TNF-α ; IL-6 ; NF-κB p65. [1]

In STZ-induced diabetic rats, oral administration of Allyl methyl sulfide at 50, 100, or 200 mg/kg body weight (b.w) daily for 30 days significantly decreased plasma glucose levels and increased plasma insulin levels in a dose-dependent manner. The most effective dose was 100 mg/kg b.w. [1]
• Allyl methyl sulfide (100 mg/kg b.w) significantly reduced elevated levels of lipid peroxidation markers (TBARS and hydroperoxides) in the liver of diabetic rats. TBARS: diabetic control 1.93 ± 0.14 mM/100g tissue vs. diabetic + AMS 0.97 ± 0.07 mM/100g tissue; hydroperoxides: diabetic control 121.45 ± 9.24 mM/100g tissue vs. diabetic + AMS 90.91 ± 6.95 mM/100g tissue. [1]
• Allyl methyl sulfide treatment significantly increased non-enzymatic antioxidant levels (vitamin C, vitamin E, reduced GSH) in the liver of diabetic rats. Vitamin C: diabetic control 0.57 ± 0.04 μg/mg protein vs. diabetic + AMS 1.02 ± 0.92 μg/mg protein; vitamin E: diabetic control 0.21 ± 0.01 μg/mg protein vs. diabetic + AMS 0.64 ± 0.04 μg/mg protein; GSH: diabetic control 2.62 ± 0.19 mg/100g tissue vs. diabetic + AMS 3.43 ± 0.26 mg/100g tissue. [1]
• Allyl methyl sulfide (100 mg/kg b.w) significantly enhanced the activities of enzymatic antioxidants (SOD, CAT, GPx, GST) in the liver of diabetic rats. SOD: diabetic control 3.94 ± 0.30 Min/mg protein vs. diabetic + AMS 6.87 ± 0.52 Min/mg protein; CAT: diabetic control 49.74 ± 3.78 μmol/min vs. diabetic + AMS 65.46 ± 5.01 μmol/min; GPx: diabetic control 4.42 ± 0.33 μg/min/mg protein vs. diabetic + AMS 8.68 ± 0.66 μg/min/mg protein; GST: diabetic control 4.32 ± 0.32 μg/min/mg protein vs. diabetic + AMS 7.45 ± 0.57 μg/min/mg protein. [1]
• Allyl methyl sulfide treatment significantly reduced serum liver toxicity markers (ALT, AST, ALP) in diabetic rats. ALT: diabetic control 53.40 ± 4.06 U/L vs. diabetic + AMS 30.11 ± 2.29 U/L; ALP: diabetic control 112.29 ± 8.55 U/L vs. diabetic + AMS 84.50 ± 6.43 U/L. [1]
• Western blot analysis showed that Allyl methyl sulfide down-regulated the protein expression of pro-inflammatory cytokines TNF-α and IL-6, and the transcription factor NF-κB p65 in the liver of STZ-induced diabetic rats. [1]
• Histopathological examination (H&E staining) revealed that Allyl methyl sulfide ameliorated severe necrosis, inflammatory cell infiltration, and periportal fatty deposition in the liver of diabetic rats. [1]
• Immunohistochemical staining demonstrated that Allyl methyl sulfide reduced the expression of TNF-α, IL-6, and NF-κB p65 in hepatic tissues of diabetic rats. [1]
• Allyl methyl sulfide treatment (100 mg/kg b.w) also improved body weight, reduced food and water intake, and increased liver weight compared to untreated diabetic rats. Body weight final: diabetic control 158 ± 12.03 g vs. diabetic + AMS 205 ± 15.23 g; food intake after treatment: diabetic control 69.23 ± 6.64 g/rat/day vs. diabetic + AMS 29.06 ± 2.98 g/rat/day; water intake after treatment: diabetic control 118.00 ± 8.99 mL/rat/day vs. diabetic + AMS 40.07 ± 3.05 mL/rat/day. [1]

Adult male Wistar rats (12 weeks old, 170-190 g) were housed under specific pathogen-free conditions at 25±2°C, 40-60% humidity, with 12h light-dark cycles and free access to food and water. [1]
• Diabetes was induced by a single intraperitoneal injection of STZ (40 mg/kg b.w) dissolved in citrate buffer (pH 4.4, 0.1 M). After 72 hours, rats with blood glucose ≥14.1 mmol/L were considered diabetic. [1]
• Allyl methyl sulfide was dissolved in 1 mL corn oil and administered intragastrically daily in the morning for 30 days. Doses used: 50, 100, and 200 mg/kg b.w. [1]
• Experimental groups (6 rats per group): Group I: normal untreated control; Group II: normal rats receiving AMS (200 mg/kg b.w); Group III: diabetic control (vehicle treated); Group IV: diabetic + AMS (50 mg/kg b.w); Group V: diabetic + AMS (100 mg/kg b.w); Group VI: diabetic + AMS (200 mg/kg b.w). [1]
• After 30 days of treatment, rats were fasted for 12 hours and sacrificed by cervical decapitation. Blood was collected for plasma and serum separation; liver was excised, weighed, and processed for biochemical and histological analyses. [1]

[1]. Allyl methyl sulfide, an organosulfur compound alleviates hyperglycemia mediated hepatic oxidativestress and inflammation in streptozotocin - induced experimental rats. Biomed Pharmacother. 2018 Nov;107:292-302.

3-(methylthio)-1-propene is an organosulfur compound. Allyl methyl sulfide has been reported in plants of the genera Allium ampeloprasum and Allium victorialis, as well as other organisms with relevant data.

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Allyl methyl sulfide is a volatile garlic metabolite and a leading compound among garlic organosulfur compounds. It has been reported to exert antioxidant, antibacterial, and anticancer properties. [1]
• The mechanism of action of AMS in diabetes involves enhancing insulin sensitivity of peripheral organs, stimulating insulin secretion from existing or regenerated pancreatic β-cells, reducing oxidative stress by scavenging free radicals, and suppressing pro-inflammatory cytokines (TNF-α, IL-6) and NF-κB activation. [1]
• This study concludes that Allyl methyl sulfide supplementation alleviates hyperglycemia-mediated hepatic oxidative stress and inflammation, preserves structural and functional integrity of hepatocytes, and could be a promising compound against glucotoxicity-mediated hepatic dysfunction. Clinical trials are warranted. [1]

C4H8S

88.17132

88.034

10152-76-8

66282

Colorless to light yellow liquid

0.9±0.1 g/cm3

88.6±9.0 °C at 760 mmHg

18.3±0.0 °C

68.4±0.2 mmHg at 25°C

1.459

1.68

0

1

2

5

24.8

0

C=CCSC

NVLPQIPTCCLBEU-UHFFFAOYSA-N

InChI=1S/C4H8S/c1-3-4-5-2/h3H,1,4H2,2H3

3-methylsulfanylprop-1-ene

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~1134.17 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (23.59 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (23.59 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (23.59 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)