Danggui-Shaoyao-San Can Ameliorate Alzheimer's Disease by Inhibiting Hippocampal Neuron Apoptosis: Findings from Serum Pharmacology

当归芍药散可通过抑制海马神经元凋亡改善阿尔茨海默病:血清药理学研究结果

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作者:Kai-Xin Zhang, Ji-Wei Zhang, Yan-Hong Jiang, Yi-Ran Wang, Zhen-Ling Liu, Peng-Li Ding, Xiang-Ying Wang, Wen-Qiang Cui, Xiang-Qing Xu #, Ya-Han Wang #

Background

Danggui-Shaoyao-San (DSS) is a traditional Chinese medicine prescription with a history of nearly 2000 years, originally widely used for gynecological diseases, and in recent years research has found that DSS also has a good therapeutic effect on Alzheimer's disease (AD).

Conclusion

DSS can modulate the calcium signaling pathway and enhance the cAMP/PKA/CREB signaling pathway to ameliorate Tau aberrant phosphorylation, cognitive deficits and neuronal apoptosis after AD.

Methods

Liquid chromatography‒mass spectrometry (LC-MS) combined with gas chromatography‒mass spectrometry (GC-MS) based non-targeted metabolomics were used to conduct in-depth research. Serum Pharmacology was used to analyze potential mechanisms of DSS for AD. C57BL/6J mice and Hippocampal neuronal cell line (HT-22) were used to prepare the AD model. Enzyme linked immunosorbent assay (Elisa), quantitative polymerase chain reaction (q-PCR), Morris water maze,Western blot (WB), Immunohistochemical and Immunofluorescence were used to study the effect of DSS on AD. Flow cytometry and Cell Counting Kit-8 (CCK-8) reveal the effect of DSS serum on HT-22 proliferation and apoptosis.

Purpose

The objective is to investigate the metabolic components of the DSS in the blood and the potential mechanisms for AD. Materials and

Results

A total of 57 metabolic components were screened in DSS serum. Serum Pharmacology revealed that the calcium signaling pathway and cAMP/PKA/CREB pathway may be a potential mechanism through which DSS treated AD. DSS can reduce aberrant phosphorylation of Tau and modulates cAMP/PKA/CREB pathway to improve cognition and apoptosis in AD mice. DSS serum can increase the cell viability of HT-22 and reduce apoptosis mainly by alleviating mitochondrial calcium overloading.

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