학술논문
Neuroprotective Effect of Salvia sahendica is Mediated by Restoration of Mitochondrial Function and Inhibition of Endoplasmic Reticulum Stress.
Document Type
Article
Author
Source
Subject
*OXIDATIVE stress
*SALVIA
*MITOCHONDRIA
*ENDOPLASMIC reticulum
*PHYSIOLOGICAL stress
*LABORATORY rats
*PHEOCHROMOCYTOMA
*APOPTOSIS
*CYTOCHROME c
*THERAPEUTICS
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Language
ISSN
0364-3190
Abstract
Herein, we investigated the protective effect of Salvia sahendica against HO-induced cell death in rat pheochromocytoma (PC12) cells. Our data show that S. sahendica blocks apoptosis pathway by inhibition of cytochrome c release from mitochondria and leakage of calcium from endoplasmic reticulum. It also activates/inactivates two members of Bcl-2 family, Bax and Bcl-2. Bax inhibition and Bcl-2 activation suppress release of cytochrome c from mitochondria that prevents cleavage of caspase-3. Besides S. sahendica suppresses ER stress via attenuation of intracellular levels of calcium. Suppression of ER stress decreased calpain activation and subsequently cleavage of caspase-12. Altogether, these results indicate that S. sahendica protects PC12 cells treated with HO via suppression of upstream factors of apoptosis pathway. While oxidative stress is an early event in Alzheimer disease, it seems that S. sahendica prevents deleterious effects of reactive oxygen species by stabilizing mitochondrial membranes and inhibiting ER stress. [ABSTRACT FROM AUTHOR]