Garlic oil (synthetic)
Based on 1 Customer Validation
Garlic oil (synthetic) is an orally effective anti-inflammatory, antioxidant, and anticancer agent. Garlic oil (synthetic) inhibits the activation of NF-κB, NFκB2 and NLRP3 inflammasome, and induces the expression of GSTA1, HO-1 and NQO-1. Garlic oil (synthetic) reduces the Bcl-2/Bax protein ratio and activates NNK-induced apoptosis (apoptosis) in lung tissues. Garlic oil (synthetic) attenuates NNK-induced apoptosis in MRC-5 cells and reduces excessive ROS production. Garlic oil (synthetic) alleviates pyroptosis (pyroptosis) and exerts a protective effect against acute lung injury in mice. Garlic oil (synthetic) inhibits lung tumorigenesis in mice and improves small intestinal motility in rats with type 2 diabetes. Garlic oil (synthetic) can be used in research related to acute lung injury, lung cancer, peptic ulcer, type 2 diabetes and hypertension.
For research use only. We do not sell to patients.
- CAS No.: 8000-78-0
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Storage:
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Garlic oil (1-4 μg/mL; 48 h) (synthetic) dose-dependently reverses the decrease in MRC-5 cell viability induced by NNK (HY-126477)[2].
Garlic oil (2 μg/mL; 48 h) (synthetic) significantly reduces NNK-induced apoptosis in MRC-5 cells[2].
Garlic oil (48 h) (synthetic) significantly reduces NNK-induced excessive ROS production in MRC-5 cells, reverses GSH depletion, protects cells against NNK-induced DNA strand breaks and loss of mitochondrial membrane potential, and reduces endoplasmic reticulum stress[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MRC-5 cells
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Concentration:1 μg/mL, 2 μg/mL, 4 μg/mL
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Incubation Time:48 h
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Result:Had no significant effect on MRC-5 cell viability at 1 μg/mL or 2 μg/mL for 48 h.
Significantly decreased cell viability compared to the control at 4 μg/mL for 48 h.
Dose-dependently reversed NNK-induced cell viability loss at 1 μg/mL or 2 μg/mL for 48 h.
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Cell Line:MRC-5 cells
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Concentration:2 μg/mL
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Incubation Time:48 h
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Result:Reduced the NNK-induced apoptosis rate from 38.3% to 14.4% in MRC-5 cells.
Garlic oil (25-50 mg/kg; p.o.; daily; 18 weeks) (synthetic) dose-dependently inhibits NNK-induced lung tumorigenesis in A/J mice[2].
Garlic oil (5 mL/kg/day; oral administration; once daily for consecutive 2 weeks) (synthetic) improves intestinal motility, alleviates oxidative stress, reduces blood glucose levels and improves insulin resistance, reverses histological damage, and increases BMI and Lee index in female Wistar rats with experimental type 2 diabetes[4].
Garlic oil (5 mL/kg/day; p.o.; daily administration for 2 consecutive weeks) (synthetic) reduces intestinal contractility and motility index in healthy female Wistar rats, increases BMI, Lee index and waist circumference, enhances oxidative stress levels in the duodenum, and decreases GSH-Px activity in the jejunum, but exerts no effect on glycemic control[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (male, 6-8 weeks old, LPS-induced acute lung injury model)[1]
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Dosage:100 mg/kg
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Administration:i.t.; single dose; 4 hours before LPS instillation
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Result:Reduced LPS-induced lung injury scores, myeloperoxidase (MPO) activity in lung tissue, total cell counts and total protein levels in bronchoalveolar lavage fluid (BALF), and mRNA/protein levels of inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-18) in lung tissue and BALF.
Decreased LPS-induced activation of NF-κB (reduced p-p65/p65 ratio), expression of NLRP3 inflammasome components (NLRP3, ASC, cleaved caspase-1), and levels of pyroptosis markers (cleaved GSDMD-N, cleaved GSDME-N) in lung tissue, lowering the pyroptosis rate of primary alveolar epithelial cells from 9.06% to 5.15%.
Increased lung tissue expression of H2S-producing enzymes (CBS, CSE) and H2S production levels.
Reversed all protective effects when H2S production was inhibited via IAM or AOAA + PAG.
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Animal Model:A/J mice (5-8 weeks old, 5 male and 5 female per group, intraperitoneal injection of 100 mg/kg NNK to induce tumorigenesis)[2]
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Dosage:25 mg/kg; 50 mg/kg
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Administration:p.o.; daily; 18 weeks
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Result:Significantly reduced lung tumor number compared to the NNK model group.
Significantly reduced lung tumor number compared to the NNK model group, with greater efficacy than the 25 mg/kg dose.
Reversed NNK-induced increases in Bcl-2 protein expression and decreases in Bax protein expression, reducing the Bcl-2/Bax ratio.
Increased protein expression of phase II drug-metabolizing enzymes HO-1, NQO1, and GSTA1 in lung tissue in a dose-dependent manner.
Increased mRNA expression of HO-1 and NQO1 in lung tissue.
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Animal Model:Wistar rats (adult female, 150-180 g, experimentally induced type 2 diabetes mellitus)[4]
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Dosage:5 mL/kg/day
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Administration:p.o.; daily; 2 consecutive weeks
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Result:Significantly increased average duration of contraction in duodenum, jejunum, and ileum.
Significantly elevated average force of contraction and motility index in duodenum, jejunum, and ileum, bringing duodenal values to levels insignificantly different from control rats.
Significantly lowered fasting blood glucose compared to untreated diabetic rats.
Significantly reduced HOMA-IR score compared to untreated diabetic rats, to levels insignificantly different from control rats.
Significantly reduced duodenal and ileal malondialdehyde (MDA) levels compared to untreated diabetic rats.
Significantly lowered jejunal CAT activity compared to untreated diabetic rats (reducing it to levels insignificantly different from controls), while duodenal CAT activity was unchanged.
Significantly decreased duodenal glutathione peroxidase (GSH-Px) activity compared to untreated diabetic rats (but unchanged compared to controls).
Significantly decreased jejunal GSH-Px activity compared to untreated diabetic rats (and unchanged in untreated diabetic rats compared to controls).
Significantly reduced ileal GSH-Px activity compared to untreated diabetic rats.
Significantly increased body mass index (BMI) compared to untreated diabetic rats.
Significantly increased Lee index compared to untreated diabetic rats.
Showed restored villi and muscle arrangement, reduced mononuclear cell infiltration, and myenteric nervous plexus with basophilic cytoplasm and normal vesicular nuclei in duodenum, jejunum, and ileum, compared to the distorted, inflamed tissue of untreated diabetic rats.
Waist circumference was insignificantly changed compared to untreated diabetic rats.
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Animal Model:Wistar rats (adult female, 150-180 g, healthy)[4]
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Dosage:5 mL/kg/day
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Administration:p.o.; daily; 2 consecutive weeks
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Result:Significantly lowered average force of contraction and motility index in duodenum, jejunum, and ileum compared to control rats.
No significant changes were observed in frequency of contraction or average duration of contraction across all small intestinal segments.
No significant changes were observed in fasting blood glucose, fasting insulin level, HOMA-IR score, or HbA1c compared to control rats.
Significantly elevated duodenal MDA level compared to control rats.
No significant changes were observed in jejunal or ileal MDA, or CAT activity in any small intestinal segment.
Significantly decreased jejunal GSH-Px activity compared to control rats, while duodenal and ileal GSH-Px activity was unchanged compared to control rats.
Significantly increased BMI, Lee index, and waist circumference compared to control rats.
Showed regular villi and crypts with basophilic cytoplasm, vesicular nuclei, and normal myenteric nervous plexus in duodenum and jejunum; ileum showed normal villi and crypts but with mononuclear cell infiltration.
Chemical Information
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CAS No. 8000-78-0
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Appearance Liquid
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Color Light yellow to yellow
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SMILES
[Garlic oil (synthetic)]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Solvent & Solubility
DMSO : 200 mg/mL (Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
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.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: 5 mg/mL; Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (50.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 5 mg/mL; Clear solution
This protocol yields a clear solution of ≥ 5 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (50.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
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.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation
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Data Sheet (282 KB)
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SDS (545 KB)
- English - EN (545 KB)
- Français - FR (545 KB)
- Deutsch - DE (545 KB)
- Norwegian - NO (545 KB)
- Español - ES (545 KB)
- Swedish - SV (545 KB)
- Italian - IT (545 KB)
- Korean - KR (545 KB)
- Portuguese - PT (545 KB)
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Handling Instructions (2659 KB)
References
[1]. Dilxat T, et al. Garlic oil supplementation blocks inflammatory pyroptosis-related acute lung injury by suppressing the NF-κB/NLRP3 signaling pathway via HS generation. Aging. 2024 Apr 12;16(7):6521-6536. [Content Brief]
[2]. Zhang L, et al. Garlic oil blocks tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis by inducing phase II drug-metabolizing enzymes. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association. 2021 Nov;157:112581. [Content Brief]
[3]. Kuna L, et al. Pretreatment of Garlic Oil Extracts Hampers Epithelial Damage in Cell Culture Model of Peptic Ulcer Disease. Medicina (Kaunas, Lithuania). 2022 Jan 07;58(1):91. [Content Brief]
[4]. Saleh NKM, et al. Garlic oil improves small intestinal motility in experimentally induced type II diabetes mellitus in female Wistar rats. PloS one. 2024;19(4):e0301621. [Content Brief]
[5]. Tain YL, et al. Perinatal Garlic Oil Supplementation Averts Rat Offspring Hypertension Programmed by Maternal Chronic Kidney Disease. Nutrients. 2022 Nov 02;14(21):4624. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Garlic oil (synthetic) Related Classifications
HY-N14116A Related Classifications
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- Garlic oil (synthetic)
- 8000-78-0
- NF-κB
- NOD-like Receptor (NLR)
- Glutathione S-transferase
- Heme Oxygenase (HO)
- Quinone Reductase
- Bcl-2 Family
- Apoptosis
- Reactive Oxygen Species (ROS)
- Pyroptosis
- MRC-5 cells
- NFκB2
- NQO-1
- GSTA1
- lung cancer
- NLRP3 inflammasome
- HO-1
- type II diabetes mellitus
- acute lung injury
- Inhibitor
- inhibitor
- inhibit