ArticleNeuroscience letters2017
Thymosin β4 for the treatment of acute stroke in aged rats.
Article in Neuroscience letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Thymosin β4 Mitigates Acute Cerebral Infarction Via Inhibition of the TLR4/NF-κB Pathway and Suppression of Neuronal Pyroptosis.Applied biochemistry and biotechnology · 2026Article
- Injectable hyaluronic acid hydrogel loaded with BMSC and NGF for traumatic brain injury treatment.Materials today. Bio · 2022Article
- Tβ4-Ac-SDKP pathway: Any relevance for the cardiovascular system?Canadian journal of physiology and pharmacology · 2019Review
- Thymosin β4 prevents oxygen-glucose deprivation/reperfusion-induced injury in rat cortical neurons.Neuropsychiatric disease and treatment · 2019Article
- Thymosin β4 for the treatment of acute stroke: neurorestorative or neuroprotective?Expert opinion on biological therapy · 2018Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Thymosin β4 (Tβ4) is a 5K peptide which influences cellular migration by inhibiting organization of the actin-cytoskeleton. Tβ4 has neurorestorative properties and is a potential candidate for the treatment of sub-acute stroke. Previous research demonstrated that Tβ4 improved neurological outcome in a young (3 months) rat model of embolic stroke. We hypothesized that Tβ4 would improve neurological outcome in an aged rat model of embolic stroke when administered 24h after embolic stroke. Aged Male Wistar rats (Charles River, France 18-21 months) were subjected to embolic middle cerebral artery occlusion (MCAo). Rats were randomized to receive Tβ4 (12mg/kg, RegeneRx Biopharmaceuticals, Inc.) or control 24h after MCAo and then every 3days for 4 additional doses. The dose of 12mg/kg was the maximal dose of Tβ4 that showed functional improvement in a young rat model of embolic stroke. Functional tests (adhesive-removal test (ART), foot fault test (FFT) and the modified Neurological Severity Score (mNSS)) were performed weekly. The rats were sacrificed 56days after MCAo and lesion volumes were measured. Immunohistochemical analysis for oligodendrogenesis, myelination and gliosis was also performed. Twenty-three rats were included in the study: control group (n=12) and Tβ4 group (n=11). After randomization, there were three deaths in both the control and Tβ4 groups. The Tβ4 treatment reduced infarct volume by more than 50% (12.8%±9.3%, mean±SE, p<0.05) compared to the control group (26.0%±4.3%). However, Tβ4 did not show improvement in functional outcome compared to control. There was no significant increase in oligodendrogenesis, myelination and gliosis between control and treatment with Tβ4, however, we unexpectedly observed that overall (control and Tβ4 groups) astrocytic gliosis as measured by GFAP immunoreactivity was significantly inversely correlated with neurological outcome measured using the modified Neurological Severity Score (mNSS) (p<0.01), suggesting that greater gliosis may be related to improvement of neurological outcome in aged rats. In summary, Tβ4 treatment of stroke aged rats significantly reduces infarct volume compared to vehicle treated stroke, however, Tβ4 treatment did not show improvement in functional outcome, myelination or gliosis when compared to control. GFAP staining was significantly inversely correlated to improvement in the mNSS, suggesting that gliosis in the aged rat may be of benefit in improvement of functional outcome.
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Registered trials
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