DL-Homocysteine
(Synonyms: DL-高半胱氨酸) 目录号 : GC30684
DL-Homocysteine是一种含硫非必需氨基酸,具有弱神经毒性。
Cas No.:454-29-5
Sample solution is provided at 25 µL, 10mM.
DL-Homocysteine is a thiol-containing non-essential amino acid that acts a weak neurotoxin[1]. DL-Homocysteine has been widely used in both cell and animal models to regulate cardiovascular functions[2].
In vitro, DL-Homocysteine treatment at 100μM for 18 hours significantly induced adhesion of U937 cells without affecting the viability of cells[3]. Treatment with 50μM DL-Homocysteine for 8 hours significantly upregulated the expression of monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) in human aortic endothelial cells[4]. Exposure of rat neuronal cells to 100μM DL-Homocysteine for 6 days resulted in a significant decrease in cell viability and a large number of cell deaths[5]. Treatment with 500μM DL-Homocysteine for 24 hours significantly inhibited the proliferation of bovine aortic endothelial cells[6].
In vivo, DL-Homocysteine treatment via oral administration at 3g/kg/day for 5 months can counteract the inflammation caused by cholesterol in male Sprague Dawley rats and improve the spatial learning ability[7]. A single intraperitoneal injection of 1.3mmol/kg of DL-Homocysteine for 60 minutes can significantly promote the production of kynurenic acid (KYNA) in the male Wistar rats' bodies[8].
References:
[1] Bleich S, Degner D, Sperling W, et al. Homocysteine as a neurotoxin in chronic alcoholism[J]. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2004, 28(3): 453-464.
[2] Stühlinger M C, Tsao P S, Her J H, et al. Homocysteine impairs the nitric oxide synthase pathway: role of asymmetric dimethylarginine[J]. Circulation, 2001, 104(21): 2569-2575.
[3] Silverman M D, Tumuluri R J, Davis M, et al. Homocysteine upregulates vascular cell adhesion molecule-1 expression in cultured human aortic endothelial cells and enhances monocyte adhesion[J]. Arteriosclerosis, thrombosis, and vascular biology, 2002, 22(4): 587-592.
[4] Poddar R, Sivasubramanian N, DiBello P M, et al. Homocysteine induces expression and secretion of monocyte chemoattractant protein-1 and interleukin-8 in human aortic endothelial cells: implications for vascular disease[J]. Circulation, 2001, 103(22): 2717-2723.
[5] Lipton S A, Kim W K, Choi Y B, et al. Neurotoxicity associated with dual actions of homocysteine at the N-methyl-D-aspartate receptor[J]. Proceedings of the National Academy of Sciences, 1997, 94(11): 5923-5928.
[6] Wejksza K, Rzeski W, Turski W A. Kynurenic acid protects against the homocysteine-induced impairment of endothelial cells[J]. Pharmacological Reports, 2009, 61(4): 751-756.
[7] Pirchl M, Ullrich C, Sperner-Unterweger B, et al. Homocysteine has anti-inflammatory properties in a hypercholesterolemic rat model in vivo[J]. Molecular and Cellular Neuroscience, 2012, 49(4): 456-463.
[8] Luchowska E, Luchowski P, Paczek R, et al. Dual effect of DL‐homocysteine and S‐adenosylhomocysteine on brain synthesis of the glutamate receptor antagonist, kynurenic acid[J]. Journal of neuroscience research, 2005, 79(3): 375-382.
DL-Homocysteine是一种含硫非必需氨基酸,具有弱神经毒性[1]。DL-Homocysteine已广泛应用于细胞和动物模型的心血管功能调控研究[2]。
在体外,100μM 的DL-Homocysteine处理U937细胞18小时可显著诱导细胞黏附且不影响细胞活力[3]。50μM的DL-Homocysteine处理人主动脉内皮细胞8小时能显著上调单核细胞趋化蛋白-1(MCP-1)和白细胞介素-8(IL-8)表达[4]。100μM的DL-Homocysteine处理大鼠神经元细胞6天会导致细胞活力显著下降并引发大量细胞死亡[5]。500μM的DL-Homocysteine处理牛主动脉内皮细胞24小时可显著抑制细胞增殖[6]。
在体内,雄性Sprague Dawley大鼠每日口服DL-Homocysteine(3g/kg;持续5个月)可拮抗胆固醇引起的炎症并改善空间学习能力[7]。雄性Wistar大鼠单次腹腔注射1.3mmol/kg的DL-Homocysteine(60分钟)能显著促进体内犬尿喹啉酸(KYNA)生成[8]。
Cell experiment [1]: | |
Cell lines | Human aortic endothelial cells |
Preparation Method | Human aortic endothelial cells were cultured in M199 medium, with 150μg/mL endothelial cell growth factor, 8% 90μg/mL heparin, 20% fetal bovine serum, and antibiotic/antifungal agent mixture added to the medium. Confluent cell cultures (5th to 7th generation) were incubated in fresh medium for 24 hours, and then treated with or without DL-Homocysteine (10, 50, 100, 500, 5000, and 10000μM) for 8 hours. The protein concentrations of MCP-1 and IL-8 in the culture supernatants were determined by ELISA. |
Reaction Conditions | 10, 50, 100, 500, 5000, and 10000μM; 8h |
Applications | DL-Homocysteine treatment significantly upregulated the expression of MCP-1 and IL-8 in human aortic endothelial cells. |
Animal experiment [2]: | |
Animal models | Female FVB/NJ mice |
Preparation Method | Female FVB/NJ mice (8-10 weeks old) were divided into 5 groups and were fed with one of the following 5 diets for a total of 14 days: (a) The control diet was the same as the choline-deficient (MCD) diet, but with added methionine and choline; (b) The control diet was supplemented with homocysteine; (c) The MCD diet; (d) The MCD diet was supplemented with DL-Homocysteine; and (e) The MCD diet was supplemented with methionine. DL-Homocysteine and L-Methionine were added to the drinking water at concentrations of 1.8g/L/day and 5g/L/day, respectively. The mice were housed in group cages, with a 12-hour light-dark cycle with free access to food and water. The mice were fasted for 4 hours before being sacrificed. Body weight was recorded at the beginning and end of the experimental protocol. The mice were euthanized by inhalation of carbon dioxide. Plasma and liver samples were collected for analysis. |
Dosage form | 1.8g/L/day for 15 days; p.o. |
Applications | DL-Homocysteine treatment significantly inhibited the liver cholesterol accumulation and elevated plasma alanine aminotransferase (ALT) caused by MCD in mice. |
References: |
Cas No. | 454-29-5 | SDF | |
别名 | DL-高半胱氨酸 | ||
Canonical SMILES | O=C(O)C(N)CCS | ||
分子式 | C4H9NO2S | 分子量 | 135.19 |
溶解度 | Water : 75 mg/mL (554.77 mM) | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg |
1 mM | 7.397 mL | 36.985 mL | 73.97 mL |
5 mM | 1.4794 mL | 7.397 mL | 14.794 mL |
10 mM | 739.7 μL | 3.6985 mL | 7.397 mL |
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