Research Paper Volume 13, Issue 12 pp 16816—16833

Celastrol protects against early brain injury after subarachnoid hemorrhage in rats through alleviating blood-brain barrier disruption and blocking necroptosis

Celastrol down-regulated RIP3/MLKL signaling pathway after SAH induction. (A) Representative WB showing protein levels of RIP3, MLKL and cleaved caspase-8 in the ipsilateral cortex in each group at 72 h after SAH induction. (B–D) Protein quantification of RIP3, MLKL and cleaved caspase-8. The densities of the protein bands were analyzed and normalized to β-actin, and compared to the mean value of the sham group. Data were presented as mean±SEM. n = 6. *P P

Figure 8. Celastrol down-regulated RIP3/MLKL signaling pathway after SAH induction. (A) Representative WB showing protein levels of RIP3, MLKL and cleaved caspase-8 in the ipsilateral cortex in each group at 72 h after SAH induction. (BD) Protein quantification of RIP3, MLKL and cleaved caspase-8. The densities of the protein bands were analyzed and normalized to β-actin, and compared to the mean value of the sham group. Data were presented as mean±SEM. n = 6. *P < 0.05, **P < 0.01.