Research Paper Volume 13, Issue 16 pp 20149—20163

25-Hydroxycholesterol protecting from cerebral ischemia-reperfusion injury through the inhibition of STING activity

Model describing the mechanism by which 25-Hydroxycholesterol protects against cerebral ischemiareperfusion injury. Left Figure: After cerebral ischemia and reperfusion, the expression of STING protein is activated and mTOR phosphorylation is inhibited, thereby increasing the expression of autophagy and achieving cerebral ischemia effect. Right image: After administration of 25-hydroxycholesterol, the expression of STING protein was inhibited, and mTOR phosphorylation was activated, thus inhibiting the expression of autophagy and achieving the effect of cerebral ischemia tolerance.

Figure 6. Model describing the mechanism by which 25-Hydroxycholesterol protects against cerebral ischemiareperfusion injury. Left Figure: After cerebral ischemia and reperfusion, the expression of STING protein is activated and mTOR phosphorylation is inhibited, thereby increasing the expression of autophagy and achieving cerebral ischemia effect. Right image: After administration of 25-hydroxycholesterol, the expression of STING protein was inhibited, and mTOR phosphorylation was activated, thus inhibiting the expression of autophagy and achieving the effect of cerebral ischemia tolerance.