Atorvastatin |
| Katalog-Nr.GC35419 |
Atorvastatin ist ein oral aktiver HMG-CoA-Reduktase-Hemmer und hat die Fähigkeit, Blutfette wirksam zu senken.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 134523-00-5
Sample solution is provided at 25 µL, 10mM.
Atorvastatin ist ein oral aktiver HMG-CoA-Reduktase-Hemmer und hat die Fähigkeit, Blutfette wirksam zu senken[1]. Atorvastatin hemmt die Proliferation und Invasion menschlicher SV-SMC mit IC50-Werten von 0,39 µM und 2,39 mM.
PMA-differenzierte THP-1-Zellen wurden als surrogate Mikrogliazellen verwendet, und LPS wurde zur Induktion entzündlicher Zustände eingesetzt. Die Vorbehandlung mit Atorvastatin konnte die LPS-induzierte Freisetzung von Interleukin (IL)-1β und Tumornekrosefaktor (TNF)-α sowie die LPS-induzierte Prostaglandin E2 (PGE2) signifikant reduzieren. Ebenso wurden die globale Produktion von reaktiven Sauerstoffspezies (ROS) und Stickstoffmonoxid (NO) nach der Vorbehandlung mit Atorvastatin reduziert[5]. In Ratten-NP-Zellen könnte Atorvastatin den durch TNF-α induzierten Matrixabbau durch Hemmung der NLRP3-Inflammasom-Aktivität und Induktion des autophagischen Flusses unterdrücken. Darüber hinaus unterdrückte Atorvastatin die durch TNF-α induzierte NF-κB-Signalisierung. Die Hemmung der NF-κB-Signalisierung unterdrückte die Aktivität des NLRP3-Inflammasoms, und die Hemmung von NLRP3 unterdrückte die durch TNF-α induzierte Aktivierung der NF-κB-Signalisierung. Die Hemmung oder der Knockdown von NLRP3 induzierte den autophagischen Fluss in Anwesenheit von TNF-α[7].
Bei Mäusen förderte die Vorbehandlung mit Atorvastatin die erhöhte Zellviabilität nach OGD und Reoxygenierung von Hippocampusschnitten. Die durch Atorvastatin induzierte Neuroprotektion könnte mit vermindertem oxidativem Stress zusammenhängen, da es den durch OGD induzierten Rückgang der nicht-proteinhaltigen Thiolspiegel (NPSH) und die Zunahme der Produktion von reaktiven Sauerstoffspezies (ROS) verhinderte[3]. Die orale Behandlung mit Atorvastatin (10 mg/kg/Tag) konnte Kurzzeitgedächtnisbeeinträchtigungen und depressionsähnliches Verhalten bei Ratten verhindern, die in den sozialen Erkennungs- und erzwungenen Schwimmtests an Tag 7 und 14 nach einer einzigen intranasalen Verabreichung von 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP) (1 mg/Nasenloch) getestet wurden[4]. Die antidepressiven Effekte von Atorvastatin stehen im Zusammenhang mit der Regulation der serotonergen Übertragung, der Hemmung des NMDA-Rezeptors und der NO-CGMP-Synthese sowie der Aktivierung des peroxisomproliferator-aktivierten Rezeptors γ[6]. Die Behandlung mit Atorvastatin zeigte neuroprotektive Effekte gegen LPS-induziertes depressionsähnliches Verhalten, was möglicherweise mit der Reduktion der TNF-α-Freisetzung, des oxidativen Stresses und der Modulation der BDNF-Expression zusammenhängt[2].
References:
[1]: Taciak PP, Lysenko N, et,al. Drugs which influence serotonin transporter and serotonergic receptors: Pharmacological and clinical properties in the treatment of depression. Pharmacol Rep. 2018 Feb;70(1):37-46. doi: 10.1016/j.pharep.2017.07.011. Epub 2017 Jul 16. PMID: 29309998.
[2]: Taniguti EH, Ferreira YS, et,al. Atorvastatin prevents lipopolysaccharide-induced depressive-like behaviour in mice. Brain Res Bull. 2019 Mar;146:279-286. doi: 10.1016/j.brainresbull.2019.01.018. Epub 2019 Jan 25. PMID: 30690060.
[3]: Vandresen-Filho S, Martins WC, et,al. Atorvastatin prevents cell damage via modulation of oxidative stress, glutamate uptake and glutamine synthetase activity in hippocampal slices subjected to oxygen/glucose deprivation. Neurochem Int. 2013 Jun;62(7):948-55. doi: 10.1016/j.neuint.2013.03.002. Epub 2013 Mar 14. PMID: 23500607.
[4]: Castro AA, Wiemes BP, et,al. Atorvastatin improves cognitive, emotional and motor impairments induced by intranasal 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration in rats, an experimental model of Parkinson's disease. Brain Res. 2013 Jun 4;1513:103-16. doi: 10.1016/j.brainres.2013.03.029. Epub 2013 Mar 30. PMID: 23548600.
[5]: McFarland AJ, Davey AK, et,al. Statins Reduce Lipopolysaccharide-Induced Cytokine and Inflammatory Mediator Release in an In Vitro Model of Microglial-Like Cells. Mediators Inflamm. 2017;2017:2582745. doi: 10.1155/2017/2582745. Epub 2017 May 4. PMID: 28546657; PMCID: PMC5435995.
[6]: Ludka FK, Constantino LC, et,al. Atorvastatin evokes a serotonergic system-dependent antidepressant-like effect in mice. Pharmacol Biochem Behav. 2014 Jul;122:253-60. doi: 10.1016/j.pbb.2014.04.005. Epub 2014 Apr 21. PMID: 24769309.
[7]: Chen J, Yan J, et,al.Atorvastatin inhibited TNF-α induced matrix degradation in rat nucleus pulposus cells by suppressing NLRP3 inflammasome activity and inducing autophagy through NF-κB signaling. Cell Cycle. 2021 Oct;20(20):2160-2173. doi: 10.1080/15384101.2021.1973707. Epub 2021 Sep 8. PMID: 34494933; PMCID: PMC8565837.
| Cell experiment [1]: | |
Cell lines | Differentiated THP-1 human monocytes |
Preparation Method | Following differentiation, cells were treated with either vehicle control or one of the six statins (atorvastatin;0-100 µM) and incubated at 37 ℃,5% CO2 for 60 minutes. |
Reaction Conditions | 0-100uM atorvastatin at 37 ℃ for 60 minutes |
Applications | Pretreatment with atorvastatin was able to significantly reduce LPS-induced interleukin (IL)-1β and tumour necrosis factor (TNF)-α release, as well as decrease LPS-induced prostaglandin E2 (PGE2). Similarly, global reactive oxygen species (ROS) and nitric oxide (NO) production were decreased following pretreatment with atorvastatin. |
| Animal experiment [2]: | |
Animal models | Male adult Swiss albino mice (30-50 g) |
Preparation Method | Animals were pretreated with 10 mg/kg/day of atorvastatin, orally or vehicle (saline, 0.9%) once a day for 7 days before preparing hippocampal slices for ex vivo OGD induction and measurement of cellular viability, oxidative stress and glutamatergic transmission parameters. |
Dosage form | 10 mg/kg atorvastatin, orally once a day for 7 days |
Applications | Atorvastatin pretreatment promoted increased cell viability after OGD and reoxygenation of hippocampal slices. Atorvastatin-induced neuroprotection may be related to diminished oxidative stress, since it prevented OGD-induced decrement of non-proteic thiols (NPSH) levels and increase in the production of reactive oxygen species (ROS). |
References: | |
| Cas No. | 134523-00-5 | SDF | |
| Canonical SMILES | O=C(C(C(C1=CC=CC=C1)=C(C2=CC=C(F)C=C2)N3CC[C@@H](O)C[C@@H](O)CC(O)=O)=C3C(C)C)NC4=CC=CC=C4 | ||
| Formula | C33H35FN2O5 | M.Wt | 558.64 |
| Löslichkeit | DMSO: 100 mg/mL (179.01 mM) | Storage | Store at -20°C |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
||
| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
|
1 mg | 5 mg | 10 mg |
| 1 mM | 1.7901 mL | 8.9503 mL | 17.9006 mL |
| 5 mM | 0.358 mL | 1.7901 mL | 3.5801 mL |
| 10 mM | 0.179 mL | 0.895 mL | 1.7901 mL |
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- Purity: >98.00%
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Average Rating: 5 (Based on Reviews and 25 reference(s) in Google Scholar.)
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