2. Membrane Transporter/Ion Channel Neuronal Signaling Apoptosis Immunology/Inflammation NF-κB
  3. Na+/K+ ATPase CaMK Apoptosis Cholinesterase (ChE) NO Synthase NF-κB
  4. Bacoside A

Bacoside A is an orally active, blood-brain barrier-permeable triterpenoid saponin that modulates the activities of ATPases, AChE, CaMK2A and iNOS. Derived from Bacopa monniera. Bacoside A exerts significant antioxidant, anti-inflammatory and anti-apoptotic effects by maintaining ion balance, scavenging reactive oxygen species, stabilizing cell membranes, and regulating the expression of NF-κB and apoptosis-related proteins. Bacoside A counteracts morphine-induced reductions in Na+/K+-ATPase, Ca2+-ATPase and Mg2+-ATPase activities, increases mitochondrial membrane potential, and decreases intracellular reactive oxygen species levels. Bacoside A specifically binds to calcium/calmodulin-dependent protein kinase IIA to trigger endoplasmic reticulum calcium release. Bacoside A exhibits non-apoptotic cytotoxicity against glioblastoma cells while protecting normal nerve cells from stress-induced damage. Bacoside A is applicable to the research of Parkinson's disease and glioblastoma multiforme.

For research use only. We do not sell to patients.

Bacoside A

Bacoside A Chemical Structure

CAS No. : 11028-00-5

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Bacoside A Related Antibodies

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Description

Bacoside A is an orally active, blood-brain barrier-permeable triterpenoid saponin that modulates the activities of ATPases, AChE, CaMK2A and iNOS. Derived from Bacopa monniera. Bacoside A exerts significant antioxidant, anti-inflammatory and anti-apoptotic effects by maintaining ion balance, scavenging reactive oxygen species, stabilizing cell membranes, and regulating the expression of NF-κB and apoptosis-related proteins. Bacoside A counteracts morphine-induced reductions in Na+/K+-ATPase, Ca2+-ATPase and Mg2+-ATPase activities, increases mitochondrial membrane potential, and decreases intracellular reactive oxygen species levels. Bacoside A specifically binds to calcium/calmodulin-dependent protein kinase IIA to trigger endoplasmic reticulum calcium release. Bacoside A exhibits non-apoptotic cytotoxicity against glioblastoma cells while protecting normal nerve cells from stress-induced damage. Bacoside A is applicable to the research of Parkinson's disease and glioblastoma multiforme[1][2][3].
IC50 & Target

AChE

 

CaMK IIα

 

iNOS

 

In Vitro

Bacoside A (8 μg/mL) induces non-apoptotic, macropinocytosis-driven cell death in LN229, U87MG and U251 glioblastoma cells, but exerts no cytotoxic effects on normal HaCaT or SVG cells[3].
Bacoside A (8 μg/mL) induces the formation of lysosome-precursor and caveolin-1-positive macropinosomes in LN229 and U87MG glioblastoma cells, thereby driving fluid accumulation and cell swelling[3].
Bacoside A (8 μg/mL; 24 h) specifically enhances the phosphorylation level of T286 in CaMK2A in LN229, U87MG and U251 glioblastoma cells, but exerts no effect on normal HaCaT or SVG cells[3].
Bacoside A (8 μg/mL; 24 h) induces CaMK2A phosphorylation in a calmodulin- and calcium-independent manner, whereas subsequent intracellular calcium release is required for macropinocytosis, cytoskeleton damage and cytotoxicity in LN229 and U87MG glioblastoma cells[3].
Bacoside A (0.2-1.0 mg/mL; 3 h) does not significantly reduce the viability of N2a neuroblastoma cells at concentrations up to 0.4 mg/mL, but decreases cell viability at higher concentrations; the cell viability remains above 100% at 0.6 mg/mL[4].
Bacoside A (0.4 mg/mL; 1 h) maintains nuclear integrity, reduces ROS production, and restores mitochondrial membrane potential in N2a neuroblastoma cells subjected to H2O2 (0.42 mM; 3 h) stress[4].
Bacoside A (0.4 mg/mL; 1 h) exhibits anti-apoptotic activity in N2a neuroblastoma cells stressed by H2O2 (0.42 mM; 3 h), but its effect is weaker than that of its monomeric components Bacoside A3 (HY-N5064), Bacopaside II (HY-N6016) and Bacopasaponin C (HY-N6015)[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Bacoside A Related Antibodies

Cell Cytotoxicity Assay[3]

Cell Line: LN229, U87MG, U251 (human glioblastoma cell lines); HaCaT (normal human epidermal keratinocytes), SVG (normal human subventricular radial glial progenitors)
Concentration: 2, 4, 6, 8 μg/mL (12 h); 8 μg/mL (12-24 h, 24-48 h, 24 h, 48 h)
Incubation Time: 12 h (2, 4, 6, 8 μg/mL); 12-24 h, 24-48 h, 24 h, 48 h (8 μg/mL)
Result: Induced phase-lucent macropinosome-like vacuoles in LN229, U87MG, and U251 glioblastoma cells by 12-24 h at 8 μg/mL, which fused to occupy the entire cell space, causing cellular hypertrophy, swelling, rounding, and necrotic morphology by 24-48 h.
Caused near-complete cell death in treated glioblastoma cultures, while normal HaCaT and SVG cells showed no morphological changes or cytotoxicity at 8 μg/mL.
Resulted in negative TUNEL assay for apoptotic DNA fragmentation in treated LN229 and U87MG cells, confirming non-apoptotic cell death.

Immunofluorescence[3]

Cell Line: LN229, U87MG, U251 (human glioblastoma cell lines); HaCaT (normal human epidermal keratinocytes), SVG (normal human subventricular radial glial progenitors)
Concentration: 8 μg/mL
Incubation Time: 24 h
Result: Increased the ratio of phospho-CaMK2A (T286) to non-phospho CaMK2A significantly in LN229, U87MG, and U251 glioblastoma cells compared to untreated controls.
Caused no significant increase in phospho-CaMK2A levels in treated normal HaCaT or SVG cells.

Apoptosis Analysis[4]

Cell Line: H2O2-stressed N2a neuroblastoma cells
Concentration: 0.4 mg/mL (post 3 h 0.42 mM H2O2 treatment)
Incubation Time: 1 h (post 3 h 0.42 mM H2O2 treatment)
Result: Reduced Annexin V-FITC green fluorescence intensity in H2O2-stressed N2a cells, indicating decreased phosphatidylserine exposure.
Showed insignificant red fluorescence via PI staining, indicating minimal necrotic cell death.
Was less effective at alleviating apoptosis compared to individual bacoside A components bacoside A3, bacopaside II, and bacopasaponin C.
In Vivo

Bacoside A (10 mg/kg/day; intragastric administration; daily dosing for 21 days) significantly alleviates morphine-induced oxidative stress in rat brain tissue by normalizing the activities of antioxidant enzymes, reducing lipid peroxidation and protein carbonylation, and restoring the function of membrane-bound ATPases; it exerts no effect on these biomarkers when administered alone[1].
Bacoside A (5-20 mg/kg; i.p.; single administration 24 h prior to modeling) exerts a dose-dependent protective effect against Parkinson's disease-induced oxidative damage and neuronal degeneration in male Wistar rats. Among these doses, 20 mg/kg completely eliminates PD-induced changes in rotational behavior and restores multiple pathological markers to the levels observed in the sham-operated group[2].
Bacoside A exhibits chemopreventive efficacy against N-Nitrosodiethylamine (HY-N7434)-induced hepatocellular carcinoma in rats[3].
Bacoside A exerts anti-tumorigenic effects in mouse models of breast cancer, prostate cancer, and lung cancer[3].
Bacoside A has a good safety profile and does not impair the learning and memory abilities of mouse models with learning and memory impairment[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: albino Wistar (adult male, 150-200 g, morphine-induced oxidative stress model)[1]
Dosage: 10 mg/kg b.w./day
Administration: p.o.; daily; 21 days
Result: Restored superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities to near normal, with significant increases relative to morphine-only treated rats.
Normalized reduced glutathione (GSH) levels relative to morphine-only treated rats.
Significantly decreased basal, FeSO4-induced, ascorbate-induced, and H2O2-induced lipid peroxide levels relative to morphine-only treated rats.
Reduced protein carbonyl content to 2.09 n mole/mg protein, a significant decrease relative to morphine-only treated rats.
Restored Na+/K+-ATPase activity to 0.54±0.03 mmol of phosphorous liberated/min/mg protein, Ca2+-ATPase activity to 0.53 mmol of phosphorous liberated/min/mg protein, and Mg2+-ATPase activity to 0.64 mmol of phosphorous liberated/min/mg protein, all significant increases relative to morphine-only treated rats.
Caused no significant changes in antioxidant enzyme activities, GSH levels, lipid peroxide levels, protein carbonyl content, or membrane-bound ATPase activities relative to control rats when administered alone.
Animal Model: Wistar rats (male, 8-10 weeks old, 295-340 g; Parkinson's disease model induced by 6-hydroxydopamine injection)[2]
Dosage: 5 mg/kg; 10 mg/kg; 20 mg/kg
Administration: i.p.; single dose 24 hours pre-PD induction
Result: Reduced PD-induced elevated turning values in a dose-dependent manner; the 20 mg/kg dose completely eliminated the PD-induced increase in turning values.
Reversed PD-mediated suppression of serum CAT and GSH-Px activities in a dose-dependent manner; the 20 mg/kg dose effectively restored these enzyme activities to near sham levels.
Dose-dependently suppressed PD-induced elevated hippocampal AChE and iNOS activities; the 20 mg/kg dose reduced these activities to levels close to the sham group.
Dose-dependently reduced PD-induced elevated serum levels of IL-1β, IL-6, TNF-α, and NF-κB p65; the 20 mg/kg dose effectively reversed PD-mediated elevations of IL-1β and IL-6.
Dose-dependently reduced PD-induced elevated hippocampal levels of COX-2, p53, Bax, caspase-3, caspase-9, and cytochrome c; the 20 mg/kg dose reduced COX-2, p53, and cytochrome c levels to near sham group values.
Molecular Weight

768.97

Formula

C41H68O13
CAS No.
SMILES

C/C(C)=C\CC[C@@]([C@@H]1[C@H]2CC[C@H]3[C@](CC[C@@H]4[C@]3(CO)CCC(O[C@H]5[C@H](O)[C@@H](O)[C@H](O[C@H]6[C@H](O)[C@@H](O)[C@@H](O)CO6)[C@@H](CO)O5)C4(C)C)(C)[C@]2(C)CC1=O)(O)C
Structure Classification
Initial Source
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Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Bacoside A Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Bacoside A11028-00-5Na+/K+ ATPaseCaMKApoptosisCholinesterase (ChE)NO SynthaseNF-κBSodium potassium pumpCalmodulin-dependent protein kinasesCalmodulin-dependent kinasesNitric oxide synthasesNOSNuclear factor-κBNuclear factor-kappaBrat brainNa+/K+-ATPaseBacopa monnieraParkinson's diseaseCa2+-ATPaseinducible nitric oxide synthaseglioblastoma cellsMg2+-ATPaseCaMK2AacetylcholinesteraseInhibitorinhibitorinhibit

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