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| Ferulic acid is an antioxidant found in some skin creams and serums. Foods: popcorn, bamboo, whole-grain rye bread, whole-grain oat flakes, sweet corn (cooked) Ferulic acid (FA) is a hydroxycinnamic acid 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. -Ferulic acid found in dietary strand fractions, especially its free form, has important functions for protecting the human health. -AChE inhibitor (AD) -Cooking results in an increase in free ferulic acid quantity and in a reduction in bound ferulic acid quantity. 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
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
Time-Scale Flag (TSF): P / R / G
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| Once the cancer has begun, NO seems to play a protumoral role rather than antitumoral one as the concentration required to cause tumor cell cytotoxicity cannot be achieved by cancer cells. The mechanistic roles of nitric oxide (NO) during cancer progression have been important considerations since its discovery as an endogenously generated free radical. Nonetheless, the impacts of this signaling molecule can be seemingly contradictory, being both pro-and antitumorigenic, which complicates the development of cancer treatments based on the modulation of NO fluxes in tumors. At a fundamental level, low levels of NO drive oncogenic pathways, immunosuppression, metastasis, and angiogenesis, while higher levels lead to apoptosis and reduced hypoxia and also sensitize tumors to conventional therapies. However, clinical outcome depends on the type and stage of the tumor as well as the tumor microenvironment. Nitric oxide is generated by three main nitric oxide synthase isoforms: neuronal (nNOS), endothelial (eNOS), and inducible (iNOS). – In many cancers, especially under inflammatory conditions, iNOS expression is upregulated. In contrast, eNOS levels may also be altered in cancers such as breast or prostate cancer. • Expression Patterns in Tumors: – Elevated iNOS expression is commonly observed in various tumor types (e.g., colon, breast, lung, and melanoma) and is often associated with an inflammatory microenvironment. – Changes in eNOS and nNOS expression have also been reported and may contribute to angiogenesis and tumor blood flow regulation. |
| 3716- | FA, | Ferulic Acid as a Protective Antioxidant of Human Intestinal Epithelial Cells |
| - | in-vitro, | IBD, | NA | - | in-vivo, | NA, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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