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Arctigenin Attenuates Learning and Memory Deficits through PI3k/Akt/GSK-3β Pathway Reducing Tau Hyperphosphorylation in Aβ-Induced AD Mice.
Planta Med. 2017 Jan; 83(1-02):51-56.PM

Abstract

Arctigenin is a phenylpropanoid dibenzylbutyrolactone lignan compound possessing antitumor, anti-inflammatory, anti-influenza, antioxidant, antibacterial, and hypoglycaemic activities. Our previous study demonstrated that arctigenin exerts neuroprotective effects both in vitro and in vivo in a Parkinson's disease model. However, the exact mechanism through which arctigenin improves amyloid beta-induced memory impairment by inhibiting the production of the hyperphosphorylated tau protein is unknown. Amyloid β1-42 was slowly administered via the intracerebroventricular route in a volume of 3 µL (≈ 410 pmmol/mouse) to mice. The mice were administered arctigenin (10, 40, or 150 mg/kg) or vehicle starting from the second day after amyloid β1-42 injection to the end of the experiment. Behavioural tests were performed from days 9 to 15. On day 16 after the intracerebroventricular administration of amyloid β1-42, the mice were sacrificed for biochemical analysis. Arctigenin (10-150 mg/kg) significantly attenuated the impairment of spontaneous alternation behaviours in the Y-maze task, decreased the escape latency in the Morris water maze test, and increased the swimming times and swimming distances to the platform located in the probe test. Arctigenin attenuated the level of phosphorylated tau at the Thr-181, Thr-231, and Ser-404 sites in the hippocampus, and increased the phosphorylation levels of phosphatidylinositol-3-kinase, threonine/serine protein kinase B, and glycogen synthase kinase-3β. Arctigenin effectively provides protection against learning and memory deficits and in inhibits hyperphosphorylated tau protein expression in the hippocampus. The possible mechanism may occur via the phosphatidylinositol-3-kinase/protein kinase B-dependent glycogen synthase kinase-3β signalling pathway.

Authors+Show Affiliations

Department of Pharmacology, The Second Hospital Affiliated to Liaoning Chinese Medical University, Shenyang, P. R. China.College of Pharmacy, Liaoning University of Traditional Chinese Medicine, Shenyang, P. R. China.Department of Pharmacology, The Second Hospital Affiliated to Liaoning Chinese Medical University, Shenyang, P. R. China.College of Pharmacy, Liaoning University of Traditional Chinese Medicine, Shenyang, P. R. China.Department of Pharmacology, The Second Hospital Affiliated to Liaoning Chinese Medical University, Shenyang, P. R. China.College of Pharmacy, Liaoning University of Traditional Chinese Medicine, Shenyang, P. R. China.College of Pharmacy, Liaoning University of Traditional Chinese Medicine, Shenyang, P. R. China.Department of Pharmacology, The Second Hospital Affiliated to Liaoning Chinese Medical University, Shenyang, P. R. China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27224270

Citation

Qi, Yue, et al. "Arctigenin Attenuates Learning and Memory Deficits Through PI3k/Akt/GSK-3β Pathway Reducing Tau Hyperphosphorylation in Aβ-Induced AD Mice." Planta Medica, vol. 83, no. 1-02, 2017, pp. 51-56.
Qi Y, Dou DQ, Jiang H, et al. Arctigenin Attenuates Learning and Memory Deficits through PI3k/Akt/GSK-3β Pathway Reducing Tau Hyperphosphorylation in Aβ-Induced AD Mice. Planta Med. 2017;83(1-02):51-56.
Qi, Y., Dou, D. Q., Jiang, H., Zhang, B. B., Qin, W. Y., Kang, K., Zhang, N., & Jia, D. (2017). Arctigenin Attenuates Learning and Memory Deficits through PI3k/Akt/GSK-3β Pathway Reducing Tau Hyperphosphorylation in Aβ-Induced AD Mice. Planta Medica, 83(1-02), 51-56. https://doi.org/10.1055/s-0042-107471
Qi Y, et al. Arctigenin Attenuates Learning and Memory Deficits Through PI3k/Akt/GSK-3β Pathway Reducing Tau Hyperphosphorylation in Aβ-Induced AD Mice. Planta Med. 2017;83(1-02):51-56. PubMed PMID: 27224270.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Arctigenin Attenuates Learning and Memory Deficits through PI3k/Akt/GSK-3β Pathway Reducing Tau Hyperphosphorylation in Aβ-Induced AD Mice. AU - Qi,Yue, AU - Dou,De-Qiang, AU - Jiang,Hong, AU - Zhang,Bing-Bing, AU - Qin,Wen-Yan, AU - Kang,Kai, AU - Zhang,Na, AU - Jia,Dong, Y1 - 2016/05/25/ PY - 2016/5/26/pubmed PY - 2017/5/23/medline PY - 2016/5/26/entrez SP - 51 EP - 56 JF - Planta medica JO - Planta Med. VL - 83 IS - 1-02 N2 - Arctigenin is a phenylpropanoid dibenzylbutyrolactone lignan compound possessing antitumor, anti-inflammatory, anti-influenza, antioxidant, antibacterial, and hypoglycaemic activities. Our previous study demonstrated that arctigenin exerts neuroprotective effects both in vitro and in vivo in a Parkinson's disease model. However, the exact mechanism through which arctigenin improves amyloid beta-induced memory impairment by inhibiting the production of the hyperphosphorylated tau protein is unknown. Amyloid β1-42 was slowly administered via the intracerebroventricular route in a volume of 3 µL (≈ 410 pmmol/mouse) to mice. The mice were administered arctigenin (10, 40, or 150 mg/kg) or vehicle starting from the second day after amyloid β1-42 injection to the end of the experiment. Behavioural tests were performed from days 9 to 15. On day 16 after the intracerebroventricular administration of amyloid β1-42, the mice were sacrificed for biochemical analysis. Arctigenin (10-150 mg/kg) significantly attenuated the impairment of spontaneous alternation behaviours in the Y-maze task, decreased the escape latency in the Morris water maze test, and increased the swimming times and swimming distances to the platform located in the probe test. Arctigenin attenuated the level of phosphorylated tau at the Thr-181, Thr-231, and Ser-404 sites in the hippocampus, and increased the phosphorylation levels of phosphatidylinositol-3-kinase, threonine/serine protein kinase B, and glycogen synthase kinase-3β. Arctigenin effectively provides protection against learning and memory deficits and in inhibits hyperphosphorylated tau protein expression in the hippocampus. The possible mechanism may occur via the phosphatidylinositol-3-kinase/protein kinase B-dependent glycogen synthase kinase-3β signalling pathway. SN - 1439-0221 UR - https://www.unboundmedicine.com/medline/citation/27224270/Arctigenin_Attenuates_Learning_and_Memory_Deficits_through_PI3k/Akt/GSK_3β_Pathway_Reducing_Tau_Hyperphosphorylation_in_Aβ_Induced_AD_Mice_ L2 - http://www.thieme-connect.com/DOI/DOI?10.1055/s-0042-107471 DB - PRIME DP - Unbound Medicine ER -