Figure 6.

Schematic illustration of the proposed molecular mechanism by which baicalein facilitates functional recovery after spinal cord ischemia-reperfusion injury (SCIRI) by activating autophagy and subsequently reducing ER stress-induced apoptosis and attenuating pyroptosis. Spinal cord ischemia-reperfusion (I/R) injury leads to the accumulation of unfolded proteins in the endoplasmic reticulum (ER) and mitochondrial damage. Autophagy is then activated by baicalein to contribute to the elimination of damaged mitochondria and unfolded proteins by forming autolysosomes with lysosomes. Subsequently, ER stress-induced apoptosis and pyroptosis are inhibited, which further results in the promotion of functional recovery.