Research Paper Volume 13, Issue 16 pp 20149—20163

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

25-Hydroxycholesterol (25-HC) suppressed the middle cerebral artery occlusion (MCAO)-induced enhanced autophagy, and the effects of 25-HC on autophagy, oxidative injury, apoptosis, and inflammation were reversed by oxygen-10-acridine acetic acid (CMA). (A) Expression of p-mTOR, STING, P62, Beclin1, LC3 I, and LC3 II were tested by Western blot (N = 5 per group, **PPPB) Expression of p-mTOR, STING, P62, Beclin1, LC3 I, and LC3 II were tested by Western blot (N = 5-6 per group, **PPPC) Levels of interleukin (IL)-6, tumor necrosis factor-α, and IL-1β were measured by commercially available ELISA kits (N = 6 per group, **PPPP

Figure 3. 25-Hydroxycholesterol (25-HC) suppressed the middle cerebral artery occlusion (MCAO)-induced enhanced autophagy, and the effects of 25-HC on autophagy, oxidative injury, apoptosis, and inflammation were reversed by oxygen-10-acridine acetic acid (CMA). (A) Expression of p-mTOR, STING, P62, Beclin1, LC3 I, and LC3 II were tested by Western blot (N = 5 per group, **P<0.001 versus sham group, ##P<0.001, #P<0.05 versus MCAO group). (B) Expression of p-mTOR, STING, P62, Beclin1, LC3 I, and LC3 II were tested by Western blot (N = 5-6 per group, **P<0.01, ***P<0.001, *P<0.05 versus sham group, versus MCAO group). (C) Levels of interleukin (IL)-6, tumor necrosis factor-α, and IL-1β were measured by commercially available ELISA kits (N = 6 per group, **P<0.01 versus sham group, ##P<0.01, #P<0.05 versus MCAO group, P<0.05 versus MCAO+CMA group).