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RETRACTED ARTICLE

Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats with Parkinson's Disease.
Cell Physiol Biochem. 2018; 46(5):1793-1806.CP

Abstract

BACKGROUND/AIMS

Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease, and recent studies suggested that oxidative stress (OS) contributes to the cascade that leads to dopamine cell degeneration in PD. In this study, we hypothesized that salidroside (SDS) offers protection against OS injury in 6-hydroxydopamine (6-OHDA) unilaterally lesioned rats as well as the underlying mechanism.

METHODS

SDS and LiCl (activators of the Wnt/β-catenin signaling pathway) administration alone and in combination with 6-OHDA injection in rats was performed 3 days before modeling for 17 consecutive days to verify the regulatory mechanism by which SDS affects the Wnt/β-catenin signaling pathway as well as to evaluate the protective effect of SDS on PD in relation to OS in vivo. In addition, pheochromocytoma 12 (PC12) cells were incubated with 10 µmol/L SDS or LiCl alone or with both in combination for 1 h followed by a 24-h incubation with 100 µmol/L 6-OHDA to obtain in vitro data.

RESULTS

In vivo the administration of LiCl was found to ameliorate behavioral deficits and dopaminergic neuron loss; increase superoxide dismutase (SOA) activity, glutathione peroxidase (GSH-Px) levels, and glycogen synthase kinase 3β phosphorylation (GSK-3β-Ser9); reduce malondialdehyde (MDA) accumulation in the striatum and the GSK-3β mRNA level; as well as elevate β-catenin and cyclinD1 mRNA and protein levels in 6-OHDA-injected rats. This SDS treatment regimen was found to strengthen the beneficial effect of LiCl on 6-OHDA-injected rats. In vitro LiCl treatment decreased the toxicity of 6-OHDA on PC12 cells and prevented apoptosis. Additionally, LiCl treatment increased SOA activity, GSH-Px levels, and GSK-3β-Ser9 phosphorylation; decreased MDA accumulation in the striatum and GSK-3β mRNA levels; as well as increased β-catenin and cyclinD1 mRNA and protein levels in 6-OHDA-treated PC12 cells. Additionally, SDS treatment increased the protective effect of LiCl on 6-OHDA-treated PC12 cells.

CONCLUSION

Evidence from experimental models suggested that SDS may confer neuroprotection against the neurotoxicity of 6-OHDA in response to OS injury and showed that these beneficial effects may be related to regulation of the Wnt/β-catenin signaling pathway. Therefore, SDS might be a potential therapeutic agent for treating PD.

Authors+Show Affiliations

Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. School of Environment Science and Spatial Informatics, China University of Mining and Technology, Xuzhou, China. Jiangsu Key Laboratory for Eco-Agricultural Biotechnology around Hongze Lake, School of Life Sciences, Huaiyin Normal University, Huaian, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Science, Jiangsu Normal University, Xuzhou, China. College of Health Sciences, Jiangsu Normal University, Xuzhou, China.

Pub Type(s)

Journal Article
Retracted Publication

Language

eng

PubMed ID

29705802

Citation

Wu, Dong-Mei, et al. "Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats With Parkinson's Disease." Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology, vol. 46, no. 5, 2018, pp. 1793-1806.
Wu DM, Han XR, Wen X, et al. Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats with Parkinson's Disease. Cell Physiol Biochem. 2018;46(5):1793-1806.
Wu, D. M., Han, X. R., Wen, X., Wang, S., Fan, S. H., Zhuang, J., Wang, Y. J., Zhang, Z. F., Li, M. Q., Hu, B., Shan, Q., Sun, C. H., Lu, J., & Zheng, Y. L. (2018). Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats with Parkinson's Disease. Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology, 46(5), 1793-1806. https://doi.org/10.1159/000489365
Wu DM, et al. Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats With Parkinson's Disease. Cell Physiol Biochem. 2018;46(5):1793-1806. PubMed PMID: 29705802.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats with Parkinson's Disease. AU - Wu,Dong-Mei, AU - Han,Xin-Rui, AU - Wen,Xin, AU - Wang,Shan, AU - Fan,Shao-Hua, AU - Zhuang,Juan, AU - Wang,Yong-Jian, AU - Zhang,Zi-Feng, AU - Li,Meng-Qiu, AU - Hu,Bin, AU - Shan,Qun, AU - Sun,Chun-Hui, AU - Lu,Jun, AU - Zheng,Yuan-Lin, Y1 - 2018/04/25/ PY - 2017/08/03/received PY - 2018/03/05/accepted PY - 2018/5/1/pubmed PY - 2018/8/2/medline PY - 2018/4/30/entrez KW - 6-OHDA KW - Apoptosis KW - Oxidative stress KW - Parkinson’s disease KW - Salidroside KW - Wnt/β-catenin signaling pathway SP - 1793 EP - 1806 JF - Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology JO - Cell Physiol Biochem VL - 46 IS - 5 N2 - BACKGROUND/AIMS: Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease, and recent studies suggested that oxidative stress (OS) contributes to the cascade that leads to dopamine cell degeneration in PD. In this study, we hypothesized that salidroside (SDS) offers protection against OS injury in 6-hydroxydopamine (6-OHDA) unilaterally lesioned rats as well as the underlying mechanism. METHODS: SDS and LiCl (activators of the Wnt/β-catenin signaling pathway) administration alone and in combination with 6-OHDA injection in rats was performed 3 days before modeling for 17 consecutive days to verify the regulatory mechanism by which SDS affects the Wnt/β-catenin signaling pathway as well as to evaluate the protective effect of SDS on PD in relation to OS in vivo. In addition, pheochromocytoma 12 (PC12) cells were incubated with 10 µmol/L SDS or LiCl alone or with both in combination for 1 h followed by a 24-h incubation with 100 µmol/L 6-OHDA to obtain in vitro data. RESULTS: In vivo the administration of LiCl was found to ameliorate behavioral deficits and dopaminergic neuron loss; increase superoxide dismutase (SOA) activity, glutathione peroxidase (GSH-Px) levels, and glycogen synthase kinase 3β phosphorylation (GSK-3β-Ser9); reduce malondialdehyde (MDA) accumulation in the striatum and the GSK-3β mRNA level; as well as elevate β-catenin and cyclinD1 mRNA and protein levels in 6-OHDA-injected rats. This SDS treatment regimen was found to strengthen the beneficial effect of LiCl on 6-OHDA-injected rats. In vitro LiCl treatment decreased the toxicity of 6-OHDA on PC12 cells and prevented apoptosis. Additionally, LiCl treatment increased SOA activity, GSH-Px levels, and GSK-3β-Ser9 phosphorylation; decreased MDA accumulation in the striatum and GSK-3β mRNA levels; as well as increased β-catenin and cyclinD1 mRNA and protein levels in 6-OHDA-treated PC12 cells. Additionally, SDS treatment increased the protective effect of LiCl on 6-OHDA-treated PC12 cells. CONCLUSION: Evidence from experimental models suggested that SDS may confer neuroprotection against the neurotoxicity of 6-OHDA in response to OS injury and showed that these beneficial effects may be related to regulation of the Wnt/β-catenin signaling pathway. Therefore, SDS might be a potential therapeutic agent for treating PD. SN - 1421-9778 UR - https://www.unboundmedicine.com/medline/citation/29705802/Salidroside_Protection_Against_Oxidative_Stress_Injury_Through_the_Wnt/β_Catenin_Signaling_Pathway_in_Rats_with_Parkinson's_Disease_ L2 - https://www.karger.com?DOI=10.1159/000489365 DB - PRIME DP - Unbound Medicine ER -