Description: <b>Flowering plant</b> uses ginger root for help with nausea, weight loss, arthritis, diabetes. Anti-inflammatory and antioxidant. <br>
Gingerol is a phenolic phytochemical compound found in fresh ginger that activates heat receptors on the tongue. It is normally found as a pungent yellow oil in the ginger rhizome.<br>
Ginger contains multiple bioactive compounds including 6-gingerol, 8-gingerol, 10-gingerol, 6-shogaol, paradols, and zingerone.<br>
<pre>
In cancer-focused literature, the majority of mechanistic work centers on 6-gingerol and 6-shogaol.
Mechanistic themes (preclinical):
-Anti-inflammatory (NF-κB↓, COX-2↓)
-Survival pathway modulation (PI3K/AKT↓, STAT3↓ reported)
-MAPK modulation (ERK/JNK/p38 context-dependent)
-ROS modulation (antioxidant in normal cells; pro-oxidant at higher doses in tumor models)
-Cell-cycle arrest (G1 or G2/M reported)
-Apoptosis induction (mitochondrial pathway)
-Anti-angiogenic and anti-metastatic signaling (VEGF↓, MMPs↓ reported)
Bioavailability note:
-Gingerols are rapidly metabolized (glucuronidation/sulfation)
-Plasma levels after dietary intake are far below many in-vitro micromolar doses
-6-Shogaol is generally more potent than 6-gingerol in cell systems
</pre>
<br>
<!-- Ginger (Zingiber officinale) — Cancer-Oriented Time-Scale Flagged Pathway Table -->
<table border="1" cellpadding="4" cellspacing="0">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer / Tumor Context</th>
<th>Normal Tissue Context</th>
<th>TSF</th>
<th>Primary Effect</th>
<th>Notes / Interpretation</th>
</tr>
<tr>
<td>1</td>
<td>NF-κB inflammatory transcription</td>
<td>NF-κB ↓; COX-2 ↓; pro-inflammatory cytokines ↓ (reported)</td>
<td>Inflammation tone ↓</td>
<td>R, G</td>
<td>Anti-inflammatory / anti-survival transcription</td>
<td>One of the most consistent ginger signatures; reduction of inflammatory tumor-support signaling.</td>
</tr>
<tr>
<td>2</td>
<td>PI3K → AKT (± mTOR) survival axis</td>
<td>PI3K/AKT ↓ (reported; model-dependent)</td>
<td>↔</td>
<td>R, G</td>
<td>Growth/survival modulation</td>
<td>Often described in conjunction with apoptosis and proliferation reduction.</td>
</tr>
<tr>
<td>3</td>
<td>ROS / redox modulation (biphasic)</td>
<td>ROS ↑ (at higher doses); apoptosis ↑</td>
<td>ROS ↓; antioxidant activity</td>
<td>P, R</td>
<td>Redox destabilization (tumor) / buffering (normal)</td>
<td>Gingerols and shogaols may act antioxidant in normal tissue but pro-oxidant in tumor systems under higher concentrations.</td>
</tr>
<tr>
<td>4</td>
<td>Intrinsic apoptosis (mitochondrial pathway)</td>
<td>ΔΨm ↓; Bax ↑; caspase-3 ↑ (reported)</td>
<td>↔ (less activation)</td>
<td>G</td>
<td>Apoptosis execution</td>
<td>Often downstream of ROS and survival-pathway suppression.</td>
</tr>
<tr>
<td>5</td>
<td>Cell-cycle arrest (G1 or G2/M)</td>
<td>Cell-cycle arrest ↑ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Cytostasis</td>
<td>Associated with modulation of Cyclins/CDKs; phase varies by tumor type.</td>
</tr>
<tr>
<td>6</td>
<td>MAPK pathways (ERK / JNK / p38)</td>
<td>Stress-MAPK modulation (context-dependent)</td>
<td>↔</td>
<td>P, R, G</td>
<td>Signal reprogramming</td>
<td>JNK/p38 activation often linked to stress-induced apoptosis; ERK direction varies.</td>
</tr>
<tr>
<td>7</td>
<td>STAT3 signaling</td>
<td>STAT3 ↓ (reported)</td>
<td>↔</td>
<td>R, G</td>
<td>Transcriptional survival suppression</td>
<td>Observed in certain tumor models; contributes to reduced proliferation and invasion.</td>
</tr>
<tr>
<td>8</td>
<td>Angiogenesis signaling (VEGF)</td>
<td>VEGF ↓ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Anti-angiogenic support</td>
<td>Typically a downstream effect of inflammatory and survival pathway suppression.</td>
</tr>
<tr>
<td>9</td>
<td>Invasion / metastasis (MMPs / EMT)</td>
<td>MMP-2/MMP-9 ↓; migration ↓ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Anti-invasive phenotype</td>
<td>Frequently linked to NF-κB and STAT3 suppression.</td>
</tr>
<tr>
<td>10</td>
<td>Bioavailability constraint</td>
<td>Systemic free gingerol levels low; rapid conjugation</td>
<td>—</td>
<td>—</td>
<td>Translation constraint</td>
<td>In-vitro cytotoxic concentrations often exceed achievable plasma levels after dietary intake.</td>
</tr>
</table>
<p><b>Time-Scale Flag (TSF):</b> P / R / G</p>
<ul>
<li><b>P</b>: 0–30 min (early redox and kinase interactions)</li>
<li><b>R</b>: 30 min–3 hr (acute signaling shifts: NF-κB, PI3K/AKT, MAPK)</li>
<li><b>G</b>: >3 hr (gene-regulatory adaptation, apoptosis, phenotype outcomes)</li>
</ul>