Description: <b>Ferulic acid</b> is an antioxidant found in some skin creams and serums.<br>
Foods: popcorn, bamboo, whole-grain rye bread, whole-grain oat flakes, sweet corn (cooked)<br>
Ferulic acid (FA) is a
<a href="https://nestronics.ca/dbx/tbProdEdit.php?pid=95">hydroxycinnamic acid </a> abundant in plant cell walls (notably cereals/whole grains) with strong antioxidant and cytoprotective activity. Mechanistically, FA is frequently described as inducing Nrf2/HO-1 antioxidant programs and suppressing NF-κB-linked inflammation, with additional model-dependent anticancer effects (cell-cycle arrest, apoptosis, reduced invasion). Oral exposure is variable because FA is rapidly metabolized (often as conjugates) and bioaccessibility depends on the food matrix.<br>
<br>
-Ferulic acid found in dietary strand fractions, especially its free form, has important functions for protecting the human health.<br>
-AChE inhibitor (AD)<br>
-Cooking results in an increase in free ferulic acid quantity and in a reduction in bound ferulic acid quantity.<br>
<pre>
Bamboo shoots 243.6 mg/100g
Sugar-beet pulp 800 mg/100g
Popcorn 313 mg/100g
Wheat bran 500–1500mg/100g
Whole wheat flour 100–300mg/100g
</pre>
<table Border="1" rules="rows">
<tr><th>Type of corn</th> <th>p-coumaric acid</th> <th>ferulic acid</th></tr>
<tr><td> </td> <td> mg/kg, DW </td> <td>mg/kg, DW</td></tr>
<tr><td>Yellow dent</td> <td>18.9 </td> <td>265</td></tr>
<tr><td>American blue</td> <td>N.D. </td> <td>927</td></tr>
<tr><td>Mexican blue</td> <td>1.3 </td> <td>202</td></tr>
<tr><td>white</td> <td>6.6 </td> <td>2484</td></tr>
</table>
<pre>
Pathway / Target Modulation by FA / Direction
Aβ aggregation ↓ Inhibits fibril formation and destabilizes existing Aβ fibrils
BACE‑1 & APP ↓ Reduces BACE-1 and APP expression; ↑ MMP‑2/‑9 expression promoting Aβ clearance
Tau hyperphosphorylation Implicitly ↓ through modulation of Ca²⁺/CDK5/GSK3β pathways
Ca²⁺ ↓ FA lowers STEP levels via chelation of Ca²⁺, suppressing PP2B → restores synaptic plasticity
(AChE / BChE) ↓ Inhibition of AChE (FA IC₅₀~15 µM, derivatives IC₅₀ down to 0.006 µM); also BChE
(MAO‑A/B) ↓ Inhibits MAO‑B (derivatives IC₅₀ ~0.3–0.7 µM), reducing ROS
ROS ↓ Scavenges ROS, enhances antioxidant enzymes (e.g., catalase), ↓ MDA
(COX‑2, 5‑LOX, NLRP3) ↓ Derivatives inhibit COX‑2/5‑LOX; derivative 13a ↓ NLRP3 inflammasome
Iron/Cu²⁺ chelation ↓ Metal-induced Aβ aggregation via chelation by FA and derivatives
Autophagy & Aβ clearance ↗ Suggested promotion of autophagy mechanisms targeting Aβ
</pre>
<!-- Ferulic Acid (FA) — Time-Scale Flagged Pathway Table (web-page ready) -->
<table border="1" cellpadding="4" cellspacing="0">
<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>Nrf2 → HO-1 / ARE antioxidant response</td>
<td>Stress adaptation modulation (context-dependent)</td>
<td>Nrf2 ↑; HO-1 ↑; antioxidant defenses ↑</td>
<td>R, G</td>
<td>Endogenous antioxidant upshift</td>
<td>FA is repeatedly reported to promote Nrf2 nuclear translocation and HO-1 induction; this is one of the most defensible “core” mechanisms.</td>
</tr>
<tr>
<td>2</td>
<td>NF-κB inflammatory transcription (COX-2 / iNOS / cytokines)</td>
<td>NF-κB ↓; COX-2/iNOS and pro-inflammatory cytokine programs ↓ (reported)</td>
<td>Inflammation tone ↓ (tissue protective)</td>
<td>R, G</td>
<td>Anti-inflammatory signaling</td>
<td>Often described as downstream of redox changes and upstream of reduced inflammatory mediators; direction is consistent across many inflammation models.</td>
</tr>
<tr>
<td>3</td>
<td>ROS / oxidative stress tone</td>
<td>Oxidative stress ↓ (often); ROS direction can vary by tumor model</td>
<td>Oxidative injury ↓</td>
<td>P, R, G</td>
<td>Redox buffering (context-dependent)</td>
<td>FA is classically antioxidant; in tumor systems, effects may be secondary to signaling changes and vary with baseline redox instability.</td>
</tr>
<tr>
<td>4</td>
<td>Cell-cycle control (Cyclin D1 / CDK4/6; checkpoints)</td>
<td>Cell-cycle arrest ↑ (reported); Cyclin D1 ↓; proliferation ↓</td>
<td>↔</td>
<td>G</td>
<td>Cytostasis</td>
<td>Frequently reported as later phenotype-level outcomes; direction and checkpoint phase (G1 vs G2/M) vary by model.</td>
</tr>
<tr>
<td>5</td>
<td>Apoptosis (intrinsic caspase-linked; p53 axis in some models)</td>
<td>Apoptosis ↑; caspase activation ↑ (reported); p53/p21 ↑ (model-dependent)</td>
<td>↔ (generally less activation)</td>
<td>G</td>
<td>Cell death execution</td>
<td>Apoptosis is commonly observed in cancer models but is not as “signature-direct” as for mitochondrial toxins; best treated as downstream/conditional.</td>
</tr>
<tr>
<td>6</td>
<td>MAPK re-wiring (ERK / JNK / p38)</td>
<td>MAPK modulation (context-dependent)</td>
<td>↔</td>
<td>P, R, G</td>
<td>Signal reprogramming</td>
<td>MAPK direction depends on whether FA is acting primarily as anti-inflammatory/anti-stress vs antiproliferative; avoid hard arrows for p38/JNK/ERK unless model-specific.</td>
</tr>
<tr>
<td>7</td>
<td>PI3K → AKT (± mTOR) survival axis</td>
<td>PI3K/AKT modulation (reported; model-dependent)</td>
<td>↔</td>
<td>R, G</td>
<td>Survival/growth modulation</td>
<td>Often listed in anticancer summaries; treat as “reported” rather than universal primary mechanism.</td>
</tr>
<tr>
<td>8</td>
<td>Invasion / metastasis programs (MMPs / migration)</td>
<td>MMPs ↓; migration/invasion ↓ (reported)</td>
<td>↔</td>
<td>G</td>
<td>Anti-invasive phenotype</td>
<td>Observed as later outcomes (gene expression + phenotype assays) and commonly linked to NF-κB/MAPK context.</td>
</tr>
<tr>
<td>9</td>
<td>Radiation/chemo injury mitigation (supportive care framing)</td>
<td>Adjunct potential: may reduce treatment-associated oxidative/inflammatory injury (context)</td>
<td>Tissue protection ↑ (reported)</td>
<td>G</td>
<td>Cytoprotection</td>
<td>Animal models report radioprotective/anti-inflammatory effects; present as supportive/adjunct rather than standalone anticancer therapy.</td>
</tr>
<tr>
<td>10</td>
<td>Bioavailability / metabolism constraint (conjugation; food-matrix dependence)</td>
<td>Systemic exposure variable; much appears as glucuronide/sulfate conjugates</td>
<td>—</td>
<td>—</td>
<td>Translation constraint</td>
<td>FA is absorbed and rapidly metabolized; “bioavailability” varies widely with food matrix and binding to polysaccharides in grains.</td>
</tr>
</table>
<p><b>Time-Scale Flag (TSF):</b> P / R / G</p>
<ul>
<li><b>P</b>: 0–30 min (primary/rapid effects; early redox interactions / rapid signaling shifts)</li>
<li><b>R</b>: 30 min–3 hr (acute stress-response + transcription signaling shifts)</li>
<li><b>G</b>: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)</li>
</ul>