Shankhpushpi / MAOB Cancer Research Results

Shank, Shankhpushpi: Click to Expand ⟱
Features:
Shankhpushpi (Convolvulus pluricaulis) is a traditional Ayurvedic herb renowned for its nootropic (cognitive-enhancing), anxiolytic, and adaptogenic properties.
-5 druglike phytochemicals from CP constituents: scopoletin, 4-hydroxycinnamic acid, kaempferol, quercetin, and ayapanin.

Shankhpushpi — Ayurvedic nootropic “brain tonic” herbal drug; most commonly standardized/treated as Convolvulus prostratus Forssk. (syn. Convolvulus pluricaulis Choisy), but the name “Shankhpushpi” is also used for other botanicals in different regions (major source-of-variation risk).

Primary mechanisms (conceptual rank)
1) Cholinergic support (AChE inhibition / pro-cholinergic nootropic profile)
2) Antioxidant / redox buffering (ROS↓, lipid peroxidation↓; antioxidant enzymes↑)
3) Anti-inflammatory neuroprotection (glial/inflammatory signaling dampening; model-dependent)
4) Proteinopathy-related neuroprotection (tau-associated neurotoxicity mitigation; model-dependent) }

Bioavailability / pharmacokinetics relevance
Human PK for defined Shankhpushpi extracts is not well-established in the clinical literature; composition varies by species, plant part, extraction solvent, and polyherbal formulations.

In-vitro vs systemic exposure
Many mechanistic studies use extracts/fractions at concentrations not directly translatable to achievable systemic exposure; translational relevance hinges on standardized extract chemistry and demonstrated CNS delivery (often not reported).

Clinical evidence status
Predominantly preclinical + traditional use; human evidence exists mostly in small/heterogeneous studies and often in polyherbal products rather than single-extract RCT-grade data.


-Acetylcholinesterase (AChE) inhibition
-Antioxidant activity Scavenges ROS
-Memory enhancement

Cancer:
-Antioxidant/anti-inflammatory May reduce chronic inflammation, a driver of tumor progression.

Shankhpushpi — AD/Neuro axis table

Rank Pathway / Axis Neural / Glial Systems TSF Primary Effect Notes / Interpretation
1 Cholinergic axis (AChE) ↓ (model-dependent) R→G Memory/cognition support Frequently presented as a nootropic mechanism; evidence base varies by extract and assay type. :contentReference[oaicite:22]{index=22}
2 ROS / antioxidant defense ↓ (often primary) P→R→G Oxidative stress reduction Reports include decreased lipid peroxidation markers and increased antioxidant defense metrics in cognitive impairment paradigms. :contentReference[oaicite:23]{index=23}
3 Neuroinflammation (broad cytokine/glial tone) ↓ (model-dependent) R→G Neuroprotection / slower degeneration pressure Often included in dementia-herb reviews as part of multi-target neuroprotection; direct causal evidence depends on study design. :contentReference[oaicite:24]{index=24}
4 Proteinopathy stress (tau-associated toxicity) ↓ (protective; model-dependent) R→G Protection from tau-driven neuronal injury Aqueous extract reported to mitigate hMAPτ-induced neurotoxicity (cell-based). :contentReference[oaicite:25]{index=25}
5 Ca²⁺ signaling (excitotoxicity / ER-mito coupling) ↔/↓ (secondary; context-dependent) R Stress-amplification modulation Mechanistically relevant when excitotoxic/mitochondrial stress endpoints are present; often not directly quantified in Shankhpushpi experiments.
6 NRF2 antioxidant response ↑ (adaptive/protective; context-dependent) R→G Transcriptional antioxidant program Frequently inferred from antioxidant enzyme changes and redox outcomes rather than directly measured NRF2 pathway activation in many studies. :contentReference[oaicite:26]{index=26}
7 Clinical Translation Constraint ↔ — Standardization + PK/BBB uncertainty Multiple botanicals sold as “Shankhpushpi,” variable extraction/chemistry, and limited human PK/CNS delivery data constrain translation to AD claims. :contentReference[oaicite:27]{index=27}

TSF legend: P: 0–30 min | R: 30 min–3 hr | G: >3 hr
MAOB, Monoamine oxidase B: Click to Expand ⟱
Source:
Type:
Monoamine oxidase B (MAO-B) is an enzyme involved in the metabolism of monoamines, especially dopamine and phenylethylamine, primarily in the brain. Its activity has been implicated in both Alzheimer's disease (AD) and cancer, but in very different contexts. -Increased MAO-B expression is observed in the brains of aging individuals and even more so in AD patients, particularly in astrocytes.
-High MAO-B activity may accelerate β-amyloid (Aβ) and tau pathology.
-MAO-B inhibitors are potential agents to combat neurodegenerative diseases, including AD and Parkinson’s disease

MAO-B inhibitors have shown anti-cancer effects in preclinical models:
   Inducing apoptosis in tumor cells.
   Sensitizing cells to chemotherapy or radiotherapy.
   Inhibiting tumor angiogenesis and invasion.


Scientific Papers found: Click to Expand⟱
3943- Shank,    Protective Mechanisms of Nootropic Herb Shankhpushpi (Convolvulus pluricaulis) against Dementia: Network Pharmacology and Computational Approach
- Review, AD, NA
*neuroP↑, *memory↑, *other↝, *AChE↓, *MAOA↓, *MAOB↓, *TrkB↓, *tau↓, *APP↓, *ROS↓, *Mood↑,

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:


Redox & Oxidative Stress ⓘ

ROS↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Migration ⓘ

APP↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   MAOA↓, 1,   tau↓, 1,   TrkB↓, 1,  

Protein Aggregation ⓘ

MAOB↓, 1,  

Functional Outcomes ⓘ

memory↑, 1,   Mood↑, 1,   neuroP↑, 1,  
Total Targets: 11

Scientific Paper Hit Count for: MAOB, Monoamine oxidase B
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#:355  Target#:1352  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

Home Page