β-Sitosterol Alleviates Inflammatory Response via Inhibiting the Activation of ERK/p38 and NF-κB Pathways in LPS-Exposed BV2 Cells.

Abstract

Neurodegenerative disease is a disease state in which neurons in the spinal cord and brain are lost. Studies show that sustained neuroinflammatory reactions release toxic factors, damage neurons, and lead to neurodegenerative diseases. Therefore, inhibiting neuroinflammation may be an effective measure to alleviate neurodegenerative diseases. Microglia is an important participant in the neuroinflammatory response. β-Sitosterol (BS) is widely found in various vegetable oils, nuts, and other plant seeds. Studies have found that BS has a wide range of anti-inflammatory effects in peritoneal macrophages and other peripheral tissues. However, no studies have reported the effect of BS that impacts microglia activity. Herein, we further study the effect of BS on impacts microglia activity. Firstly, BV2, a murine microglial cell, was treated with different concentrations of BS prior to stimulation of LPS, and then the inflammatory mediators and the expression of related signaling molecules were tested. The inflammatory response results illustrated that BS treatment can reduce the LPS-induced expression of inflammatory mediators (interleukin-6 (IL-6), inducible nitric oxide (iNOS), tumor necrosis factor-α (TNF-α), and cyclooxygenase-2(COX-2)). The related signaling pathway analysis demonstrated that BS treatment can inhibit the LPS-induced activation of p38, ERK, and NF-κB pathways. To sum up, the results demonstrated that BS impacts microglia activity via repressing the activation of p38, ERK, and NF-κB pathways.