2. Academic Validation
  3. Salidroside Prevents Hypoxia-Induced Human Retinal Microvascular Endothelial Cell Damage Via miR-138/ROBO4 Axis

Salidroside Prevents Hypoxia-Induced Human Retinal Microvascular Endothelial Cell Damage Via miR-138/ROBO4 Axis

  • Invest Ophthalmol Vis Sci. 2021 Jul 1;62(9):25. doi: 10.1167/iovs.62.9.25.
Xiaoling Shi 1 2,  Nuo Dong 2,  Qi Qiu 1,  Shanhua Li 1,  Jiaxing Zhang 1
Affiliations

Affiliations

  • 1 Institute of Brain Diseases and Cognition, Medical College of Xiamen University, Xiamen, Fujian, China.
  • 2 Affiliated Xiamen Eye Center, Medical College of Xiamen University, Xiamen, Fujian, China.
PMID: 34269814 DOI: 10.1167/iovs.62.9.25
Abstract

Purpose: Retinopathies are associated with the injury of retinal microvascular endothelial cells. Salidroside (SAL) is a medicinal supplement that has antioxidative and cytoprotective properties. We hypothesized that SAL might have a protective function in retinopathies. This research aims to explore the function and mechanism of SAL in hypoxia-induced retinal microvascular endothelial cell injury.

Methods: Human retinal microvascular endothelial cells (HRMECs) injury was induced by culturing under hypoxic condition. The function of SAL on HRMECs injury was investigated using cell counting kit-8, 5-ethynyl-2'-deoxyuridine (EdU) staining, flow cytometry, Western blotting, and Enzyme linked immunosorbent assay. MicroRNA (miR)-138, roundabout 4 (ROBO4), and proteins in the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathways were examined using quantitative reverse transcription polymerase chain reaction or Western blotting. The target correlation was determined by dual-luciferase reporter analysis and RNA immunoprecipitation.

Results: Hypoxia resulted in proliferation inhibition, cycle arrest, Apoptosis, inflammatory reaction, and oxidative stress in HRMECs. SAL attenuated hypoxia-induced HRMECs injury via increasing cell proliferation, and mitigating cycle arrest, Apoptosis, inflammatory reaction, and oxidative stress. MiR-138 expression was enhanced by hypoxia, and decreased via SAL stimulation. MiR-138 upregulation reversed the influence of SAL on hypoxia-induced HRMECs injury. ROBO4 was targeted via miR-138. ROBO4 overexpression weakened the role of miR-138 in HRMECs injury. The PI3K/Akt/mTOR pathway was inactivated under hypoxic condition, and SAL increased the activation of PI3K/Akt/mTOR pathways by decreasing miR-138.

Conclusions: SAL protected against hypoxia-induced HRMECs injury through regulating miR-138/ROBO4 axis, indicating the protective potential of SAL in retinopathies.

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