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eISSN: 1643-3750

Comparative Study on the Protective Effects of Salidroside and Hypoxic Preconditioning for Attenuating Anoxia-Induced Apoptosis in Pheochromocytoma (PC12) Cells

Yao Hu, Xiumei Lv, Jing Zhang, Xianli Meng

Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China (mainland)

Med Sci Monit 2016; 22:4082-4091

DOI: 10.12659/MSM.897640

Available online: 2016-10-30

Published: 2016-10-30


#897640

BACKGROUND: Hypoxia is an important sign that can result from body injuries or a special condition such as being at a high altitude or deep water diving. In the current studies, hypoxic preconditioning (HPC) plays a key role in reducing hypoxia-induced apoptosis. We aimed to study the pharmacologic preconditioning effects of salidroside versus those of HPC in hypoxia-/anoxia-induced apoptosis in PC12 cells (pheochromocytoma).
MATERIAL AND METHODS: PC12 cells were treated by different experimental conditions: control condition, hypoxia condition, HPC condition, low-/middle-/high-dose condition of salidroside, cyclosporine A (CsA), and oratractyloside (ATR). The cell viability, lactate dehydrogenase (LDH) activity, apoptosis, mitochondrial membrane potential (MMP), intracellular Ca2+, caspase-3 activity, and expression of Bcl-2 were detected in PC12 cells after the hypoxia treatment. Salidroside, extracted from the traditional Chinese herb Rhodiola rosea L, plays an essential role in reducing hypoxia-induced apoptosis in PC12 cells by the mitochondrial pathway.
RESULTS: Salidroside decreased the apoptosis and increased the viability of hypoxia-induced PC12 cells more effectively than HPC Moreover, salidroside markedly stabilized MMP and intracellular Ca2+, reduced or inhibited LDH and caspase-3 activity, and up-regulated Bcl-2; CsA and ATR showed corresponding function.
CONCLUSIONS: Salidroside administration restrains apoptosis induced by hypoxia in PC12 cells. The protective effects are mediated by preservation of mitochondrial integrity and MMP to inhibit the excessive Ca2+ influx and caspase-3 activity and to promote the Bcl-2 expression, providing a potential clinical and effective therapeutic mechanism to reduce deaths from ischemic or hypoxic injury.

Keywords: Apoptosis - physiology, Animals, Cell Hypoxia - drug effects, Cell Survival - drug effects, Glucosides - pharmacology, Hypoxia - prevention & control, Ischemic Preconditioning, Membrane Potential, Mitochondrial - drug effects, Mitochondria - metabolism, Neuroprotective Agents - pharmacology, Oxidative Stress - drug effects, PC12 Cells, Phenols - pharmacology, Rats, Reactive Oxygen Species - metabolism



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