Abstract | BACKGROUND: Some degree of spontaneous recovery is usually observed after stroke. Experimental studies have provided information about molecular mechanisms underlying this recovery. However, the majority of pre-clinical stroke studies are performed in male rodents, and females are not well studied. This is a clear discrepancy when considering the clinical situation. Thus, it is important to include females in the evaluation of recovery mechanisms for future therapeutic strategies. This study aimed to evaluate spontaneous recovery and molecular mechanisms involved in the recovery phase two weeks after stroke in female rats. METHODS: RESULTS: Spontaneous recovery after stroke was observed from day 2 to day 14 and was accompanied by a significantly higher expression of nestin, p-Akt, p-ERK1/2 and TGF-β in ischemic regions compared to contralateral side at day 14. In addition, a significantly higher expression of TGF-β was observed in occluded versus non-occluded middle cerebral arteries. The expression of Tie-2 and IL-10 did not differ between the ischemic and contralateral sides. CONCLUSION: Spontaneous recovery after ischemic stroke in female rats was coincided by a difference observed in the expression of molecular markers. The alteration of these markers might be of importance to address future therapeutic strategies.
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Authors | Maryam Mostajeran, Lars Edvinsson, Hilda Ahnstedt, Kajsa Arkelius, Saema Ansar |
Journal | BMC neuroscience
(BMC Neurosci)
Vol. 23
Issue 1
Pg. 23
(04 12 2022)
ISSN: 1471-2202 [Electronic] England |
PMID | 35413803
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2022. The Author(s). |
Chemical References |
- Nestin
- Transforming Growth Factor beta
- Interleukin-10
- Proto-Oncogene Proteins c-akt
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Topics |
- Animals
- Brain Ischemia
- Female
- Infarction, Middle Cerebral Artery
(drug therapy)
- Interleukin-10
- Ischemic Stroke
- Male
- Nestin
- Pregnancy
- Proto-Oncogene Proteins c-akt
- Rats
- Rats, Wistar
- Recovery of Function
(physiology)
- Stroke
(metabolism)
- Transforming Growth Factor beta
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