Pyrroloquinoline Quinone Protects SMA560 Astrocytes Against Thrombin-Induced Cell Death by Improving Mitochondrial Function

Thrombin activation after cerebral hemorrhage induces the death of neurons and astrocytes. Pyrroloquinoline quinone (PQQ) shows nutritional functions and cell protection. This study aimed to clarify the protective effects of PQQ on thrombin-induced cell death in astrocytes. Murine SMA560 astrocytoma cells were used in this study. The cell viability was measured by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. The changes in reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were observed by CellROX (R) Deep Red and JC-1, respectively. The expression of apoptotic genes was measured by reverse transcription-quantitative polymerase chain reaction. Thrombin dose- and time-dependently induced SMA560 cell death. PQQ significantly repressed thrombin-induced SMA560 cell death in a dose-dependent manner. Thrombin led to the diminishment of MMP, increased production of ROS, and the upregulated expression of apoptotic genes including c-Jun, TP53, Bim, Puma, and Noxa in SMA560 cells. Meanwhile, PQQ treatment significantly attenuated the effects of thrombin on ROS, MMP, and gene expression in SMA560 cells. In conclusion, PQQ protects SMA560 astrocytes against thrombin-induced cell death by inhibiting oxidative stress and improving mitochondrial function in vitro.

Automated summary

This study showed that PQQ has protective effects against thrombin-induced cell death in astrocytes by inhibiting oxidative stress and improving mitochondrial function.