i>Panax ginseng</i>) and American ginseng (<i>Panax quinquefolius</i>). Active constituents: ginsenosides (Rb1, Rg1, Rg3, Rh2), polysaccharides, and other saponins.<br>
<b>Primary mechanisms (conceptual rank):</b><br>
1) Multi-pathway signaling modulation (PI3K/Akt, MAPK, NF-κB; isoform-dependent).<br>
2) Redox regulation (bidirectional ROS modulation; NRF2 interaction).<br>
3) Anti-inflammatory and immunomodulatory effects.<br>
4) Anti-proliferative and pro-apoptotic effects in cancer (notably Rg3, Rh2; dose-dependent).<br>
5) Neurotrophic and cholinergic modulation (BDNF, ACh support).<br>
<b>PK / bioavailability:</b> ginsenosides have variable oral absorption; gut microbiota convert to active metabolites (e.g., Compound K); plasma levels generally lower than many in-vitro doses.<br>
<b>In-vitro vs systemic exposure:</b> many cancer studies use ≥10–100 µM; achievable plasma concentrations after oral dosing are typically lower and metabolite-driven.<br>
<b>Clinical evidence status:</b> supportive oncology (fatigue reduction) supported by RCTs; direct anti-cancer efficacy largely preclinical; cognitive and fatigue benefits better substantiated.</p>
<b>Ginseng (Panax ginseng)</b> – This herb has been studied for its ability to enhance the immune system.<br>
-Antioxidant Properties: Ginseng contains ginsenosides, which have antioxidant properties.<br>
-Immune System Support<br>
-Inhibition of Tumor Growth<br>
-Chemopreventive Effects<br>
-Synergistic Effects with Cancer Treatments: ginseng may enhance the effectiveness of certain cancer treatments, such as chemotherapy, and may help reduce side effect<br>
Dose: Standardized Extract:<br>
Dosage: extract containing 4-7% ginsenosides 200-400mg/d<br>
Dried Root:1-2g/d<br>
Tea: 1-2g dried root, 1-3x/d<br>
<br>
<h3>Ginseng (Panax spp.) — Cancer-Relevant Pathways</h3>
<table>
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer Cells</th>
<th>Normal Cells</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
<tr>
<td>1</td>
<td>PI3K/Akt / MAPK signaling</td>
<td>↓ proliferation (isoform-dependent)</td>
<td>↔ / adaptive support</td>
<td>R→G</td>
<td>Growth signaling attenuation</td>
<td>Ginsenosides Rg3/Rh2 most studied; context- and tumor-type dependent.</td>
</tr>
<tr>
<td>2</td>
<td>Apoptosis (caspase / mitochondrial)</td>
<td>↑ (dose-dependent)</td>
<td>↔ / protective</td>
<td>R→G</td>
<td>Pro-apoptotic signaling</td>
<td>Mitochondrial depolarization reported; supra-physiologic concentrations common in vitro.</td>
</tr>
<tr>
<td>3</td>
<td>ROS modulation</td>
<td>↑ (high concentration) / ↓ (adaptive)</td>
<td>↓</td>
<td>P→R</td>
<td>Redox modulation</td>
<td>Bidirectional: pro-oxidant cytotoxicity in tumors at high dose; antioxidant in normal cells.</td>
</tr>
<tr>
<td>4</td>
<td>NF-κB / inflammation</td>
<td>↓</td>
<td>↓</td>
<td>R→G</td>
<td>Anti-inflammatory</td>
<td>Reduces pro-tumor inflammatory microenvironment signals.</td>
</tr>
<tr>
<td>5</td>
<td>Angiogenesis (VEGF)</td>
<td>↓ (preclinical)</td>
<td>↔</td>
<td>G</td>
<td>Anti-angiogenic</td>
<td>Reported particularly with Rg3; human oncologic outcome data limited.</td>
</tr>
<tr>
<td>6</td>
<td>NRF2 axis</td>
<td>↔ / ↑ (adaptive)</td>
<td>↑</td>
<td>G</td>
<td>Antioxidant enzyme induction</td>
<td>Protective in normal tissues; tumor resistance context-dependent.</td>
</tr>
<tr>
<td>7</td>
<td>Clinical Translation Constraint</td>
<td>—</td>
<td>—</td>
<td>—</td>
<td>Adjunct role</td>
<td>RCTs support fatigue reduction in cancer patients; direct anti-tumor efficacy not established.</td>
</tr>
</table>
<p><b>TSF Legend:</b> P: 0–30 min | R: 30 min–3 hr | G: >3 hr</p>
<br>
<h3>Ginseng (Panax spp.) — Alzheimer’s Disease–Relevant Axes</h3>
<table>
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cells (neurons/glia)</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
<tr>
<td>1</td>
<td>BDNF / neuroplasticity</td>
<td>↑</td>
<td>G</td>
<td>Neurotrophic support</td>
<td>Rg1 and metabolites reported to enhance BDNF signaling; supports cognition in mild impairment models.</td>
</tr>
<tr>
<td>2</td>
<td>Cholinergic modulation</td>
<td>↑ (mild)</td>
<td>R→G</td>
<td>ACh support</td>
<td>May increase ACh release or inhibit AChE modestly; relevance additive to standard therapy unclear.</td>
</tr>
<tr>
<td>3</td>
<td>Neuroinflammation (NF-κB)</td>
<td>↓</td>
<td>R→G</td>
<td>Microglial modulation</td>
<td>Reduces pro-inflammatory cytokines in animal models.</td>
</tr>
<tr>
<td>4</td>
<td>ROS / oxidative stress</td>
<td>↓</td>
<td>P→R</td>
<td>Antioxidant support</td>
<td>Induces antioxidant enzymes; may protect against Aβ-induced oxidative injury.</td>
</tr>
<tr>
<td>5</td>
<td>Aβ processing</td>
<td>↓ (preclinical)</td>
<td>G</td>
<td>Reduced amyloid burden</td>
<td>Animal studies suggest modulation of APP processing; human AD RCT data limited.</td>
</tr>
<tr>
<td>6</td>
<td>Clinical Translation Constraint</td>
<td>—</td>
<td>—</td>
<td>Modest cognitive benefit</td>
<td>Small human trials suggest mild cognitive improvement; not disease-modifying.</td>
</tr>
</table>
<p><b>TSF Legend:</b> P: 0–30 min | R: 30 min–3 hr | G: >3 hr</p>