Astaxanthin relieves HT22 cells from LPS-induced inflammation and apoptosis by inhibiting oxygen species and regulating the TLR4/MyD88/NFκB signaling pathway

Abstract

Astaxanthin exhibits promising anti-inflammatory effects in the treatment of neurodegenerative diseases. Our aim was to explore the mechanisms by which astaxanthin mitigates inflammation associated with these conditions. We treated HT22 cells with lipopolysaccharide (LPS), astaxanthin (ATX), and the TLR4 inhibitor TAK-242, employing CCK-8 assays, flow cytometry, and Western blotting to assess cell survival, oxidative stress, inflammation, and apoptosis. We found that LPS decreased the survival rate of HT22 cells, induced reactive oxygen species (ROS) accumulation and apoptosis, and increased the expression of inflammation-related proteins. Conversely, ATX diminished LPS-induced ROS accumulation and apoptosis, as well as the expression of inflammation-related proteins. The application of TLR4 inhibitors further enhanced the anti-inflammatory effects of ATX on LPS. In summary, we demonstrated that ATX can alleviate LPS-induced ROS accumulation, inflammation, and apoptosis, with its anti-inflammatory effects closely linked to the TLR4/MyD88/NFκB signaling pathway.

Keywords

• Neurodegenerative disorders
• Astaxanthin
• Inflammation
• Apoptosis
• Oxidative stress