Up-regulation of miR-137 can inhibit PTN in target manner to regulate PTN/PTPRZ pathway to prevent cognitive dysfunction caused by propofol

Area of Science:

• Neuroscience
• Molecular Biology
• Pharmacology

Background:

• Propofol (PRO) is an anesthetic agent known to potentially induce cognitive dysfunction.
• MicroRNA-137 (miR-137) plays a role in neuronal function and has been implicated in various neurological processes.
• The precise mechanisms by which propofol affects cognitive function at the molecular level require further elucidation.

Purpose of the Study:

• To investigate the impact of miR-137 on propofol-induced cognitive dysfunction in a rat model.
• To explore the regulatory relationship between miR-137 and PTN (Pleiotrophin) in the context of propofol exposure.
• To assess the effects of modulating miR-137 and PTN on cellular functions, including apoptosis and proliferation.

Main Methods:

• Establishment of rat models and SK-N-SH cell cultures exposed to propofol.
• Manipulation of miR-137 and PTN expression levels (upregulation and downregulation).
• Assessment of cognitive function (escape latency, exploration time), cell apoptosis, proliferation, and PTN/PTPRZ pathway phosphorylation.

Main Results:

• Propofol significantly prolonged escape latency and reduced exploration in rats, indicating cognitive impairment.
• miR-137 expression decreased, while PTN expression increased in cells treated with propofol.
• Upregulation of miR-137 or downregulation of PTN reversed propofol-induced cognitive deficits and cellular dysfunction, including apoptosis and proliferation.

Conclusions:

• miR-137 upregulation can inhibit PTN expression in a targeted manner, thereby modulating the PTN/PTPRZ pathway.
• This mechanism effectively reduces propofol-induced cell apoptosis.
• Upregulation of miR-137 offers a protective effect against propofol-induced cognitive dysfunction.