tbResList Print — PTS Pterostilbene

Description: <b>Antioxidant</b> found in blueberries, cranberries and grapes.<br>
Pterostilbene (trans-3,5-dimethoxy-40-hydroxystilbene) is a naturally occurring stilbene, found mainly in blueberries and grapes. It is a dimethylated derivative of resveratrol with comparable antioxidant, anti-inflammatory and anticarcinogenic properties [26].<br>
-more bioavailable than resveratrol<br>
-Antioxidant activity: Reduces reactive oxygen species and lipid peroxidation<br>
-Anti-inflammatory: Downregulates pro-inflammatory cytokines- IL-1β, TNF-α, NF-κB<br>
-Amyloid pathology:inhibits Aβ aggregation and promotes clearance- Aβ, APP, BACE1<br>
-Reduces hyperphosphorylation of tau protein<br>
-Inhibits histone deacetylases (HDACs)<br>
-Increases acetylcholine by inhibiting acetylcholinesterase<br>
-Sirtuin activation<br>
<br>

<table border="1" cellspacing="0" cellpadding="4">
<tr>
<th>Rank</th>
<th>Pathway / Axis</th>
<th>Cancer Cells</th>
<th>Normal Cells</th>
<th>Label</th>
<th>Primary Interpretation</th>
<th>Notes</th>
</tr>

<tr>
<td>1</td>
<td>SIRT1 / AMPK metabolic sensing</td>
<td>↑ AMPK; context-dependent SIRT1 modulation</td>
<td>↑ SIRT1 / ↑ AMPK</td>
<td>Driver</td>
<td>Energy-stress signaling</td>
<td>Pterostilbene strongly engages energy-sensing pathways due to high bioavailability</td>
</tr>

<tr>
<td>2</td>
<td>PI3K → AKT → mTOR axis</td>
<td>↓ AKT / ↓ mTOR</td>
<td>↔ adaptive suppression</td>
<td>Driver</td>
<td>Growth and survival inhibition</td>
<td>AKT/mTOR suppression explains cytostatic and pro-apoptotic effects in cancer cells</td>
</tr>

<tr>
<td>3</td>
<td>Reactive oxygen species (ROS)</td>
<td>↑ ROS (mild, dose-dependent)</td>
<td>↓ ROS / buffered</td>
<td>Conditional Driver</td>
<td>Biphasic redox modulation</td>
<td>More balanced redox profile than resveratrol; weaker pro-oxidant behavior</td>
</tr>

<tr>
<td>4</td>
<td>Mitochondrial integrity / intrinsic apoptosis</td>
<td>↓ ΔΨm; ↑ caspase activation</td>
<td>↔ preserved</td>
<td>Secondary</td>
<td>Execution of apoptosis</td>
<td>Mitochondrial apoptosis follows metabolic and redox stress</td>
</tr>

<tr>
<td>5</td>
<td>NF-κB signaling</td>
<td>↓ NF-κB activation</td>
<td>↓ inflammatory NF-κB tone</td>
<td>Secondary</td>
<td>Suppression of inflammatory survival programs</td>
<td>NF-κB inhibition contributes to anti-invasive and chemosensitizing effects</td>
</tr>

<tr>
<td>6</td>
<td>Cell cycle regulation</td>
<td>↑ G1 or G2/M arrest</td>
<td>↔ spared</td>
<td>Phenotypic</td>
<td>Cytostatic growth control</td>
<td>Cell-cycle arrest reflects upstream metabolic and signaling effects</td>
</tr>

<tr>
<td>7</td>
<td>NRF2 antioxidant response</td>
<td>↑ NRF2 (adaptive)</td>
<td>↑ NRF2 (protective)</td>
<td>Adaptive</td>
<td>Redox compensation</td>
<td>NRF2 activation contributes to stress buffering rather than primary cytotoxicity</td>
</tr>

</table>