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Endoplasmic Reticulum Stress and NF-[Formula: see text]B Pathway in Salidroside Mediated Neuroprotection: Potential of Salidroside in Neurodegenerative Diseases.

Authors
  • Wang, Chenggui1, 2
  • Lou, Yiting1, 2
  • Xu, Jianxiang1, 2
  • Feng, Zhenhua1, 2
  • Chen, Yu1, 2
  • Tang, Qian1, 2
  • Wang, Qingqing1, 2
  • Jin, Haiming1, 2
  • Wu, Yaosen1, 2
  • Tian, Naifeng1, 2
  • Zhou, Yifei1, 2
  • Xu, Huazi1, 2
  • Zhang, Xiaolei1, 2, 3
  • 1 * Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, P. R. China. , (China)
  • 2 † Key Laboratory of Orthopaedics of Zhejiang Province, Wenzhou 325000, P. R. China. , (China)
  • 3 ‡ Chinese Orthopaedic Regenerative Medicine Society, Hangzhou, P. R. China. , (China)
Type
Published Article
Journal
The American journal of Chinese medicine
Publication Date
Jan 01, 2017
Volume
45
Issue
7
Pages
1459–1475
Identifiers
DOI: 10.1142/S0192415X17500793
PMID: 28946765
Source
Medline
Keywords
License
Unknown

Abstract

Microglial activation leads to increased production of proinflammatory enzymes and cytokines, which is considered to play crucial role in neurodegenerative diseases, however there are only a few drugs that target microglia activation. Recent studies have indicated that the Traditional Chinese Medicine, salidroside (Sal), exerted anti-inflammatory effects. According to this evidence, our present study aims to explore the effect of the Sal (a phenylpropanoid glycoside compound which is isolated from rhodiola), on microglia activation in lipopolysaccharide (LPS)-stimulated BV-2 cells. Our results showed that Sal could significantly inhibit the excessive production of Nitric Oxide (NO) and Prostaglandin E2 (PGE2) in LPS-stimulated BV2 cells. Moreover, Sal treatment could suppress the mRNA and protein expressions of inflammatory enzymes, including Inducible Nitric Oxide Synthase (iNOS) and Cyclooxygenase-2 (COX-2). The mechanisms may be related to the inhibition of the activation of Nuclear Factor-kappaB (NF-[Formula: see text]B) and endoplasmic reticulum stress. Our study demonstrated that salidroside could inhibit lipopolysaccharide-induced microglia activation via the inhibition of the NF-[Formula: see text]B pathway and endoplasmic reticulum stress, which makes it a promising therapeutic agent for human neurodegenerative diseases.

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