Autophagy activation is associated with neuroprotection against apoptosis via a mitochondrial pathway in a rat model of subarachnoid hemorrhage

RETRACTED ARTICLE: Preconditioning with pitavastatin, an HMG-CoA reductase inhibitor, attenuates C-Jun N-terminal kinase activation in experimental subarachnoid hemorrhage-induced apoptosis

“…Despite more than 50 years of subarachnoid hemorrhage (SAH) studies focusing on the correction and prevention of delayed vasospasm, attempts to reverse this condition have proven problematic in patients following a ruptured aneurysm [2,3,6,11,15,18,19,31,33,46]. Delayed ischemic neurological deficit and acute cerebral ischemia occurring prior to 72 h after SAH are defined as early brain injury (EBI) [25,31,32,35,49,50].…”

Rapamycin protects dopaminergic neurons against rotenone-induced cell death in primary mesencephalic cell culture

“…Counting of apoptotic nuclei using blue-fluorescent DAPI nucleic acid stain indicated that rapamycin decreased rotenone-induced apoptotic cell death in primary mesencephalic cell cultures. Yin et al [41] and Jing et al [17] similarly reported an antiapoptotic effect for rapamycin against transient focal cerebral ischemia/reperfusion and subarachnoid hemorrhage in mice and rats, respectively. The antiapoptotic effect of rapamycin was reported to be mediated by decreasing Bax production and the downstream release of cytochrome c from mitochondria to the cytosol [17].…”

“…Yin et al [41] and Jing et al [17] similarly reported an antiapoptotic effect for rapamycin against transient focal cerebral ischemia/reperfusion and subarachnoid hemorrhage in mice and rats, respectively. The antiapoptotic effect of rapamycin was reported to be mediated by decreasing Bax production and the downstream release of cytochrome c from mitochondria to the cytosol [17]. In addition to aforementioned mechanisms of neuroprotection, rapamycin was found to protect neuronal cells through some other pathways.…”

Autophagy in Critical Illness

“…Upregulation of autophagy in this early phase was first described by Lee et al in rats subjected to the endovascular perforation technique: examination of the ipsilateral fronto-basal cortex by electron microscopy revealed increased autophagosomes and autolysosomes, with Western blot and immunohistochemical evidence of increased LC shift as seen by LC3-II/LC3-I ratio, and elevation of cathepsin D and Beclin 1 levels within the first 72 hours following SAH (Lee et al, 2009). Using the same model, Jing et al showed the presence of autophagic vacuole formation, increased LC3-II to LC3-I ratio, and increased Beclin 1 and Atg5 expression 24 h after SAH (Jing et al, 2012). Wang et al (2012) simulated SAH by injecting autologous blood into the prechiasmatic cistern of rats.…”