Related Experiment Video
Updated: Oct 7, 2025
Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
MiR-10b-3p alleviates cerebral ischemia/reperfusion injury by targeting Krüppel-like factor 5 (KLF5)
Ke Sun1, Jiangang Zhang1, Qingcheng Yang2
1Department of Neurology, Anyang People's Hospital, No. 1120 Yuefei Street, Wenfeng District, Anyang City, Henan Province, 455000, People's Republic of China.
Abstract:
Although miR-10b-3p has been identified to be involved in cerebral ischemia injury, its impact and specific mechanism in cerebral ischemia injury remain unclear. The effects of Mir-10b-3p were investigated by establishing rat and cell models of ischemia/reperfusion (I/R) injury. Oxygen-glucose deprivation/reperfusion (OGD/R) was performed on pheochromocytoma-12 (PC12) cells. MiR-10b-3p expression levels in brain tissues and PC12 cells were detected by qRT-PCR. The impacts of miR-10b-3p on neurological deficits, infarct volume, inflammatory factor expression, in vivo brain water content, cell viability, and cell apoptosis were assessed. The relationship between miR-10b-3p and KLF5 was determined by TargetScan and luciferase reporter assay. The rescue experiments were performed to confirm the role of this axis in cerebral ischemia injury. Mir-10b-3p levels in rat brain tissue and PC12 cells were significantly decreased after I/R injury. MiR-10b-3p overexpression obviously reduced neurological deficits, infarct volume, brain water content, inflammatory factors expression, and neuronal apoptosis in the brain of ischemia-stroked rats. Meanwhile, miR-10b-3p upregulation also inhibited cell viability and apoptosis of OGD/R-induced PC12 cells. Besides, KLF5 was identified as a target of miR-10b-3p, and rescue experiments revealed that KLF5 was involved in the regulation of miR-10b-3p in ischemic injury. Our results demonstrated that miR-10b-3p had the neuroprotective effects against ischemia injury by targeting KLF5 and provided a potential underlying target for ischemic stroke treatment.
Insights
MicroRNA-10b-3p (miR-10b-3p) protects the brain from ischemia injury by targeting KLF5. This study reveals miR-10b-3p as a potential therapeutic target for ischemic stroke treatment.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Cerebral ischemia injury, including stroke, poses a significant health burden.
- The precise role and mechanism of microRNA-10b-3p (miR-10b-3p) in cerebral ischemia injury are not fully understood.
- Identifying novel therapeutic targets is crucial for improving outcomes in ischemic stroke patients.
Purpose of the Study:
- To investigate the neuroprotective effects of miR-10b-3p in cerebral ischemia/reperfusion (I/R) injury.
- To elucidate the underlying molecular mechanism of miR-10b-3p in I/R injury, focusing on its interaction with KLF5.
- To evaluate miR-10b-3p as a potential therapeutic target for ischemic stroke.
Main Methods:
- Establishment of rat and pheochromocytoma-12 (PC12) cell models of ischemia/reperfusion (I/R) and oxygen-glucose deprivation/reperfusion (OGD/R) injury.
- Quantification of miR-10b-3p expression using qRT-PCR.
- Assessment of neurological deficits, infarct volume, brain water content, inflammatory markers, cell viability, and apoptosis.
- Bioinformatic analysis (TargetScan) and luciferase reporter assays to identify and validate KLF5 as a direct target of miR-10b-3p.
- Rescue experiments to confirm the functional role of the miR-10b-3p/KLF5 axis.
Main Results:
- miR-10b-3p expression was significantly downregulated in both in vivo and in vitro models of I/R injury.
- Overexpression of miR-10b-3p ameliorated neurological deficits, reduced infarct volume, decreased brain water content, and suppressed inflammatory factor expression in ischemic rats.
- miR-10b-3p upregulation inhibited OGD/R-induced neuronal apoptosis and improved cell viability in PC12 cells.
- KLF5 was confirmed as a direct target of miR-10b-3p, and its modulation was involved in the protective effects of miR-10b-3p against ischemic injury.
Conclusions:
- miR-10b-3p exerts significant neuroprotective effects against cerebral ischemia injury.
- The neuroprotective mechanism involves the downregulation of KLF5.
- miR-10b-3p represents a promising therapeutic target for the treatment of ischemic stroke.
