MicroRNA‑497 attenuates cerebral infarction in patients via the TLR4 and CREB signaling pathways

Area of Science:

• Biochemistry
• Molecular Biology
• Neuroscience

Background:

• Cerebral infarction is a major cause of disability and death.
• The role of microRNAs in cerebral infarction pathogenesis is not fully understood.

Purpose of the Study:

• To investigate the function and mechanism of microRNA-497 (miR-497) in cerebral infarction.
• To explore miR-497's regulatory role in the Toll-like receptor 4 (TLR4) and CREB signaling pathways.

Main Methods:

• Serum miR-497 expression was measured in patients with cerebral infarction and healthy controls.
• N2A cells were used to study the effects of miR-497 overexpression on cell proliferation, apoptosis, and inflammatory markers.
• Western blotting was used to assess protein expression levels of TLR4, MyD88, NF-κB, IRAK1, and p-CREB.
• Inhibitors of TLR4 and CREB were used to elucidate the signaling pathways involved.

Main Results:

• Serum miR-497 expression was significantly upregulated in patients with cerebral infarction compared to healthy controls.
• Overexpression of miR-497 in N2A cells promoted cell proliferation, reduced apoptosis, and decreased the activity of caspase-3 and caspase-9.
• miR-497 overexpression suppressed inflammatory factors and the protein expression of TLR4, MyD88, NF-κB, IRAK1, and p-CREB.
• TLR4 and CREB inhibition mimicked the protective effects of miR-497, reducing inflammation and apoptosis.

Conclusions:

• miR-497 plays a protective role in cerebral infarction.
• miR-497 attenuates cerebral infarction by regulating the TLR4 and CREB signaling pathways.
• miR-497 may serve as a potential therapeutic target for cerebral infarction.