Study on Cellular Mechanism of Improving Inflammatory Effect of Gastrodin.

Abstract

Neuroinflammation is a major pathological mechanism of neurodegenerative disease-triggered cognitive disorders. Currently, no preventative measures or therapies are available. Gastrodin (GAS), an effective monomer derived from Gastrodia, is considered to be an anti-inflammatory candidate to attenuate microglia-induced neuroinflammation and neurodegenerative diseases. The present study first modelled the inflammatory activation of BV2 cells, which was induced by lipopolysaccharide (LPS) at the molecular level. The optimal concentration of GAS was screened out to preliminarily investigate its role in improving the inflammatory activation of BV2 cells during cellular death. Then, the research further discussed how GAS ameliorated inflammation via regulating ferroptosis. According to the results of our study, GAS up-regulates downstream heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1) expression while lowers reactive oxygen species (ROS) expression by Nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear transposition. Experimental results showed that 100 µM is the optimal concentration for gastrodin in the inflammatory activation model. GAS can promote Nrf2 nuclear translocation and the expression of HO-1 and NQO1 while reduce ROS level. Therefore, GAS can regulate ferroptosis in LPS-induced BV2 cellular inflammation model, thus attenuating inflammatory occurrence. In conclusions, GAS is considered to be an anti-inflammatory candidate that acts in LPS-induced BV2 cellular inflammation model by regulating ferroptosis.