OBJECTIVETo observe the effects of danshensu on function of endothelial progenitor cells (EPCs) from peripheral blood which were damaged by oxidative low density lipoprotein (Ox-LDL). And study its possible mechanism.

METHODTotal mononuclear cells (MNCs) were isolated from peripheral blood by ficoll density gradient centrifugation, and were identified by demonstrating the expression of CD34, VEGFR-2 and AC133 with flow cytometry, to sure that all the cells needed were EPCs. Then the cells were plated on fibronectin-coated culture dishes. After incubation for 7 days, attached cells were collected and divided into three groups: Control group, Ox-LDL group, danshensu intervention group, stimulated with different cencentrations of danshensu (2, 10 and 50 mg x L(-1)), adhesion assay respectively. EPCs adhesion assay were performed by replating those on fibronectin-coated dishes, then adherent cells were counted. And take cell supernate of each group to carry on the SOD, MDA content examination.

RESULTOx-LDL impaired EPC proliferative and adhesive capacity. In Ox-LDL group, The SOD content obviously drops, the MDA content obviously elevates. After danshensu interventing for 24 h, adhesive EPCs and migratory EPCs were significantly increased. Compared with Ox-LDL group, the SOD content of Danshensu intervention group obviously increased and the MDA content obviously reduced.

CONCLUSIONdanshensu could improve proliferative and adhesive capacity of EPCs that were impaired by Ox-LDL. The mechanism might relate to the oxidation resistance damage.

Animals ; Cell Adhesion ; drug effects ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Endothelium ; cytology ; Humans ; Lactates ; pharmacology ; Lipoproteins, LDL ; adverse effects ; Malondialdehyde ; metabolism ; Oxidative Stress ; drug effects ; Stem Cells ; cytology ; drug effects ; metabolism ; Superoxide Dismutase ; metabolism

OBJECTIVE To investigate the effects of Brassica rapa polysaccharide （BRP） on the Toll-like receptor 4 （TLR4）/ myeloid differentiation factor 88 （MyD88）/nuclear factor-κB （NF-κB）， AMP-activated protein kinase （AMPK）/sterol regulatory element-binding protein-1c （SREBP-1c） pathways， intestinal microbiota and liver metabolism of mice with alcoholic liver injury， and preliminarily elucidate its mechanism for improving alcoholic liver injury. METHODS Seventy-two mice were randomly divided into blank group （normal saline）， model group （normal saline）， bifendate group （positive control， 300 mg/kg） and BRP low-， medium- and high-dose groups （75， 150 and 300 mg/kg）. They were given relevant medicine intragastrically， once a day， for consecutive 9 d. After the last administration， mice in all groups except the blank group were gavaged with white liquor to establish an alcoholic liver injury model. The levels of alanine aminotransferase and aspartate aminotransferase in serum， total cholesterol， triglycerides， low-density lipoprotein cholesterol， interleukin-6， interleukin-1β， tumor necrosis factor- α and lipopolysaccharide， as well as protein expressions of TLR4， MyD88， NF-κB p65， phosphorylated NF-κB p65 （p-NF-κB p65）， AMPK， phosphorylated AMPK （p-AMPK）， and SREBP-1c were all detected； pathological morphological changes of liver tissue and colon were observed. 16S rRNA was used to detect the changes of intestinal microbiota in mice， and metabolomics 2022B02058） technology was used to detect the changes of liver metabolites. RESULTS Compared with model group， the above biochemical indicators and the protein expressions of TLR4， MyD88， p-NF-κB p65， and SREBP-1c in liver tissues were all significantly decreased （P＜0.05 or P＜0.01）， while the protein expression of p-AMPK was significantly increased （P＜0.05 or P＜0.01）. Pathological damage to liver and colon tissues was significantly improved. Medium dose of BRP could increase the relative abundance of Akkermansia， norank_f_Muribaculaceae and Lachnospiraceae_NK4A136_group in the intestinal contents of mice to a certain extent， and decrease the relative abundance of Lactobacillus and Escherichia-Shigella. A total of 9 differential metabolites were identified by metabolomics， including homogentisic acid， myristyl lysophosphatidylcholine， which were involved in pathways such as tyrosine metabolism. CONCLUSIONS BRP can regulate the relative abundance of beneficial flora， reduce the relative abundance of harmful flora， improve the structure of intestinal colonies， reduce the entry of pro-inflammatory mediator lipopolysaccharides into liver tissue， affect metabolic pathways such as tyrosine metabolism and the expression of TLR4/MyD88/NF- κB and AMPK/SREBP-1c signaling pathways in the liver， and ultimately improve alcoholic liver injury.