1.Relationship among plasma BNP level and cardiac function and prognosis in patients with acute heart failure
Niannian LIU ; Kangting TANG ; Pingxi XIAO
Chinese Journal of cardiovascular Rehabilitation Medicine 2017;26(4):364-367
Objective: To explore assessment value of change of brain natriuretic peptide (BNP) level for cardiac function and prognosis judgment in patients with acute heart failure (AHF).Methods: After standard medicinal treatment, according to whether BNP level after treatment reduced <30% or rose compared with at hospitalization, a total of 91 AHF inpatients were divided into BNP reduction ≥30% group (n=67) and BNP reduction <30% or rise group (n=24).Left ventricular ejection fraction (LVEF), left ventricular end-diastolic dimension (LVEDd) and 6min walking distance (6MWD) at discharge were compared between two groups.All patients were followed up for 12 months.Multi-factor Logistic regression analysis was used to analyze risk factors for cardiogenic death.and adverse cardiac events were recorded.Results: Compared with BNP reduction ≥30% group, there were significant reductions in LVEF [(46.00±5.46)% vs.(34.54±5.32)%] and 6MWD [(392.64±153.02)m vs.(136.75±56.25)m], and significant rise in LVEDd [(56.33±4.40)mm vs.(65.96±6.13)mm] in BNP reduction <30% group, P<0.01 all.Multi-factor Logistic regression analysis indicated BNP reduction <30% or rise was the only one independent risk factor for cardiogenic death (OR=2.714, P=0.039).Compared with BNP reduction ≥30% group, there was significant rise in incidence rate of adverse cardiac events (40.3% vs.62.5%) in BNP<30% group, and the Log-rank value was 30.264 (P=0.001).Conclusion: Change of plasma BNP level can be used as an important reference index for the evaluation of cardiac function and prognosis in patients with acute heart failure.
2.Effects of amifostine on formation of abdominal aortic aneurysm in mice induced by benzo[ a] pyrene
Luyuan TAO ; Shaoze WU ; Jiaoni WANG ; Guoqiang WANG ; Yangjing XUE ; Zhiqiang XU ; Jie WANG ; Jifei TANG ; Kangting JI
Chinese Journal of Pathophysiology 2016;32(12):2168-2176
AIM:To study the role of amifostine on the formation of benzo [a]pyrene (BaP)-induced abdomi-nal aortic aneurysm ( AAA) in C57BL/6J mice and the underlying mechanism .METHODS: RAW246.7 mononuclear macrophage in vitro were divided into control group , DMSO group, BaP group, low dose (1 μmol/L) amfostine treated group, middle dose (5 μmol/L) amfostine treated group and high dose (25μmol/L) amfostine treated group .The influ-ence of BaP on the expression of matrix metalloproteinase (MMP)-9, MMP-12, TNF-α, NF-κB in the RAW246.7 mono-nuclear macrophages in vitro was determined by Western blot .Male C57BL/6J mice (8 months old) were divided into con-trol group, model group (AngII+BaP group), low dose (50 mg/kg) amfostine treated group and high dose (100 mg/kg) amfostine treated group.After 6 weeks, the abdominal aorta were isolated .The aortic tissues were subjected to HE and Masson staining.The vascular wall structure , infiltration of macrophage , the expression of MMP-9, MMP-12, TNF-α, NF-κB were evaluated by Western blot and immunochemistry staining .RESULTS:Amifostine attenuated BaP-induced expres-sion of TNF-α, MMP-9, MMP-12, NF-κB in the RAW246.7 mononuclear macrophages (P<0.05).The results of animal experiments showed that the incidence of AAA in high dose amifostine treated group were significantly lower than that in low dose amifostine treated group and model group (P<0.05).Immunohistochemistry staining observation showed that amifos-tine inhibited the aortic macrophage infiltration more obviously in high amifostine treated group compared with model group and low dose amifostine treated group (P<0.05).Compared with model group and low dose amifostine treated group , the MMP-9, MMP-12, TNF-αand NF-κB expression of abdominal aorta in high amifostine treated group was reduced signifi -cantly ( P<0.05 ) .CONCLUSION: Amifostine inhibits BaP-induced activation of macrophages , and also prevents the formation of abdominal aortic aneurysm in C 57BL/6J mice induced by BaP by inhibition of the NF-κB pathway, macro-phage infiltration and the expression of TNF-αand MMPs.
3.Effects of danshensu on function of EPCs which were damaged by Ox-LDL and study its possible mechanism.
Junde CHAI ; Kangting JI ; Jiafeng LIN ; Ruiyin YE ; Jifei TANG ; Penglin YANG
China Journal of Chinese Materia Medica 2009;34(7):904-907
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