Liposomal Coenzyme Q10
Based on 1 Customer Validation
Liposomal Coenzyme Q10 is an orally effective delivery system that encapsulates fat-soluble Coenzyme Q10 (CoQ10) (HY-N0111) via liposomal nanocarriers. Liposomal Coenzyme Q10 alleviates hepatic oxidative stress, attenuates hepatic inflammatory responses, reduces hepatocyte apoptosis, and ameliorates liver fibrosis. Liposomal Coenzyme Q10 activates the ferroptosis suppressor protein 1 (FSP1)/Coenzyme Q10 system, reduces the accumulation of malondialdehyde and ROS, and inhibits neuronal ferroptosis. Liposomal Coenzyme Q10 can be used in studies related to Propanoic acid (HY-W020017)-induced liver injury and subarachnoid hemorrhage.
For research use only. We do not sell to patients.
- Purity: 98%
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
Biological Activity
Description
In Vitro
Liposomal coenzyme Q10 (equivalent to 10 μM CoQ10) activates FSP1, alleviates iron overload, inhibits oxidative stress, and alleviates Hb-stimulated ferroptosis in N2A neuronal cells, with a potency weaker than that of neuron-targeted liposomal coenzyme Q10 (CoQ10-Tet1-Lipos)[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
Liposomal Coenzyme Q10 (100 mg/kg; i.v.; daily; 3 days) activates the FSP1/CoQ10 system, inhibits neuronal ferroptosis, and improves neurological function in SAH-induced mice relative to vehicle and non-targeted liposomes, though less effectively than neuron-targeted CoQ10-Tet1-Lipos[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Albino rats (adult male, 150-170 g, propionic acid-induced liver injury)[1]
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Dosage:10 mg/kg/day; 100 mg/kg/day (acetyl-L-carnitine, combination group)
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Administration:p.o.; daily; 5 days (administered one hour after propionic acid)
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Result:Marked reduction in serum AST, ALT, and LDH activity levels compared to the propionic acid-only group.
Significant reduction in hepatic malondialdehyde (MDA) levels, and significant restoration of hepatic reduced glutathione (GSH) levels and superoxide dismutase (SOD) enzyme activity compared to the propionic acid-only group.
Significant downregulation of hepatic proinflammatory cytokines IL-6 and TNF-α levels compared to the propionic acid-only group.
Significant reduction in hepatic caspase-3 levels, and significant downregulation of hepatic cytokeratin-18 (CK18) mRNA expression compared to the propionic acid-only group.
Significant downregulation of hepatic transforming growth factor-beta1 (TGF-β1) and SMAD3 protein expression compared to the propionic acid-only group.
Significant downregulation of hepatic high-mobility group box-1 (HMGB1) mRNA expression compared to the propionic acid-only group.
Showed intact lobular hepatic architecture, with hepatocytes arranged in thin plates and only mild hydropic degeneration, compared to the propionic acid-only group which exhibited intracytoplasmic vacuoles, congested/dilated sinusoids, and necrotic areas; combination group showed almost normal hepatic structure and architecture.
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Animal Model:C57BL/6 (male, 6-8 weeks old, 20-25 g, intracranial vessel puncture via external carotid artery insertion of a monofilament)[2]
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Dosage:100 mg/kg
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Administration:i.v.; daily; 3 days
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Result:Increased FSP1 levels at the lesion site relative to SAH-only, Lipos, and Tet1-Lipos groups, though to a lesser extent than the CoQ10-Tet1-Lipos group.
Reduced lesion-site iron content relative to SAH-only, Lipos, and Tet1-Lipos groups, though to a lesser extent than the CoQ10-Tet1-Lipos group.
Reduced lesion-site MDA concentration relative to SAH-only, Lipos, and Tet1-Lipos groups, though to a lesser extent than the CoQ10-Tet1-Lipos group.
Reduced oxidative stress (measured via 8-OHdG fluorescence intensity) relative to SAH-only, Lipos, and Tet1-Lipos groups, though to a lesser extent than the CoQ10-Tet1-Lipos group.
Increased the number of morphologically normal neurons at the lesion site relative to SAH-only, Lipos, and Tet1-Lipos groups, though to a lesser extent than the CoQ10-Tet1-Lipos group.
Inhibited neuronal ferroptosis (preserved mitochondrial morphology via TEM) relative to SAH-only, Lipos, and Tet1-Lipos groups, though to a lesser extent than the CoQ10-Tet1-Lipos group.
Produced shorter latency to find the platform and longer time spent in the correct quadrant in the Morris water maze test relative to SAH-only, Lipos, and Tet1-Lipos groups, though to a lesser extent than the CoQ10-Tet1-Lipos groups, indicating improved spatial memory.
Achieved a higher modified Garcia score relative to SAH-only, Lipos, and Tet1-Lipos groups, though to a lesser extent than the CoQ10-Tet1-Lipos group, indicating improved sensory and motor function.
Resulted in shorter time to reach the 20 cm mark in the chimney behavioral test relative to SAH-only, Lipos, and Tet1-Lipos groups, though to a lesser extent than the CoQ10-Tet1-Lipos group, indicating improved motor function.
Had a mortality rate of 15.63% (10/64) in behavioral test groups and 17.24% (5/29) in tissue collection groups, comparable to other SAH treatment groups.
Chemical Information
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Appearance Powder
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Color Yellow to orange
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SMILES
[Liposomal Coenzyme Q10]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Solvent & Solubility
In Vitro:
H2O : < 0.1 mg/mL (insoluble)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Working solution concentration: 0.22 mg/mL
Purity & Documentation
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Data Sheet (279 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- Liposomal Coenzyme Q10
- Liposomal Coenzyme Q 10
- Liposomal Coenzyme Q-10
- Liposome
- Apoptosis
- Ferroptosis
- Reactive Oxygen Species (ROS)
- N2A neuronal cells
- ferroptosis suppressor protein 1
- cytokeratin-18
- subarachnoid hemorrhage
- reactive oxygen species
- high-mobility group box-1
- malondialdehyde
- SMAD3
- transforming growth factor-beta1
- propionic acid-induced liver injury
- Inhibitor
- inhibitor
- inhibit