Ginseng / VEGF Cancer Research Results

Gins, Ginseng: Click to Expand ⟱
Features:

Ginseng = adaptogenic herbal root from the genus Panax; main species: Asian ginseng (Panax ginseng) and American ginseng (Panax quinquefolius). Active constituents: ginsenosides (Rb1, Rg1, Rg3, Rh2), polysaccharides, and other saponins.
Primary mechanisms (conceptual rank):
1) Multi-pathway signaling modulation (PI3K/Akt, MAPK, NF-κB; isoform-dependent).
2) Redox regulation (bidirectional ROS modulation; NRF2 interaction).
3) Anti-inflammatory and immunomodulatory effects.
4) Anti-proliferative and pro-apoptotic effects in cancer (notably Rg3, Rh2; dose-dependent).
5) Neurotrophic and cholinergic modulation (BDNF, ACh support).
PK / bioavailability: ginsenosides have variable oral absorption; gut microbiota convert to active metabolites (e.g., Compound K); plasma levels generally lower than many in-vitro doses.
In-vitro vs systemic exposure: many cancer studies use ≥10–100 µM; achievable plasma concentrations after oral dosing are typically lower and metabolite-driven.
Clinical evidence status: supportive oncology (fatigue reduction) supported by RCTs; direct anti-cancer efficacy largely preclinical; cognitive and fatigue benefits better substantiated.

Ginseng (Panax ginseng) – This herb has been studied for its ability to enhance the immune system.
-Antioxidant Properties: Ginseng contains ginsenosides, which have antioxidant properties.
-Immune System Support
-Inhibition of Tumor Growth
-Chemopreventive Effects
-Synergistic Effects with Cancer Treatments: ginseng may enhance the effectiveness of certain cancer treatments, such as chemotherapy, and may help reduce side effect
Dose: Standardized Extract:
Dosage: extract containing 4-7% ginsenosides 200-400mg/d
Dried Root:1-2g/d
Tea: 1-2g dried root, 1-3x/d

Ginseng (Panax spp.) — Cancer-Relevant Pathways

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 PI3K/Akt / MAPK signaling ↓ proliferation (isoform-dependent) ↔ / adaptive support R→G Growth signaling attenuation Ginsenosides Rg3/Rh2 most studied; context- and tumor-type dependent.
2 Apoptosis (caspase / mitochondrial) ↑ (dose-dependent) ↔ / protective R→G Pro-apoptotic signaling Mitochondrial depolarization reported; supra-physiologic concentrations common in vitro.
3 ROS modulation ↑ (high concentration) / ↓ (adaptive) ↓ P→R Redox modulation Bidirectional: pro-oxidant cytotoxicity in tumors at high dose; antioxidant in normal cells.
4 NF-κB / inflammation ↓ ↓ R→G Anti-inflammatory Reduces pro-tumor inflammatory microenvironment signals.
5 Angiogenesis (VEGF) ↓ (preclinical) ↔ G Anti-angiogenic Reported particularly with Rg3; human oncologic outcome data limited.
6 NRF2 axis ↔ / ↑ (adaptive) ↑ G Antioxidant enzyme induction Protective in normal tissues; tumor resistance context-dependent.
7 Clinical Translation Constraint — — — Adjunct role RCTs support fatigue reduction in cancer patients; direct anti-tumor efficacy not established.

TSF Legend: P: 0–30 min | R: 30 min–3 hr | G: >3 hr


Ginseng (Panax spp.) — Alzheimer’s Disease–Relevant Axes

Rank Pathway / Axis Cells (neurons/glia) TSF Primary Effect Notes / Interpretation
1 BDNF / neuroplasticity ↑ G Neurotrophic support Rg1 and metabolites reported to enhance BDNF signaling; supports cognition in mild impairment models.
2 Cholinergic modulation ↑ (mild) R→G ACh support May increase ACh release or inhibit AChE modestly; relevance additive to standard therapy unclear.
3 Neuroinflammation (NF-κB) ↓ R→G Microglial modulation Reduces pro-inflammatory cytokines in animal models.
4 ROS / oxidative stress ↓ P→R Antioxidant support Induces antioxidant enzymes; may protect against Aβ-induced oxidative injury.
5 Aβ processing ↓ (preclinical) G Reduced amyloid burden Animal studies suggest modulation of APP processing; human AD RCT data limited.
6 Clinical Translation Constraint — — Modest cognitive benefit Small human trials suggest mild cognitive improvement; not disease-modifying.

TSF Legend: P: 0–30 min | R: 30 min–3 hr | G: >3 hr
VEGF, Vascular endothelial growth factor: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
A signal protein produced by many cells that stimulates the formation of blood vessels. Vascular endothelial growth factor (VEGF) is a signal protein that plays a crucial role in angiogenesis, the process by which new blood vessels form from existing ones. This process is vital for normal physiological functions, such as wound healing and the menstrual cycle, but it is also a key factor in the growth and spread of tumors in cancer.
Because of its significant role in tumor growth and progression, VEGF has become a target for cancer therapies. Anti-VEGF therapies, such as monoclonal antibodies (e.g., bevacizumab) and small molecule inhibitors, aim to inhibit the action of VEGF, thereby reducing blood supply to tumors and limiting their growth. These therapies have been used in various types of cancer, including colorectal, lung, and breast cancer.
Scientific Papers found: Click to Expand⟱
4243- Gins,    Effects of Ginseng on Neurological Disorders
- Review, Stroke, NA - Review, AD, NA - Review, Park, NA
*BDNF↑, *TrkB↑, *neuroP↑, *VEGF↑, *p‑tau↓, *memory↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Angiogenesis & Vasculature ⓘ

VEGF↑, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,   p‑tau↓, 1,   TrkB↑, 1,  

Functional Outcomes ⓘ

memory↑, 1,   neuroP↑, 1,  
Total Targets: 6

Scientific Paper Hit Count for: VEGF, Vascular endothelial growth factor
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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:219  Target#:334  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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