Shankhpushpi / ChAT 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
ChAT, Choline acetyltransferase: Click to Expand ⟱
Source:
Type:
Choline acetyltransferase (ChAT) is the enzyme responsible for synthesizing acetylcholine (ACh), a key neurotransmitter involved in memory, learning, and attention.
In AD, one of the hallmark neurochemical findings is a loss of cholinergic neurons, especially in the basal forebrain, leading to:
↓ ChAT activity
↓ Acetylcholine (ACh) levels
↓ Cognitive function (especially memory and attention)

Many AD drugs aim to increase ACh levels by:
-Inhibiting acetylcholinesterase (AChE) (which breaks down ACh), e.g., donepezil, rivastigmine.


Scientific Papers found: Click to Expand⟱
3948- Shank,    Neuroprotective role of Convolvulus pluricaulis on aluminium induced neurotoxicity in rat brain
- in-vivo, AD, NA
*AChE↓, *ChAT↑, *NGF↑, *CDK5↓, *neuroP↑, *MDA↓,

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 ⓘ

MDA↓, 1,  

Migration ⓘ

CDK5↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   ChAT↑, 1,   NGF↑, 1,  

Functional Outcomes ⓘ

neuroP↑, 1,  
Total Targets: 6

Scientific Paper Hit Count for: ChAT, Choline acetyltransferase
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#:1346  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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