Figure 8

A proposed mechanism of luteolin against glutamate-induced neuronal death through autophagy-mediated neuronal cell death. Elevated glutamate levels within neurons cause an increase in mitochondrial ROS. These heightened ROS levels can damage mitochondria and trigger an excessive and specific process of removing damaged mitochondria, known as mitophagy, facilitated by BNIP3L/NIX. This sequence of events ultimately leads to the death of neurons. On the other hand, luteolin directly counteracts ROS, rescues mitochondrial health, and enhances the expression of mTORC1. Moreover, luteolin decreases autophagy-related gene expression (BNIP3 and UVRAG) and increases p62 gene expression. Furthermore, luteolin can reduce the initiation of mitophagy, resulting in a reduction of neuronal cell death. This figure was created with BioRender.com.