scholarly journals UPLC-QTOF/MS-Based Lipidomic Profiling of Liver Qi-Stagnation and Spleen-Deficiency Syndrome in Patients with Hyperlipidemia

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Piao Shenghua ◽  
Tan Shuyu ◽  
Li Kunping ◽  
Zhan Huixia ◽  
Xiao Xue ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Plasma Lipid ◽  
Deficiency Syndrome ◽  
Common Disease ◽  
Database Searching ◽  
Efficient Technology ◽  
Spleen Deficiency ◽  
Qi Stagnation ◽  
Lipid Metabolites ◽  
Spleen Deficiency Syndrome

Hyperlipidemia is a common disease caused by abnormal plasma lipid metabolism. Lipidomics is a powerful and efficient technology to study the integration of disease and syndrome of Chinese medicine. This study investigated specific changes in lipid metabolites from hyperlipidemia patients with syndrome of liver qi-stagnation and spleen-deficiency (SLQSD). Lipid profiles in plasma samples from 29 hyperlipidemia patients including 10 SLQSD and 19 non-SLQSD and 26 healthy volunteers (NC) were tested by UPLC-QTOF/MS. PLS-DA analysis and database searching were performed to discover differentiating metabolites. Differences in lipid metabolites between hyperlipidemia and healthy people mainly include phosphatidylcholines, phosphatidylethanolamines, phosphatidylglycerols, and ceramides. Hyperlipidemia patients with SLQSD and non-SLQSD could be differentiated by using identified lipid metabolites including phosphatidylcholines, phosphatidylethanolamines, phosphatidylinositols, triglycerides, diacylglycerols, lysophosphatidylethanolamines, sphingomyelins, lysophosphatidylcholines, and lactosylceramides. There were significant differences of lipid metabolism between between different syndromes of the same disease such as hyperlipidemia which showed significant differences between SLQSD and non-SLQSD.

A combination of depression and liver Qi stagnation and spleen deficiency syndrome using a rat model

2020 ◽  
Vol 303 (8) ◽  
pp. 2154-2167 ◽  
Author(s):  
Xiao‐Juan Li ◽  
Wen‐Qi Qiu ◽  
Xiao‐Li Da ◽  
Ya‐Jing Hou ◽  
Qing‐Yu Ma ◽  
...  
Keyword(s):  
Rat Model ◽  
Deficiency Syndrome ◽  
Spleen Deficiency ◽  
Qi Stagnation ◽  
Spleen Deficiency Syndrome

scholarly journals Treatment of Spleen-Deficiency Syndrome With Atractyloside A From Bran-Processed Atractylodes lancea by Protection of the Intestinal Mucosal Barrier

2020 ◽  
Vol 11 ◽  
Author(s):  
Jiyuan Tu ◽  
Ying Xie ◽  
Kang Xu ◽  
Linghang Qu ◽  
Xiong Lin ◽  
...  
Keyword(s):  
Body Weight ◽  
Deficiency Syndrome ◽  
Mucosal Barrier ◽  
Enzyme Linked Immunosorbent Assay ◽  
Residual Rate ◽  
Intestinal Mucosal Barrier ◽  
Expression Levels ◽  
Spleen Deficiency ◽  
Atractylodes Lancea ◽  
Spleen Deficiency Syndrome

Atractylodes lancea (Thunb.) DC. (AL) is used in traditional Chinese medicine for the treatment of spleen-deficiency syndrome (SDS). Bran-processed Atractylodes lancea (BAL) has been found to be more effective than unprocessed AL. However, the compound in BAL active against SDS remains unclear. The pharmacological efficacy of BAL and its mechanism of action against SDS were investigated by HPLC-ELSD. Candidate compound AA (atractyloside A) in AL and BAL extracts was identified by HPLC-MS analysis. AA was tested in a rat model of SDS in which body weight, gastric residual rate, and intestinal propulsion were measured, and motilin (MTL), gastrin (GAS), and c-Kit were quantified by enzyme-linked immunosorbent assay. Potential targets and associated pathways were identified based on network pharmacology analysis. mRNA expression levels were measured by qRT-PCR and protein expression levels were measured by Western blot analysis and immunohistochemistry. AA increased body weight, intestinal propulsion, MTL, GAS, and c-Kit levels, while decreasing gastric residual volume and intestinal tissue damage, as same as Epidermal Growth Factor Receptor and Proliferating Cell Nuclear Antigen levels. Seventy-one potential pharmacologic targets were identified. Analysis of protein interaction, Gene Ontology (GO) functional analysis, pathway enrichment analysis, and docking and molecular interactions highlighted MAPK signaling as the potential signal transduction pathway. Validation experiments indicated that treatment with AA increased MTL, GAS, ZO-1, and OCLN levels, while reducing AQP1, AQP3, and FGF2 levels. In addition, phosphorylation of p38 and myosin light-chain kinase (MLCK) expression were inhibited. AA improved gastrointestinal function by protecting the intestinal mucosal barrier via inhibition of the p38 MAPK pathway. The results have clinical implications for the therapy of SDS.

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