1. Immunology/Inflammation NF-κB Metabolic Enzyme/Protease Apoptosis Anti-infection
  2. Reactive Oxygen Species (ROS) Apoptosis MMP Bacterial Parasite
  3. Negundoside

Negundoside is an iridoid glycoside compound. Negundoside exhibits hepatoprotective effects, reduces ROS, lipid peroxidation and intracellular calcium ion levels, and prevents the decrease of mitochondrial membrane potential (MMP) and apoptosis (apoptosis). Negundoside has neuroprotective effects, improves behavioral deficits, alleviates oxidative damage, and ameliorates cerebral infarction. Negundoside also possesses antibacterial and antiparasitic activities.

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Negundoside

Negundoside Chemical Structure

CAS No. : 82451-20-5

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Description

Negundoside is an iridoid glycoside compound. Negundoside exhibits hepatoprotective effects, reduces ROS, lipid peroxidation and intracellular calcium ion levels, and prevents the decrease of mitochondrial membrane potential (MMP) and apoptosis (apoptosis). Negundoside has neuroprotective effects, improves behavioral deficits, alleviates oxidative damage, and ameliorates cerebral infarction. Negundoside also possesses antibacterial and antiparasitic activities[1][2][3][4].

In Vitro

Negundoside (5-400 mg/L; 1-24 h) shows no toxicity to HuH-7 cells and antagonizes CCl4-induced cell death, with a PC50 of 24.46 mg/L[2].
Negundoside (30-100 mg/L; 25 h) protects HuH-7 cells from CCl4-induced morphological damage to cells and nuclei, including apoptosis-like changes[2].
Negundoside (5-100 mg/L; 1 h) dose-dependently stabilizes human erythrocyte membranes against Triton X-100-induced hemolysis, with a protective rate of 91% at 100 mg/L[2].
Negundoside (5-100 mg/L; 20 min-24 h) dose-dependently inhibits lipid peroxidation (LPO) in rat liver microsomes treated with FeSO4/H2O2 and HuH-7 cells treated with CCl4, with maximum inhibition rates of 69% and 131% at the concentration of 100 mg/L, respectively[2].
Negundoside (10-100 mg/L; 25 h) dose-dependently inhibits CCl4-induced ROS and H2O2 production in HuH-7 cells, with a maximum inhibition rate of 104% for ROS and 143% for H2O2 at 100 mg/L[2].
Negundoside (10-100 mg/L; 25 h) dose-dependently reduces CCl4-induced intracellular Ca2+ elevation in HuH-7 cells, with an inhibition rate of up to 106% at 100 mg/L[2].
Negundoside (10-100 mg/L; 25 h) inhibits the activation of caspase-3 in HuH-7 cells in a dose-dependent manner, with an inhibition rate of 139% at the concentration of 100 mg/L[2].
Negundoside (50-100 mg/L; 40 min) inhibits cytochrome C release in isolated rat liver mitochondria, with an inhibition rate of up to 105% at 100 mg/L[2].
Negundoside (50-100 mg/L; 25 h) protects HuH-7 cells against CCl4-induced loss of mitochondrial membrane potential, reducing the proportion of damaged mitochondria to 20% and 11%, respectively[2].
Negundoside (25-100 mg/L; 25 h) inhibits CCl4-induced apoptosis in HuH-7 cells, as evidenced by reduced DNA fragmentation and a decreased proportion of cells in the sub-G0/G1 phase (down to 11% at 100 mg/L)[2].
Negundoside (10-100 mg/L; 25 h) restores the reduced cAMP level in HuH-7 cells treated with CCl4[2].
Negundoside (10-100 mg/L; 25 h) dose-dependently inhibits CCl4-induced activation of cPLA2 in HuH-7 cells, with an inhibition rate reaching 304% at 50 mg/L[2].
Negundoside (5-100 mg/L; 25 h) dose-dependently restores the depleted intracellular GSH levels in HuH-7 cells treated with CCl4, with a recovery rate of up to 147% at 100 mg/L[2].
Negundoside (12.5 μg/mL) inhibits the growth of Bacillus subtilis with an MIC of 12.5 μg/mL; it produces an 18 mm inhibition zone against Staphylococcus aureus, Micrococcus pyogenes, Pseudomonas aeruginosa and Escherichia coli in vitro[3].

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

In Vivo

Negundoside (1-15 mg/kg; i.p.; single administration) exerts dose-dependent neuroprotective efficacy against global cerebral ischemia-reperfusion injury in Balb/C mice[4]

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

Animal Model: Balb/C (either sex, 20-25 g, global cerebral ischemia via bilateral common carotid artery occlusion followed by reperfusion)[4]
Dosage: 1 mg/kg; 3 mg/kg; 5 mg/kg; 10 mg/kg; 15 mg/kg
Administration: i.p.; single dose; pre-treated 60 minutes before ischemia induction
Result: Reduced cerebral infarct size significantly at 3, 5, 10, and 15 mg/kg compared to ischemic controls; showed no obvious change at 1 mg/kg.
Produced a dose-dependent anxiolytic response.
Prevented ischemia-reperfusion-induced increases.
Molecular Weight

496.46

Formula

C23H28O12

CAS No.
SMILES

OC(C1=CO[C@@H](O[C@H]2[C@@H]([C@H]([C@@H]([C@H](O2)CO)O)O)OC(C3=CC=C(C=C3)O)=O)[C@@]4([H])[C@]1([H])CC[C@@]4(O)C)=O

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Purity & Documentation
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    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.

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Negundoside
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