ArticleCellular and molecular neurobiology2018
Effects of Rat Anti-mouse Interleukin-6 Receptor Antibody on the Recovery of Cognitive Function in Stroke Mice.
Article in Cellular and molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Arterial Stiffness and Indices of Left Ventricular Diastolic Dysfunction in Patients with Embolic Stroke of Undetermined Etiology.Disease markers · 2019Trial
- Translational evidence for increased central amygdala IL-6 activity in alcohol dependence.Journal of neuroinflammation · 2026Article
- Effects of long-term infliximab and tocilizumab treatment on anxiety-like behavior and cognitive function in naive rats.Pharmacological reports : PR · 2022Article
- Propofol ameliorates ischemic brain injury by blocking TLR4 pathway in mice.Translational neuroscience · 2022Article
- Neuroprotective effects of neurotropin in a mouse model of hypoxic-ischemic brain injury.Journal of anesthesia · 2019Article
- Vascular Cognitive Impairment: Information from Animal Models on the Pathogenic Mechanisms of Cognitive Deficits.International journal of molecular sciences · 2019Review
- Hydroxysafflor Yellow A (HSYA) Improves Learning and Memory in Cerebral Ischemia Reperfusion-Injured Rats via Recovering Synaptic Plasticity in the Hippocampus.Frontiers in cellular neuroscience · 2018Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate the effects of rat anti-mouse interleukin (IL)-6 receptor antibody (MR16-1) on the recovery of cognitive function in stroke mice. Adult male C57BL/6 mice were subjected to middle cerebral artery occlusion (MCAO). Mice were randomly assigned into three groups: sham group, model group, and MR16-1 group. After the treatment of MR16-1, spatial learning and memory performance of mice were evaluated by the Morris water maze (MWM) and Y-maze tests. Then, brain slices were obtained and infarct volume and neuronal apoptosis were assessed by 2,3,5-triphenyltetrazolium chloride (TTC) staining and Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay, respectively. Protein expression levels of apoptosis-associated proteins and multiple inflammatory cytokines were determined by Western blot analysis. Real-time quantitative PCR (RT-PCR) was used to examine the mRNA levels of various inflammatory cytokines in brain slices and cerebrospinal fluid (CSF). The results showed that MR16-1 improved performances of stroke mice in MWM and Y-maze tests. Moreover, MR16-1 ameliorated MCAO-induced infarct, neuronal apoptosis, and inflammatory response. Furthermore, MR16-1 promoted the expression of Bcl-2 and inhibited the expression of Bax in stroke mice, which revealed the inhibitory effect of MR16-1 on neuronal apoptosis. IL-6 levels in brain and CSF were both decreased by MR16-1 treatment in stroke mice. MR16-1 ameliorated cognitive dysfunction and apoptosis in stroke mice, involving the inhibition of inflammatory response and pro-apoptotic Bax, and the up-regulation of anti-apoptotic Bcl-2. The data supported that MR16-1 might be a potential therapeutic drug for the treatment of stroke.
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