ABSTRACT
Objective To explore the effect of dihydromyricetin (DMY) on the cholesterol efflux in macrophage derived foam cells and analyze the possible mechanisms. Methods RAW 264.7 macrophages were incubated by oxidized low densi?ty lipoprotein (ox-LDL, 50 mg/L) for 48 h to induce foam cells. Subsequently, the foam cells were subdivided into control group (RPMI1640 media) and DMY 1-4 groups (10, 20, 40 and 80μmol/L) and cultured for 24 h. Cholesterol efflux from foam cells was examined by [3H] labed cholesterol. The high performance liquid chromatography assay was used to test the cellular contents of free cholesterol (FC), cholesteryl ester (CE) and total cholesterol (TC). The expression of ATP-binding cassette transporter A1 (ABCA1) was measured by Western blot assay. Results Compared with control group, cholesterol efflux was significantly increased, the content of FC, TC CE and CE/TC ratio were significantly decreased and expression of ABCA1 was significantly up-regulated in dose dependent manner in DMY (20, 40 and 80μmol/L) groups (P0.05). Conclusion DMY promotes the cholesterol efflux in the macro?phage derived foam cells, which may be related with the increase of ABCA1 induced by DMY.
ABSTRACT
Objective To observe the protective effect of Apelin-13 on the cerebral ischemia-reperfusion injury (CIRI), and to explore the possible mechanism in rat model. Methods Fifty male SD rats were randomly divided into five groups:sham group, CIRI model group and Apelin-13 (0.1, 1.0 and 10.0 μg/kg) treatment groups. The model of CIRI was established by filament. After 2 h ischemia, the focal middle cerebral artery was followed by 72 h reperfusion. Apelin-13 was administrated by intracerebroventricular injection 30 minutes before reperfusion. The score of neural function was estimated in different time points. The 2,3,5-triphenyl tetrazolium chloride (TTC) dye was used to calculate the volume and percentage of cerebral infarction. The endoplasmic reticulum stress (ERS) protein markers including glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP) in cerebral cortex were measured by Western blot assay. Results Compared with the sham group, the score of neural function was significantly increased, the infarct rate was reached(47.63 ± 5.81)%and the protein expressions of GRP78 and CHOP were significantly up-regulated in CIRI model group (P＜0.05). There were no significant differences in these data between the CIRI model group and 0.1 μg/kg Apelin-13 treatment group (P＞0.05). Compared with the CIRI group, the neural function defect was significantly improved, the muscle strength was significantly enhanced and the infarct rate was significantly decreased, and the protein expressions of GRP78 and CHOP were significantly down-regulated in the 1.0 and 10.0 μg/kg Apelin-13 treatment groups (P＜0.05). Conclusion Apelin-13 protects the cerebral ischemia-reperfusion injury in rat model, which may be related with the inhibition of endoplasmic reticulum stress.
ABSTRACT
Objective To investigate the effect of hydrogen sulfide (H2S) on the cholesterol efflux and ATP-binding cassette transporter A1 (ABCA1) expression in foam cells .Methods RAW 264 .7 macrophages were incubated with oxidized low density lipoprotein to induce foam cells .Foam cells were incubated with H2S donor sodium hydrosulfide .Cholesterol efflux from macropha-ges was tested by labed cholesterol .The cellular levels of free cholesterol (FC) ,cholesterol ester (CE) and total cholesterol (TC) were measured by high performance liquid chromatography assays .The mRNA and protein expressions of ABCA1 were detected by Real-time PCR and Western blot .Results Compared with the foam cells ,the rates of cholesterol efflux were significantly in-creased ,the levels of TC ,FC ,CE and CE/TC ratio were significantly decreased(P<0 .05) and expression of ABCA1 was signifi-cantly increased by treatment with H2S in dose-and time-dependent manner(P<0 .05) .Conclusion H2S up-regulates of expres-sion ABCA1 and promotes cholesterol efflux in RAW 264 .7 macrophage-derived foam cells .