Paeoniflorin alleviates spinal cord injury in a cell model via regulating PTEN and PI3K/AKT signaling.

Abstract

<p>Spinal cord injury (SCI) is a prevalent form of spinal cord dysfunction, and the discovery of new effective treatments remains a critical research focus. This study investigated the role of paeoniflorin in a lipopolysaccharide (LPS)-induced PC-12 cell model of SCI and examined the involvement of phosphatase and tensin homolog (PTEN) and the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. Rat neuronal PC-12 cells were injured using LPS. Cell viability, proliferation, and apoptosis were assessed using the Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine (EdU), and Terminal deoxynucleotidyl transferase dUTP Nick End Labeling (TUNEL) assays, respectively. Western blotting and quantitative polymerase chain reaction were used to analyze PI3K, AKT, and PTEN expressions. PTEN was overexpressed to determine its functional role. LPS significantly reduced cell viability and proliferation, while increasing apoptosis. Paeoniflorin treatment ameliorated these injury markers in a dose-dependent manner, downregulated PTEN expression, and enhanced phosphorylated PI3K and AKT levels. PTEN overexpression counteracted the protective effects of paeoniflorin and its activation of PI3K/AKT signaling. Paeoniflorin alleviates LPS-induced cell injury in PC-12 cell model by inhibiting PTEN expression and subsequently activating the PI3K/AKT pathway.</p>