Propofol
(Synonyms: 丙泊酚; 2,6-Diisopropylphenol) 目录号 : GC39424
Propofol是一种广泛用于麻醉诱导和维持的静脉麻醉药，具有调节自噬、抗肿瘤或致癌活性。
Cas No.:2078-54-8
Sample solution is provided at 25 µL, 10mM.
Propofol, a widely used intravenous anesthetic for induction and maintenance, modulates autophagy and exhibits anti-tumor or carcinogenic activity[1-2]. Propofol exerts its hypnotic actions by activating the central inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the central nervous system[2]. In addition, Propofol possesses cyclooxygenase (COX)-inhibiting activity[3].
In vitro, exposure of H9c2 embryonal rat heart-derived cells to escalating concentrations of Propofol (12.5-100µmol/L) for 4h produced a dose-dependent, significant reduction in hypoxia/reoxygenation (H/R)-induced early-apoptotic cells while simultaneously elevating LC3-II levels in a dose-dependent manner. H/R alone reduced p62 protein abundance, and Propofol further amplified this H/R-induced decline in p62[4]. In neuronal PC12 cells, a 10min exposure to Propofol (10, 20, or 50µM) dose-dependently attenuated autophagy by down-regulating the autophagy-related proteins LC3-II, Beclin-1, and Beclin-1-phosphatidylinositol-3 kinase class III (class III PI3K)[5].
In vivo, in male Sprague-Dawley rats, continuous intravenous infusion of Propofol at 12mg/kg/h for 30min via the femoral vein markedly attenuated myocardial injury caused by ischemia–reperfusion (I/R) and significantly reduced the formation of cytosolic vacuoles and myofibrillar lysis in cardiomyocytes[6]. Nude mice received intraperitoneal injections of Propofol (35mg/kg) every 2 days for 14 days, resulting in significantly smaller pheochromocytoma (PCC) tumor volumes and weights and markedly enhanced tumor-cell apoptosis compared with the sham group[7].
References:
[1] Xu Y, Pan S, Jiang W, et al. Effects of propofol on the development of cancer in humans. Cell Prolif. 2020;53(8):e12867.
[2] Guo XN, Ma X. The Effects of Propofol on Autophagy. DNA Cell Biol. 2020;39(2):197-209.
[3] Inada T, Kubo K, Shingu K. Possible link between cyclooxygenase-inhibiting and antitumor properties of propofol. J Anesth. 2011;25(4):569-575.
[4] Li H, Zhang X, Tan J, et al. Propofol postconditioning protects H9c2 cells from hypoxia/reoxygenation injury by inducing autophagy via the SAPK/JNK pathway. Mol Med Rep. 2018;17(3):4573-4580.
[5] Cui D, Wang L, Qi A, et al. Propofol prevents autophagic cell death following oxygen and glucose deprivation in PC12 cells and cerebral ischemia-reperfusion injury in rats [retracted in: PLoS One. 2022 Sep 28;17(9):e0275548. doi: 10.1371/journal.pone.0275548.]. PLoS One. 2012;7(4):e35324.
[6] Noh HS, Shin IW, Ha JH, et al. Propofol protects the autophagic cell death induced by the ischemia/reperfusion injury in rats. Mol Cells. 2010;30(5):455-460.
[7] Wang H, Zhang S, Zhang A, et al. Propofol Prevents the Progression of Malignant Pheochromocytoma In Vitro and In Vivo. DNA Cell Biol. 2018;37(4):308-315.
Propofol是一种广泛用于麻醉诱导和维持的静脉麻醉药，具有调节自噬、抗肿瘤或致癌活性[1-2]。Propofol的催眠作用主要通过激活中枢神经系统中的抑制性神经递质γ-氨基丁酸（GABA）而实现[2]。此外，Propofol还具有抑制环氧合酶（COX）的活性[3]。
在体外，将H9c2胚胎大鼠心肌源性细胞暴露于递增浓度的Propofol（12.5-100µmol/L）4小时，可剂量依赖性地显著减少缺氧/复氧（H/R）诱导的早期凋亡细胞，并同时以剂量依赖性方式提高LC3-II水平。H/R本身即可降低p62蛋白含量，而Propofol进一步增强了H/R引起的p62下降[4]。在神经元PC12细胞中，10分钟Propofol处理（10、20或50µM）可剂量依赖性地抑制自噬，表现为下调LC3-II、Beclin-1及Beclin-1-Ⅲ类磷脂酰肌醇-3-激酶（class III PI3K）等自噬相关蛋白[5]。
在体内，雄性Sprague-Dawley大鼠经股静脉持续静脉输注Propofol（12mg/kg/h，30分钟），显著减轻缺血再灌注（I/R）引起的心肌损伤，并明显减少心肌细胞胞质空泡和肌原纤维溶解[6]。裸鼠每2天腹腔注射Propofol（35mg/kg），持续14天，其嗜铬细胞瘤（PCC）肿瘤体积和重量显著小于假手术组，且肿瘤细胞凋亡显著增强[7]。
| Cell experiment [1]: | |
Cell lines | H9c2 embryonal rat heart-derived (cardiac muscle) cell line |
Preparation Method | Hypoxia was modeled in the H9c2 embryonal rat heart-derived (cardiac muscle) cell line. Hypoxia was terminated by exposing the cells to fresh Dulbecco's modified Eagle's medium (DMEM) containing 10% FBS and incubating them in a normal incubator (95% air; 5% CO2) for 4h at 37°C to simulate reperfusion (reoxygenation). Propofol (12.5-100µmol/L) was added to fresh medium at the onset of reoxygenation. After reoxygenation, cells were harvested by 0.25% trypsinization at 37°C, centrifuged at 800×g for 3min at room temperature, and washed twice with PBS. |
Reaction Conditions | 12.5, 25, 50, 100µmol/L; 4h |
Applications | Treatment with 12.5-50µmol/L Propofol caused a dose-dependent and significant reduction in the proportion of early apoptotic cells induced by hypoxia/reoxygenation (H/R). Post-treatment with Propofol dose-dependently enhanced 1A/1B-light chain 3 (LC3)-II levels. H/R exposure alone already decreased p62 protein abundance, and Propofol further intensified this H/R-induced reduction in p62. |
| Animal experiment [2]: | |
Animal models | Male Sprague-Dawley rats |
Preparation Method | The animals were anesthetized with ketamine 50mg/kg and xylazine 5mg/kg into the gluteus maximus muscle, and were ventilated artificially with room air using a rodent ventilator. The chest was opened via a left thoracotomy, followed by a pericardiotomy. A 4-0 black silk suture was passed around the left ascending (LAD) coronary artery, and the ends were pulled through a small vinyl tube to form a snare and then tightened. Coronary artery occlusion was verified by epicardial cyanosis. After 25min of ischemia, the myocardium was reperfused for 24h. The rats were randomized into three groups as follows. Saline (1.2ml/kg/h) and Propofol (12mg/kg/h) were administered via a femoral vein, beginning 15 minutes before reperfusion and continuing for 30 minutes into reperfusion. Group 1 rats (sham), surgically operated on, but no tightening of the coronary sutures. Group 2 rats (ischemia–reperfusion (I/R)) received saline and were subjected to 25min of ischemia followed by reperfusion. Group 3 rats (I/R with Propofol) received Propofol and were subjected to 25min of ischemia followed by reperfusion. |
Dosage form | 12mg/kg/h, 30min; administered via femoral vein |
Applications | The weight of the infarction area of the left ventricle obtained from I/R- injured rats was 0.14±0.01g, whereas the infarction weight of I/R-injured rats treated with Propofol was significantly decreased to 0.06±0.02g (P<0.05). Propofol treatment during I/R dramatically decreased the formation of cytosolic vacuoles and myofibrillar lysis in cardiomyocytes of I/R- damaged rats. |
References: | |
| Cas No. | 2078-54-8 | SDF | |
| 别名 | 丙泊酚; 2,6-Diisopropylphenol | ||
| Canonical SMILES | OC1=C(C(C)C)C=CC=C1C(C)C | ||
| 分子式 | C12H18O | 分子量 | 178.27 |
| 溶解度 | DMSO: 100 mg/mL (560.95 mM); Water: 1 mg/mL (5.61 mM) | 储存条件 | Store at 2-8°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.6095 mL | 28.0473 mL | 56.0947 mL |
| 5 mM | 1.1219 mL | 5.6095 mL | 11.2189 mL |
| 10 mM | 0.5609 mL | 2.8047 mL | 5.6095 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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工作液浓度： mg/ml；
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2.
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