Elevated microRNA-135b-5p relieves neuronal injury and inflammation in post-stroke cognitive impairment by targeting NR3C2

Abstract

Purpose

Post-stroke cognitive impairment (PSCI) is a series of syndromes that meets the diagnostic criteria of cognitive impairment within 6 months after the clinical event of stroke. With the unpleasing treatment at present, this study aimed to investigate the role of microRNA (miR)-135b-5p in regulating mineralocorticoid receptor (NR3C2) in PSCI.

Methods

The rats were modeled via middle cerebral artery occlusion, and injected with miR-135b-5p agomir or antagomir to figure its role in post-stroke neurological deficits, neuronal injury, neuronal cell apoptosis, and inflammation via Behavioral tests, Nissl’s staining, flow cytometry, and TUNEL staining. The expression of miR-135b-5p and NR3C2 in rats was detected by RT-qPCR and western blot analysis. The targeting relationship between miR-135b-5p and NR3C2 was verified by dual luciferase reporter gene assay.

Results

Highly expressed miR-135b-5p relieved post-stroke neurological deficits, focal cerebral ischemia-reperfusion (FCIR) neuron injury, and reduced neuronal apoptosis and inflammatory response after FCIR in PSCI rats. Poorly expressed miR-135b-5p and highly expressed NR3C2 were present in FCIR injury in PSCI rats. miR-135b-5p can direct target NR3C2 3’UTR.

Conclusion

The study highlights that up regulation of miR-135b-5p can reduce neuronal injury and inflammatory response in PSCI by targeting NR3C2, which might be helpful for PSCI treatment.

Keywords:

• Post-stroke cognitive impairment
• MicroRNA-135b-5p
• Mineralocorticoid receptor
• Neuronal injury
• inflammatory factors
• Apoptosis

Disclosure statement

No potential conflict of interest was reported by the author(s).