Propofol Protects Against Angiotensin II-Induced Mouse Hippocampal HT22 Cells Apoptosis Via Inhibition of p66Shc Mitochondrial Translocation

In this study, we investigated the mechanism how propofol protected mouse hippocampal HT22 cells against angiotensin II-induced oxidative stress and apoptosis. Cell viability was evaluated with CCK8 kit. Protein expressions of active caspase 3, cytochrome c, p66Shc, p-p66shc–Ser36, protein kinase C βII (PKCβII), Pin-1 and phosphatase A2 (PP2A) were measured by Western blot. Superoxide anion (O 2 .− ) accumulation was measured with the reduction of ferricytochrome c. Compared with the control group, angiotensin II up-regulated expression of PKCβII, Pin-1 and PP2A, induced p66Shc–Ser36 phosphorylation, and facilitated p66Shc mitochondrial translocation, resulting in O 2 .− accumulation, mitochondrial cytochrome c release, caspase 3 activation, and the inhibition of cell viability. Importantly, we found propofol inhibited angiotensin II-induced PKCβII and PP2A expression and improved p66Shc mitochondrial translocation, O 2 .− accumulation, mitochondrial cytochrome c release, caspase 3 activation, inhibition of cell viability. On the other hand, propofol had no effects on angiotensin II-induced Pin-1 expression and p66Shc–Ser36 phosphorylation. Moreover, the protective effects of propofol on angiotensin II-induced HT22 apoptosis were similar with calyculin A, an inhibitor o...
Source: NeuroMolecular Medicine - Category: Neurology Source Type: research