Mechanism of Xiao Chaihutang in Treatment of Alzheimer's Disease： Based on Network Pharmacology and in vitro Experimental Verification / 中国实验方剂学杂志

ObjectiveTo investigate the potential mechanism of Xiao Chaihutang （XCHT） in the treatment of Alzheimer's disease （AD） based on network pharmacology and bioinformatics. MethodThe active components of XCHT and corresponding targets were retrieved from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）， and the differentially expressed genes related to AD were searched from Gene Expression Omnibus （GEO）. Thereby， the common targets of XCHT and AD were yielded， followed by Gene Ontology （GO） term enrichment and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis of the common targets. The component-target network and protein–protein interaction （PPI） network were constructed. Furthermore， amyloid β-protein （Aβ）1-40 was used to induce AD in PC12 cells and then the AD cells were intervened with XCHT. Afterward， cell viability was detected by Cell Counting Kit-8 （CCK-8） assay and cell morphology was observed based on 4'，6-diamidino-2-phenylindole （DAPI） staining. Cell membrane potential was determined and apoptosis was detected by flow cytometry， and cellular immunofluorescence detects the expression of B-cell lymphoma-2 （Bcl-2）/Bcl-2-related X protein （Bax）. Moreover， immunofluorescence assay was performed. ResultA total of 190 active components and 41 anti-AD targets of XCHT were screened out. The key components included mairin， quercetin， berberine， protoporphyrin， 24-ethylcholest-4-en-3-one， and β-D-ribofuranoside， and the core targets were sigma non-opioid intracellular receptor 1 （SIGMAR1）， checkpoint kinase 1 （CHEK1）， protein tyrosine phosphatase non-receptor type 6 （PTPN6）， protein kinase C（PRKCH）， inhibitor of nuclear factor kappa B kinase subunit beta （IKBKB）， cathepsin D （CTSD）， cysteine aspartate protease-3 （Caspase-3）， Bax， and Bcl-2-like protein 1 （Bcl-2L1）. The anti-AD targets of XCHT were involved in 302 GO terms （P < 0.05）， particularly the regulation of neuronal cell apoptosis， and 73 KEGG pathways （P<0.05）. The major pathways and biological processes included the apoptosis pathway， virus infection pathway， lipid and atherosclerosis pathway， and cancer-related pathways. In the in vitro experiment， the model group demonstrated the decrease in cell survival rate （P<0.05）， increase in apoptosis rate （P<0.05）， and down-regulation of mitochondrial membrane potential and Bcl-2/Bax ratio compared with the blank control. Compared with the model group， XCFT group showed the increase in cell survival rate （P<0.05）， decrease in apoptosis rate （P<0.05）， and up-regulation of mitochondrial membrane potential and Bcl-2/Bax ratio. ConclusionBased on network pharmacology， this study reveals the multi-component， multi-target， and multi-pathway characteristics of XCHT in the treatment of AD， laying a foundation for further research on the material basis and mechanism of this prescription.

The Fourier transform infrared spectra of the key organs derived from Kidney (Shen)-yang deficiency syndrome mice / 中国结合医学杂志

<p><b>OBJECTIVE</b>To explore an approach to rapidly and accurately identify the compounds as biomarkers of Chinese medicine (CM) syndromes.</p><p><b>METHOD</b>The Fourier transform infrared (FT-IR) spectrometry was applied to investigate the characteristic components of a mice model of Kidney (Shen)-yang deficiency syndrome (KDS), and the remedial effect of a typical CM formula Shenqi Pill (). Thirty-six females and 18 males of Balb/c mice were randomly divided into KDS, Shenqi or control group. The females and males of the same group freely were mated for 96 h, and the males were taken out and only the female mice were raised. Females of the KDS group were threatened by a ferocious cat every other day for 14 d. After delivery, the KDS, or gestational threatened, offspring were raised at standard condition for 11 weeks. Then 10 male offspring were randomly selected, anaesthetized and their representative organs, i.e. testes, kidneys, lungs and feet were collected, for the FT-IR scan. Mice of the Shenqi group were intragastric administered Shenqi Pill; while mice in the KDS and control groups were given the same volume of saline.</p><p><b>RESULTS</b>The attenuated birth outcomes of the KDS group were displayed. The remarkable FT-IR differences of all organs between KDS mice and healthy control were mainly at 1,735-1,745 cm(-1) (indicating the increased levels of lipids) and at 1,640-1,647 cm(-1) and 1,539-1,544 cm(-1) (displaying the decreased proteins). No statistic FT-IR difference between Shenqi and control mice was observed.</p><p><b>CONCLUSION</b>In accordance with major traits of KDS, prenatal stress extensively impaired the building up of proteins and resulting in the excessive lipid storage, and FT-IR could effectively identify the biomarkers of KDS.</p>

Research on gene expression of warm-hot drug treating cold syndrome / 中国中药杂志

<p><b>OBJECTIVE</b>To study the therapeutic molecular mechanism of the warm-hot drugs treating cold syndrome.</p><p><b>METHOD</b>A brother and his sister with deficiency-cold syndrome were chosen and treated with appropriate Chinese formula consisted chiefly of warm-hot drugs for 45 days. Then microarray technique was applied for comparing the gene expression difference of sister who had significant effect, the data was dialed with multiple analysis method and the results were mined though gene function and pathway.</p><p><b>RESULT</b>276 differential genes were obtained, which were related to metabolism and 18 pathways.</p><p><b>CONCLUSION</b>Warm-hot drugs work on the gene expression of metabolism. It may be exerting the curative action by gene network and there is distinct difference between gene expression of curative effect and syndrome.</p>