miR-590-3p protects against ischaemia/reperfusion injury in an oxygen-glucose deprivation and reoxygenation cellular model by regulating HMGB1/TLR4/MyD88/NF-κB signalling

• Yaping Wang ^[1] ; Fanfu Jin ^[1] ; Lanxiu Huang ^[1] ; Wenqian Wu ^[2] ; Wenjie Hu ^[1] ; Tingting Huang ^[1] ; Lingsong Ma ^[1] ; Zhaohu Chu ^[1] ; Yang Xu ^[1] ; Shou-cai Zhao ^[1]
  1. [1] First Affiliated Hospital of Wannan Medical College

     First Affiliated Hospital of Wannan Medical College

     China

     
  2. [2] The Second Affiliated Hospital of Wannan Medical College, Wuhu, China
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 38, Nº. 8, 2023, págs. 941-951
• Idioma: inglés
• Enlaces
  • Texto completo
• Resumen

  • miR-590-3p has been reported to be reduced in myocardial ischaemia-reperfusion (I/R) injury, but its specific role in cerebral I/R injury is still uncertain.

    Thus, we explored the function and mechanism of miR590-3p in cerebral I/R injury using a cellular model.

    miR-590-3p, high mobility group Box 1 (HMGB1), and signalling-related factor levels were assessed using qPCR or a western blot analysis. Cell apoptosis was measured by flow cytometry. Inflammatory factors were detected by ELISA. The target of miR-590-3p was confirmed by dual-luciferase reporter assay and western blot analysis. We found that miR-590-3p was decreased and HMGB1 was increased in the OGD/R model.

    Upregulation of miR-590-3p reduced cell apoptosis and inflammation in the OGD/R model, and the TLR4/MyD88/NF-κB signalling pathway was suppressed. However, inhibition of miR-590-3p showed the opposite effects. Moreover, HMGB1 was verified as a target gene of miR-590-3p. HMGB1 reversed the decrease in apoptosis and inflammation caused by overexpression of miR590-3p, and the TLR4/MyD88/NF-κB signalling pathway was activated.

    Our results suggest that miR-590-3p regulates the TLR4/MyD88/NF-κB pathway by interacting with HMGB1 to protect against OGD/R-induced I/R injury.

    Thus, miR-590-3p may serve as a potential therapeutic target in cerebral I/R repair.