RETRACTED: Ligustrazine promoted hypoxia-treated cell growth by upregulation of miR-135b in human umbilical vein endothelial cells (Retracted article. See vol. 127, 2022)

Background: Pressure ulcers are a kind of troublesome disease which caused by long-term pressure and subsequently lead to tissue festering necrosis because of sustained ischemia, hypoxia and malnutrition. In our study, we used hypoxia to stimulate human umbilical vein endothelial cells (HUVECs) to mimic pressure ulcers and investigated the effects of Ligustrazine (Lig) with multi-activities on HUVECs. Methods: HUVECs were treated by hypoxia to induce cell injury. HUVECs were administrated with Lig and/or transfected with miR-135b inhibitor or negative control. Cell viability and cell apoptosis were detected by Cell Counting kit-8 assay and flow cytometry, respectively. The protein expression of Cyclin Dl and p53, the apoptosis-related proteins (Bcl-2, Bax, pro-/Cleaved-Caspas-3), and the JNK/SAPK and PI3K/AKT/mTOR pathways related proteins was examined by western blot. Results: Hypoxia-induced injury presented by decreasing cell viability and increasing cell apoptosis. Then Lig administration enhanced cell viability and inhibited cell apoptosis. Importantly, miR-135b was upregulated by the treatment of Lig. Further studies revealed that transfection with miR-135b inhibitor led to the opposite result with decreasing cell viability and increasing cell apoptosis. In addition, Lig increased the phosphorylation of JNK, SAPK, PI3K, AKT and mTOR. Conclusion: Lig promoted hypoxia-treated HUVECs cell growth as evidenced by increasing cell viability and reducing cell apoptosis. This process might be modulated by upregulation of miR-135b and subsequent activation of JNK/SAPK and PI3K/AKT/mTOR pathways.