ARTEMIDA Trial (A Randomized Trial of Efficacy, 12 Months International Double-Blind Actovegin)

Guekht, Alla; Skoog, Ingmar; Edmundson, Sally; Vv, Zakharov; Korczyn, Amos D.

doi:10.1161/strokeaha.116.014321

Cited by 73 publications

(31 citation statements)

References 34 publications

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“…Clinically, the susceptibility and prognosis of stroke is also related to systemic inflammatory processes (Dirnagl et al, 1999). Although anti-inflammatory agents have garnered considerable interest from researchers for treating ischemic damage, and have exhibited promising effects in ischemic stroke animal models, most have failed in subsequent clinical trials (Guekht et al, 2017). Thus, new therapies that aim to re-establish brain homeostasis and restore the balance between pro-inflammatory and anti-inflammatory signals are urgently needed to improve outcome.…”

Section: Introductionmentioning

confidence: 99%

Meisoindigo Protects Against Focal Cerebral Ischemia-Reperfusion Injury by Inhibiting NLRP3 Inflammasome Activation and Regulating Microglia/Macrophage Polarization via TLR4/NF-κB Signaling Pathway

Jin

Zhou

et al. 2019

Front. Cell. Neurosci.

201

119

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Ischemic stroke is a devastating disease with long-term disability. However, the pathogenesis is unclear and treatments are limited. Meisoindigo, a second-generation derivative of indirubin, has general water solubility and is well-tolerated. Previous studies have shown that meisoindigo reduces inflammation by inhibiting leukocyte chemotaxis and migration. In the present study, we investigated the hypothesis that meisoindigo was also protective against ischemic stroke, then evaluated its underlying mechanisms. In vivo, adult male C57BL/6J wild-type mice were used to produce a middle cerebral artery occlusion (MCAO) stroke model. On day three after reperfusion, obvious improvement in neurological scores, infarct volume reduction and cerebral edema amelioration were observed in meisoindigo treatment. Moreover, immunofluorescence staining and western-blot showed that the expression of NLRP3 inflammasome and its associated proteins in neurons and microglia was inhibited by meisoindigo. The effects of Meisoindigo on NLRP3 inflammasome inactivation and increased the M2 phenotype of microglia/macrophage through shifting from a M1 phenotype, which was possibly mediated by inhibition of TLR4/NF-κB. Furthermore, we verified the inhibitory effect of meisoindigo on TLR4/NF-κB signaling pathway, and found that meisoindigo treatment could significantly suppressed the expression of TLR4/NF-κB pathway-associated proteins in a dose-dependent manner, meanwhile, which resulted in downregulation of HMGB1 and IL-1β. Next, we established an in vitro oxygen glucose deprivation/Reperfusion (OGD/R) model in HT-22 and BV2 cells to simulate ischemic conditions. Cytotoxicity assay showed that meisoindigo substantially improved relative cell vitality and in HT-22 and BV2 cells following OGD/R in vitro. After suffering OGD/R, the TLR4/NF-κB pathway was activated, the expression of NLRP3 inflammasome-associated proteins and M1 microglia/macrophage were increased, but

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Section: Introductionmentioning

confidence: 99%

Meisoindigo Protects Against Focal Cerebral Ischemia-Reperfusion Injury by Inhibiting NLRP3 Inflammasome Activation and Regulating Microglia/Macrophage Polarization via TLR4/NF-κB Signaling Pathway

Jin

Zhou

et al. 2019

Front. Cell. Neurosci.

201

119

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“…Согласно данным разных авторов, клинический эффект цереброактивных препаратов начинает проявляться уже через 1-3 мес применения. Например, у пациентов с цереброваскулярными заболеваниями 2-месячный курс терапии нафтидрофурилом (периферический вазодилататор и антагонист серотониновых 5-НТ2-рецепторов) способствовал повышению среднего балла по шкале МоСА на 3 балла [38], 4-недельный курс этилметилгидроксипиридина сукцината (антиоксидант и мембранопротектор)на 4,61 балла [39], 2-месячный курс тиоцетама (ноотропное, противоишемическое и антиоксидантное действие) -на 3 балла [40], 3-месячный курс винпоцетина (вазоди латирующее действие) -на 1,6 балла [19], 3-месячный курс депротеинизированного гемодеривата крови телят (антигипоксантное действие) -на 3,4 балла [41].…”

Section: Discussionunclassified

Diagnosis and treatment of cognitive impairment in patients with chronic cerebral ischemia: the results of observational Russian program DIAMANT

Parfenov¹,

Zhivolupov²,

Nikulina³

et al. 2018

Z. nevrol. psikhiatr. im. S.S. Korsakova

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Cognitive disorders were identified in 90.7% of patients (<26 MoCA scores). After treatment, the mean MoCA score increased from 19.58±5.13 to 23.99±4.21 (p<0.0001), the number of patients with normal cognitive functions rate (≥26 scores) increased from 9.3 to 41.3%, the number of patients with marked cognitive impairment decreased. The drug was well-tolerated by old and very old patients, adverse events were observed rarely (0.6% of cases). The majority of doctors (88.4%) noticed the effect of divaza as significant improvement or improvement, and 89.6% of patients valued the effect to be excellent or good. The use of divaza, the drug with endothelioprotective and nootropic effects, is pathogenetically justified and promising in patients with cognitive disorders of vascular etiology.

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“…В рекомендациях, подготовленных экспертами США, ноотропные, вазоактивные и метаболические средства, ан-тиоксиданты не расцениваются как эффективные при СКН [2]. Однако во многих современных обзорах по лечению СКН встречаются данные о положительном действии церебролизина при выраженных СКН по результатам метаанализа [58], препарата EGB 761 -по данным систематического обзора [59], актовегина при постинсультных КН -по результатам многоцентрового рандомизированного плацебоконтролируемого исследования [60].…”

Section: о б з о р ы к р и т е р и и к н с о с у д и с т о г о п р о unclassified

Vascular cognitive impairment and chronic cerebral ischemia (dyscirculatory encephalopathy)

Parfenov

2019

RJTAO

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The paper reviews the literature on vascular cognitive impairment (VCI), the diagnosis widely used in foreign neurological practice, as well as chronic cerebral ischemia (CCI) and dyscirculatory encephalopathy (DEP), the common diagnoses in Russian neurological practice. According to the etiology, risk factors, and manifestations, Stages I and II DEP largely corresponds to moderate VCI; Stage III DEP does to severe VCI. The results of the author’s studies show that a considerable proportion of patients followed up with a diagnosis of CCI, DEP, have no signs of chronic cerebrovascular disease (CVD), but suffer from primary or secondary headache, vertigo of various origins, emotional disorders, and other diseases. The diagnosis of CCI, DEP should be based on the presence of CCI, the reliable neuroimaging signs of chronic CVD, and the ruling out of other diseases. When treating and preventing VCI, CCI, and DEP, a premium is placed upon both non-drug (regular physical activity, smoking cessation, rational nutrition) and drug therapy aimed at normalizing blood pressure and blood lipid spectrum, preventing blood clots, and improving cognitive functions.

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ARTEMIDA Trial (A Randomized Trial of Efficacy, 12 Months International Double-Blind Actovegin)

Abstract: Supplemental Digital Content is available in the text.

Cited by 73 publications

References 34 publications

Meisoindigo Protects Against Focal Cerebral Ischemia-Reperfusion Injury by Inhibiting NLRP3 Inflammasome Activation and Regulating Microglia/Macrophage Polarization via TLR4/NF-κB Signaling Pathway

Meisoindigo Protects Against Focal Cerebral Ischemia-Reperfusion Injury by Inhibiting NLRP3 Inflammasome Activation and Regulating Microglia/Macrophage Polarization via TLR4/NF-κB Signaling Pathway

Diagnosis and treatment of cognitive impairment in patients with chronic cerebral ischemia: the results of observational Russian program DIAMANT

Vascular cognitive impairment and chronic cerebral ischemia (dyscirculatory encephalopathy)

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