3'-Daidzein sulfonate sodium protects against memory impairment and hippocampal damage caused by chronic cerebral hypoperfusion.
3'-Daidzein sulfonate sodium protects against memory impairment and hippocampal damage caused by chronic cerebral hypoperfusion.
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3α-大豆苷元磺酸钠可预防慢性脑灌注不足引起的记忆障碍和海马损伤
DOI:
10.4103/1673-5374.237119
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发表时间:
2018-09
影响因子:
6.1
通讯作者:
Xiao H
中科院分区:
文献类型:
--
作者:
Li X;Liu RZ;Zeng Q;Huang ZH;Zhang JD;Liu ZL;Zeng J;Xiao H
3′-Daidzein sulfonate sodium (DSS) is a new synthetic water-soluble compound derived from daidzein, a soya isoflavone that plays regulatory roles in neurobiology. In this study, we hypothesized that the regulatory role of DSS in neurobiology exhibits therapeutic effects on hippocampal damage and memory impairment. To validate this hypothesis, we established rat models of chronic cerebral hypoperfusion (CCH) by the permanent occlusion of the common carotid arteries using the two-vessel occlusion method. Three weeks after modeling, rat models were intragastrically administered 0.1, 0.2, and 0.4 mg/kg DSS, once a day, for 5 successive weeks. The Morris water maze test was performed to investigate CCH-induced learning and memory deficits. TUNEL assay was used to analyze apoptosis in the hippocampal CA1, CA3 regions and dentate gyrus. Hematoxylin-eosin staining was performed to observe the morphology of neurons in the hippocampal CA1, CA3 regions and dentate gyrus. Western blot analysis was performed to investigate the phosphorylation of PKA, ERK1/2 and CREB in the hippocampal PKA/ERK1/2/CREB signaling pathway. Results showed that DSS treatment greatly improved the learning and memory deficits of rats with CCH, reduced apoptosis of neurons in the hippocampal CA1, CA3 regions and dentate gyrus, and increased the phosphorylation of PKA, ERK1/2, and CREB in the hippocampus. These findings suggest that DSS protects against CCH-induced memory impairment and hippocampal damage possibly through activating the PKA/ERK1/2/CREB signaling pathway.
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影响因子:
6.1
作者:
Yuan W;Chen Q;Zeng J;Xiao H;Huang ZH;Li X;Lei Q
通讯作者:
Lei Q
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Howe, Peter R. C.
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Zhang J
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