α-Tocopherol suppresses 24(S)-hydroxycholesterol-induced cell death via inhibition of endoplasmic reticulum membrane disruption.

The brain-specific cholesterol metabolite 24(S)-hydroxycholesterol (24S-OHC) has been shown to cause neuronal cell death when subjected to esterification by acyl-CoA:cholesterol acyltransferase 1 (ACAT1). Accumulating 24S-OHC esters in the endoplasmic reticulum (ER) provoked ER membrane disruption and an integrated stress response (ISR), a signaling pathway that regulates adaptation to various stresses. We have previously reported that α-tocopherol (α-Toc) but not α-tocotrienol (α-Toc3), among vitamin E homologs, suppressed 24S-OHC-induced cell death without affecting ACAT1 activity in human neuroblastoma SH-SY5Y cells.

Integrated stress response is involved in the 24(S)-hydroxycholesterol-induced unconventional cell death mechanism.

Perturbation of proteostasis triggers the adaptive responses that contribute to the homeostatic pro-survival response, whereas disruption of proteostasis can ultimately lead to cell death. Brain-specific oxysterol-i.e.

Field Survey of Glycyrrhiza Plants in Central Asia (5). Chemical Characterization of G. bucharica Collected in Tajikistan.

One triterpene and five triterpene glycosides, including four new compounds, have been identified in the underground parts of Glycyrrhiza bucharica, which was shown to be closely related to Glycyrrhizin-producing Glycyrrhiza species, G. uralensis, G. glabra and G.

Field Survey of Glycyrrhiza Plants in Central Asia (4). Characterization of G. glabra and G. bucharica Collected in Tajikistan.

The characteristics of 2 Glycyrrhiza plants, G. glabra and G. bucharica (=Meristotropis bucharica), were investigated in Tajikistan.