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Exploring the Pharmacological Action and Molecular Mechanism of Salidroside in Inhibiting MCF-7 Cell Proliferation and Migration
Published on: June 9, 2023
Salidroside attenuates hydrogen peroxide-induced cell damage through a cAMP-dependent pathway.
Shuang Guan1, Wei Wang, Jing Lu
1Institute of Zoonoses, College of Animal Science and Veterinary Medicine, Jilin University, Changchun, Jilin 130062, China. gshuang1973@126.com
Molecules (Basel, Switzerland)
|April 23, 2011
Summary
Salidroside from Rhodiola rosea protects cells from oxidative damage by reducing calcium and reactive oxygen species via a cAMP pathway.
Area of Science:
- Pharmacology
- Cell Biology
- Biochemistry
Background:
- Salidroside, a key compound in Rhodiola rosea L., exhibits antioxidant properties.
- The precise molecular mechanisms underlying salidroside's antioxidant effects remain unclear.
Purpose of the Study:
- To investigate the signal transduction pathway involved in the antioxidant effects of salidroside.
- To elucidate how salidroside modulates cellular responses to oxidative stress.
Main Methods:
- Utilized HL-7702 cells exposed to hydrogen peroxide (H(2)O(2)) to induce oxidative stress.
- Measured cytosolic free calcium ([Ca2+]i) levels, reactive oxygen species (ROS) generation, and cyclic nucleotide (cAMP and cGMP) concentrations.
- Assessed the dose-dependent effects of salidroside.
Main Results:
- Salidroside mitigated H(2)O(2)-induced cell damage and inhibited the elevation of [Ca2+]i.
- Salidroside effectively scavenged ROS and increased intracellular cyclic adenosine monophosphate (cAMP) levels.
- No significant effect of salidroside on cyclic guanosine monophosphate (cGMP) levels was observed.
Conclusions:
- The antioxidant effects of salidroside are linked to the down-regulation of intracellular calcium and ROS.
- These protective mechanisms appear to be mediated through a cAMP-dependent signaling pathway.
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