| 包装 | 价格(元) |
| 10mg | 电议 |
| 50mg | 电议 |
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 !栩n 5% CO2 for 60 minutes. |
Reaction Conditions | 0-100uM atorvastatin at 37 !栦or 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 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). |
| 产品描述 | Atorvastatin is an orally active HMG-CoA reductase inhibitor, has the ability to effectively decrease blood lipids[1]. Atorvastatin inhibits human SV-SMC proliferation and invasion with IC50s of 0.39 µM and 2.39 mM. PMA-differentiated THP-1 cells were used as surrogate microglial cells, and LPS was used to induce inflammatory conditions. 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[5]. In rat NP cells, Atorvastatin might suppress matrix degradation induced by TNF-α by suppressing NLRP3 inflammasome activity and inducing autophagic flux. Moreover, atorvastatin suppressed NF-κB signaling induced by TNF-α. NF-κB signaling inhibition suppressed NLRP3 inflammasome activity, and NLRP3 inhibition suppressed NF-κB signaling activation induced by TNF-α. NLRP3 inhibition or NLRP3 knockdown induced autophagic flux in the presence of TNF-α[7]. In mice, 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)[3]. The oral treatment with atorvastatin (10mg/kg/day)was able to prevent short-term memory impairments and depressive-like behavior of rats assessed in the social recognition and forced swimming tests at 7 and 14 days, respectively, after a single intranasal administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (1mg/nostril)[4].The effects of atorvastatin antidepressants are related to the regulation of serotonergic transmission, the inhibition of NMDA receptor and NO-CGMP synthesis, and the activation of receptor γ dependent on peroxisome proliferators[6]. Atorvastatin treatment exerted neuroprotective effects against LPS-induced depressive-like behaviour which may be related to reduction of TNF-α release, oxidative stress and modulation of BDNF expression[2]. References: |
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