"Statins enhance expression of growth factors and activate the PI3K/Akt-mediated signaling pathway after experimental intracerebral hemorrhage"
written by Dongmei Yang, Yuxia Han, Jianfeng Zhang, Michael Chopp, Donald M. Seyfried,
published by World Journal of Neuroscience, Vol.2 No.2, 2012
has been cited by the following article(s):
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[13] Atorvastatin suppresses CD147 and MMP-3 expression and improves histological and neurological outcomes in an animal model of intracerebral hemorrhage
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[18] Simvastatin as a Potential Disease-Modifying Therapy for Patients with Parkinson's Disease: Rationale for Clinical Trial, and Current Progress
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[19] Effects of Atorvastatin in Patients with Acute Spinal Cord Injury
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[20] Neovascularization and Synaptic Function Regulation with Memantine and Rosuvastatin in a Rat Model of Chronic Cerebral Hypoperfusion
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[21] Intracerebral Hemorrhage: Perihemorrhagic Edema and Secondary Hematoma Expansion: From Bench Work to Ongoing Controversies
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[22] After Intracerebral Hemorrhage, Oligodendrocyte Precursors Proliferate and Differentiate Inside White-Matter Tracts in the Rat Striatum
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[23] Involvement of PI3K/Akt/GSK-3β and mTOR in the antidepressant-like effect of atorvastatin in mice
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[24] Neuroprotective Effects of Low-Dose Statins in the Retinal Ultrastructure of Hypercholesterolemic Rabbits
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[25] Refining a Post-Stroke Pharmacological and Physical Treatment to Reduce Infarct Volume or Improve Functional Recovery, Using Gene Expression Changes in the …
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[26] Endoplasmic reticulum stress-induced neuronal inflammatory response and apoptosis likely plays a key role in the development of diabetic encephalopathy
[27] The Association between Impaired Glucose Regulation and Prognosis of Chinese Patients with Intracerebral Hemorrhage
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[28] Activation of peroxisome proliferator-activated receptor–γ by a 12/15-lipoxygenase product of arachidonic acid: a possible neuroprotective effect in the brain after experimental intracerebral hemorrhage
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[29] Atorvastatin Protects from Aβ1–40-Induced Cell Damage and Depressive-Like Behavior via ProBDNF Cleavage
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[30] Modulation of the expression and function of dopaminergic presynaptic proteins by the statins : Potential implication for the therapeutic intervention in Parkinson’s disease
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[31] Simvastatin prevents β-amyloid 25–35-impaired neurogenesis in hippocampal dentate gyrus through α7nAChR-dependent cascading PI3K-Akt and increasing BDNF via reduction of farnesyl pyrophosphate
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[32] Gelatin Nanostructured Lipid Carriers Incorporating Nerve Growth Factor Inhibit Endoplasmic Reticulum Stress-Induced Apoptosis and Improve Recovery in Spinal Cord Injury
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[33] Does statin therapy reduce plasma VEGF levels in humans? A systematic review and meta-analysis of randomized controlled trials
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[34] Statins Reduce the Risks of Relapse to Addiction in Rats
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[35] Modulation de l’expression et de la fonction des protéines dopaminergiques présynaptiques par les statines : Application potentielle pour une intervention thérapeutique dans la maladie de Parkinson.
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[36] Effects of Delayed Pharmacological Treatment and Limb Rehabilitation on Infarct Size and Functional Recovery After Stroke
[37] Effect of atorvastatin, a HMG-CoA reductase inhibitor in monosodium iodoacetate-induced osteoarthritic pain: Implication for osteoarthritis therapy
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[38] Evaluation of Antidepressant Activity of Simvastatin in Albino Mice
[39] Atorvastatin attenuates neuropathic pain in rat neuropathy model by down-regulating oxidative damage at peripheral, spinal and supraspinal levels
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[40] Antagonism by bioactive polyphenols against inflammation: a systematic view
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[41] Treadmill exercise reduces spinal cord injury-induced apoptosis by activating the PI3K/Akt pathway in rats
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[42] Statins in nervous system-associated diseases: angels or devils?
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[43] Antihyperalgesic and anti-inflammatory effects of atorvastatin in chronic constriction injury-induced neuropathic pain in rats
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[44] Simvastatin with niaspan improves neurological outcome after experimental intracerebral hemorrhage
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