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AIM To explore the anti-atherosclerotic mechanism of Wendan decoction based on formation of foam cells. METHODS The optimal concentrations of Wendan decoction without cytotoxity to cells were selected by MTT assay. After Wendan decoction treatment， the formation of foam cells was examined by oil red O staining. The cholesterol efflux， cholesterol level， free cholesterol level and cholesterol esterification rate were analyzed using cholesterol efflux assay， total cholesterol assay and free cholesterol assay. The expression levels of macrophage membrane proteins， including CD36， scavenger receptor class A （SR-A）， ATP-binding cassette transporter A1 （ABCA1） and scavenger receptor class B type I （SR-BI）， were quantified by Western blot. RESULTS The optimal concentrations of Wendan decoction without cytotoxity to the cells were 0~6 g/L. Wendan decoction at the concentrations of 1.5， 3 and 6 g/L were selected for the experiments. Wendan decoction at these concentrations inhibited the formation of foam cells induced by oxidized low-density lipoprotein （ox-LDL）， and reduced the accumulation of intracellular lipids in a concentration-dependent manner （P <0.05 or P <0.01）. Wendan decoction also reduced intracellular total cholesterol level， cholesterol ester level and cholesterol esterification rate （P <0.05 or P <0.01）， promoted efflux of intracellular cholesterol （P <0.01）， and decreased the protein level of CD36 in THP-1 cell-derived macrophages （P <0.01） in a concentration-dependent manner. Wendan decoction at the concentration of 6 g/L significantly reduced the protein level of SR-A in THP-1 cell-derived macrophages （P <0.05）. At the concentrations of 3 and 6 g/L， Wendan decoction significantly increased the protein levels of ABCA1 and SR-BI in THP-1 cell-derived macrophages （P <0.05 or P <0.01）. CONCLUSION Wendan decoction significantly inhibits ox-LDL-induced formation of foam cells by reducing cholesterol deposition and promoting cholesterol efflux， and its mechanism may be related to the down-regulation of CD36 and SR-A and the up-regulation of ABCA1 and SR-BI. 相似文献
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AIM: To investigate the regulation of ghrelin on the expression of ATP-binding cassette transporter A1 and G1 (ABCA1/ABCG1)during the foam cell formation. METHODS: The human monocytic leukemia cell line (THP-1)was chosen in our study. The differentiation of THP-1 cells into macrophages was induced by using phorbol myristate acetate (PMA). Macrophages were then incubated with oxidized LDL (ox-LDL)to generate foam cells. Ghrelin of different concentrations were treated at different time points during foam cell formation. The ABCA1/ABCG1 protein and mRNA levels were detected by Western blotting and RT-PCR. The effect of variance of cholesterol content was measured by zymochemistry via-fluorospectrophotometer. RESULTS: Ghrelin reduced the content of lipid droplet in foam cells, and increased the efflux of intracellular cholesterol significantly. Ghrelin increased ABCA1 protein mass and mRNA level in dose-dependent manner. The changes of ABCG1 protein and mRNA level were the same as ABCA1. CONCLUSION: Ghrelin interfere atherosclerosis by up-regulating the expression of ABCA1 and ABCG1. 相似文献
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AIM: To establish the THP-1-derived foam cell formation and to evaluate the effects of angiotensin-(1-7) and MDL (an inhibitor of adenylate cyclase) on the expression of ATP-binding cassete transporter A1(ABCA1) and the content of cholesterol. METHODS: THP-1-derived macrophages were treated with oxidized low-density lipoprotein(ox-LDL) to develop into foam cells. The foam cells were divided into 4 groups: control group, MDL group, Ang-(1-7) group and MDL+Ang-(1-7) group. At 24 h after treatment, the content of cAMP was measured by ELISA. The mRNA and protein levels of ABCA1 were determined by real-time RT-PCR and Western blotting, respectively. The content of cholesterol was detected by high performance liquid chromatography. RESULTS: The cAMP, the mRNA and protein levels of ABCA1 in Ang-(1-7) group were significantly higher, and the content of cholesterol was significantly lower than those in control group (P<0.05). On the contrary, the cAMP, the mRNA and protein levels of ABCA1 in MDL group were significantly lower and the content of cholesterol was significantly higher than those in control group (P<0.05). The results in MDL+Ang-(1-7) group were between Ang-(1-7) group and control group. CONCLUSION: Ang-(1-7) inhibits the formation of foam cells by promoting the expression of ABCA1 and decreasing the content of cholesterol. MDL partly antagonizes the effect of Ang-(1-7) by inhibiting the adenylate cyclase and decreasing the content of cAMP. 相似文献
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AIM To observe the changes of lipophagy during foam cells formation， and to determine the effect of lipophagy on the lipid content and cholesterol outflow of foam cells. METHODS Human THP-1 monocytes were induced by phorbol-12-myristate-13-acetate for 48 h to differentiate into macrophages， and then were incubated with 50 mg/L oxidized low-density lipoprotein （oxLDL） to form foam cells. Lipids in foam cell were stained by oil red O， and the lipid content was determined. The total cholesterol （TC） and free cholesterol （FC） levels in foam cells were measured by cholesterol testing kit. Cholesteryl ester （CE） and CE/TC ratio were calculated. The cholesterol efflux rate was detected by cholesterol efflux assay kit. The expression of autophagy-related proteins， including autophagy-related protein 5 （Atg5）， microtubule-associated protein 1 light chain 3 （LC3） and P62， were detected by Western blot. The colocalization of lipid droplets （LD） and LC3 was detected by immunofluorescence staining. The autophagy inducer rapamycin （Rap） or blocker 3-methyladenine （3MA） was used to intervene foam cells， and the expression of Atg5， LC3 and P62， the co-expression of LD and LC3， the cholesterol content and the cholesterol efflux rate were determined. RESULTS Formation of foam cells was observed at 24 h after stimulation with oxLDL at 50 mg/L， as indicated by intracellular CE/TC ratio exceeding 50%.Cholesterol efflux assay revealed that the cholesterol efflux rate increased within 24 h during foam cell formation but decreased after 48 h （P <0.05）. Western blot results displayed that the expression of Atg5 and LC3-II/LC3-I ratio were increased within 24 h of foam cell formation， but was deceased after 48 h （P <0.05）. The expression of P62 was decreased within 24 h but was increased at 48 h （P <0.05）. The colocalization of LD and LC3 was increased at 24 h but was decreased at 48 h after oxLDL stimulation. Treatment with Rap up-regulated the expression of Atg5 and LC3-II/LC3-I ratio， reduced the level of P62， increased the colocalization of LD and LC3， promoted the cholesterol efflux， anf reduced cholesterol content in foam cells （P <0.05）. On the contrary， 3MA inhibited the expression of Atg5， reduced LC3-II/LC3-I ratio， elevated the level of P62， decreased the colocalization of LD and LC3， reduced the outflow of cholesterol， increased the content of TC and CE， and elevated CE/TC ratio in foam cells （P <0.05）. CONCLUSION Lipophagy is enhanced at 24 h but decreased at 48 h during foam cell formation. Lipophagy inhibited foam cell formation by reducing cholesterol content and increasing cholesterol efflux. 相似文献
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AIM: To investigate the expressions of peroxisome proliferator-activated receptor γ (PPAR γ) and acyl-coenzyme A: cholesterol acyltransferase-1 (ACAT1), and to discuss the mechanisms and pathways of Chlamydia pneumoniae (C.pn)-induced macrophage foam cell formation. METHODS: THP-1-derived macrophages were incubated for 48 h with or without C.pn (1×105 to 1×106 IFU) and/or rosiglitazone (1 to 20 μmol/L), a specific PPAR γ agonist. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellular cholesterol ester were detected by enzyme-fluorescence. PPAR γ, ACAT1 mRNA and protein expressions were determined by RT-PCR and Western blotting, respectively. RESULTS: THP-1-derived macrophages infected with C.pn at concentration of 5×105 and 1×106 IFU resulted in the large accumulation of lipid droplets and the ratio of cholesteryl ester (CE) to total cholesterol (TC) was much higher than 50%when co-incubated with low density lipoprotein (LDL). C.pn up-regulated the expressions of ACAT1 mRNA and protein, and down-regulated the expressions of PPAR γ mRNA and protein in a concentration-dependent manner (P<0.05). Rosiglitazone (10, 20 μmol/L) markedly suppressed the accumulation of lipid droplets and CE by C.pn. Moreover, rosiglitazone inhibited the up-regulation of ACAT1 mRNA and protein expression by C.pn infection in a concentration-dependent manner (P<0.05). CONCLUSION: C.pn induces macrophage foam cell formation by up-regulating ACAT1 expression via PPARγ pathway, which may provide new evidences for the development and progression of atherosclerosis initiated by C.pn infection. 相似文献
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WANG Yuan GAO Hong-wei FENG Gao-jie DAI Pei ZHANG Qin-feng BAI Rui QIN Wei-wei LI Hong GAO Fen 《园艺学报》2020,36(2):206-213
AIM: To compare the effects of high-density lipoprotein (HDL) from healthy subjects (HDLheathy) and HDL from the patients with coronary artery disease (HDLCAD) on the lipid deposition and apoptosis in mouse peritoneal macrophages. METHODS: HDL was isolated from healthy subjects, stable CAD patients (HDLSCAD) and acute myocar-dial infarction patients (HDLAMI). The accumulation of intracellular lipids was determined by oil red O staining. The apoptosis of macrophages was measured by fluorescence microscopy with annexin-V/PI staining. DCHF-DA, a redox-sensitive dye, was used to detect intracellular reactive oxygen species (ROS) levels. The protein expression of ATP-binding cassette transporter (ABC) A1, ABCG1, Bcl-2 and Bax was determined by Western blot analysis. RESULTS: Lipid deposition in the macrophages was increased significantly after oxidized low-density lipoprotein (ox-LDL) treatment, and the expression of ABCA1 and ABCG1 was up-regulated (P <0.05). Compared with ox-LDL treatment alone, HDLhealthy decreased lipid deposition in the macrophages and up-regulated the expression of ABCA1 and ABCG1 (P <0.05), while treatment with HDLSCAD or HDLAMI further decreased lipid deposition in the macrophages and down-regulated the expression of ABCA1 and ABCG1 (P <0.05). Compared with HDLSCAD treatment, lipid deposition in the macrophages was further increased after HDLAMI treatment, and the expression of ABCA1 and ABCG1 was down-regulated (P <0.05). HDLhealthy decreased the levels of intracellular ROS and apoptosis by increasing the level of antiapoptotic protein Bcl-2 and reducing the expression of proapoptotic protein Bax. In contrast, HDLSCAD and HDLAMI had opposite effects on the intracellular ROS, the cell apoptosis and the expression of apoptosis-related proteins Bcl-2 and Bax. CONCLUSION: HDLCAD promotes lipid accumulation in macrophages and induces macrophage apoptosis. These findings provide novel insights into mechanisms leading to altered vascular effects of HDL in CAD. 相似文献
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AIM:To study the action of ATP binding cassette transporter(ABC) A 1 on cholesterol efflux in THP-1 macrophage-derived foam cells.METHODS:After exposure of the cultured THP-1 macrophage-derived foam cells to 22(R)-hydroxycholesterol and 4, 4'-diisothiocyanostilbene-2, 2'-disulfonic acid (DIDS) at different concentration for 24 hours, cholesterol efflux and ABCA1 mRNA level were determined by FJ-2107P type liquid scintillator and reverse trancriptase-polymerase chaim reaction(RT-PCR), respectively.RESULTS:Oxidized LDL promoted cholesterol efflux in THP-1 macrophages and 22(R)-hydroxycholesterol increased cholesterol efflux in THP-1 macrophage-derived foam cells in a dose-dependent manner and DIDS inhibited cholesterol efflux in THP-1 macrophage-derived foam cells in a dose-dependent manner. Exposure of the cultured THP-1 macrophage-derived foam cells to 22(R)-hydroxycholesterol and DIDS at different concentration for 24 hours, resulted in increase and decrease in the expression of ABCA1 mRNA in THP-1 macrophage-derived foam cells in a dose-dependent manner, respectively.CONCLUSION:ABCA1 playes an important role in cholesterol efflux in THP-1 macrophage-derived foam cells. 相似文献
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AIM: To investigate the effects of ghrelin on the expression of acyl coenzyme A:cholesterol acyltransferases-1 (ACAT-1) during the formation of foam cells. METHODS: The human monocytic leukemia cell line THP-1 was used in the study. The differentiation of THP-1 cells into macrophages was induced by phorbol 12-myristate 13-acetate (PMA). Macrophages were incubated with oxidized LDL (ox-LDL) to generate foam cells. Ghrelin of different concentrations were used during the formation of foam cells. The ACAT-1 protein and mRNA levels were detected by Western blotting and RT-PCR. The variance of cholesterol content was measured by zymochemistry via-fluorospectrophotometer. RESULTS: Ghrelin reduced the content of cholesterol ester in foam cells obviously. ACAT-1 protein and mRNA levels were also decreased. Ghrelin reduced ACAT-1 protein mass and mRNA level in a dose-dependent manner. CONCLUSION: Ghrelin might retard the formation of atherosclerosis via down-regulating the expression of ACAT-1. 相似文献
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AIM To explore the anti-atherosclerotic mechanism of Wendan decoction based on reverse cholesterol transport. METHODS Eight-week-old apolipoprotein E gene knockout （ApoE -/-） mice with high-fat diet and daily drug gavage were randomly divided into model group, simvastatin group, and low-, middle- and high-dose Wendan decoction groups, with 15 mice in each group. The C57BL/6 mice of the same age served as control group. The mice were weighed once every week. After 10 weeks, the mice were anesthetized with chloral hydrate. The serum were collected for lipid level examination. The atherosclerotic plaque buildup in aortic root and whole aorta was observed by HE staining and oil red O staining, respectively. The levels of proteins related to cholesterol transport, ATP-binding cassette transporter A1 （ABCA1） and caveolin-1 in the aorta, and scavenger receptor class B type I （SR-BI） and CD36 in the liver, were quantified by Western blot. RESULTS Wendan decoction at middle dose inhibited the increase in the body weight of ApoE -/- mice fed with high-fat diet （P <0.05）. Wendan decoction at different doses significantly reduced the serum levels of triglyceride, total cholesterol and low-density lipoprotein cholesterol in the ApoE -/- mice （P <0.05 or P <0.01）, but had no effect on serum high-density lipoprotein cholesterol level （P >0.05）. Wendan decoction at different doses inhibited the formation of atherosclerotic plaques in whole aorta of the ApoE -/- mice （P <0.05 or P <0.01）. Middle- and high-dose Wendan decoction significantly inhibited the formation of atherosclerotic plaques in the aortic root （P <0.05）. Bedsides, Wendan decoction at different doses increased the protein level of ABCA1 and decreased the protein level of caveolin-1 in the aorta of the ApoE -/- mice （P <0.01）. Middle- and high-dose Wendan decoction increased the liver protein level of SR-BI in the ApoE -/- mice （P <0.01）. However, Wendan decoction at different doses had no effect on the liver protein level of CD36 in the ApoE -/- mice （P >0.05）. CONCLUSION Wendan decoction reduces the body weight, serum lipid levels and formation of atherosclerotic plaques in ApoE -/- mice fed with high-fat diet, and its mechanism is related to up-regulation of ABCA1 protein level in the aorta and SR-BI protein level in the liver as well as down-regulation of caveolin-1 protein level in the aorta. 相似文献
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AIM To investigate the role of fatty acid translocase (FAT/CD36) on differentiation of monocytes to macrophages. METHODS Human monocyte THP-1 cells were treated with phorbol 12-myristate 13-acetate (PMA) at 0, 100 and 200 μg /L. Small interfering RNA (siRNA) targeting CD36 (siCD36) was employed to knock down the expression of CD36 in THP-1 cells. The CD36 over-expression (CD36OE) cell line was constructed by transfection with a recombinant lentivirus containing CD36 cDNA. Optical microscopy and crystal violet staining were used to detect the monocyte morphological changes and adhesion ability. The protein expression of CD36 was measured by flow cytometry and Western blot. The mRNA levels of CD36, CD11b and CD80 were detected by real-time PCR. The protein levels of extracellular signal-regulated kinase (ERK） and Src tyrosine kinase were determined by Western blot. RESULTS The cellular adhesiveness of THP-1 cells was elevated in the process of monocytes differentiation, and the expression of CD36 was increased in this process as well (P <0.01). siCD36 was transfected into the THP-1 cells (CD36i group) and the silencing efficiency was approximately 80%. The cell surface area and cellular adhesiveness were significantly decreased in CD36i group compared with scrambled siRNA (NCi) group (P <0.01). The mRNA levels of CD11b and CD80 were decreased in CD36i group compared with NCi group (P <0.01). The cell surface area and cellular adhesiveness were increased in CD36OE group compared with empty vector (vector) group (P <0.05). The mRNA levels of CD11b and CD80 were increased in CD36OE group compared with vector group (P <0.01). The phosphorylation levels of ERK and Src were decreased in CD36i group compared with NCi group (P <0.05). CONCLUSION CD36 promotes the differentiation of human monocyte THP-1 cells to macrophages by increasing the phosphorylation of Src and further activating ERK. 相似文献
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AIM: To study the protective effect of puerarin on the atherosclerosis of RAW264.7-derived foam cells. METHODS: The model of foam cells was established by incubating the RAW264.7 cells with ox-LDL. The cholesterol uptake was evaluated by a DiI-ox-LDL binding assay. The ability of cholesterol efflux of the RAW264.7-derived foam cells was detected by cholesterol efflux assay. The protein levels of LC3Ⅱ, P62, CD36, ABCA1, LAL and p-AMPK were determined by Western blot. RESULTS: Puerarin treatment reduced the cholesterol uptake capacity and enhanced the cholesterol efflux rate. The protein levels of LC3Ⅱ, ABCA1 and LAL in puerarin group were higher than that in ox-LDL group, while the protein levels of P62 and CD36 were obviously decreased, and those in rapamycin treatment group had the same change as puerarin group. The protein levels of LC3Ⅱ, ABCA1 and LAL were obviously decreased and the protein level of p-AMPK was increased after co-treated with 3-MA. CONCLUSION: Puerarin promotes LAL and ABCA1-mediated cholesterol efflux in ox-LDL-treated RAW264.7 macrophages, which might enhance autophagy through AMPK-dependent pathway for cholesterol efflux regulation, and reduce the uptake of lipids by CD36 negative regulation. 相似文献
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AIM: To study the effect of acyl coenzyme A: cholesteryl acyltransferase 1 (ACAT1) antisense oligonucleotides on the formation of foam cells (FC). METHODS: THP-1 cells were cultured and differentiated into macrophages (MP) by phorbol myristate acetate (PMA). Over-expressing ACAT1 gene THP-1 cells were constructed. The ACAT1 antisense and missense oligonucleotides conducted by LipofectamineTM 2000 were incubated with above cells. Ac-LDL was added 6 h later and incubated for 24 h. The expression of ACAT1 protein was detected by Western blotting. The ACAT activity was measured by quantifying the incorporation of ［1-14C］ oleoyl CoA into cholesteryl esters. The formation of foam cells was detected by oil red O staining. RESULTS: The ACAT1 antisense oligonucleotides inhibited the activity of ACAT in macrophages and over-expressing ACAT1 gene THP-1 cells. It also inhibited the formation of foam cell in macrophages and over-expressing ACAT1 gene THP-1 cells with lipid loading. The missense oligonucleotides did not show the inhibitory effects. CONCLUSION: The ACAT1 antisense oligonucleotides inhibit the activity of ACAT and the formation of foam cells. 相似文献
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DAI Pei GAO Fen GAO Hong-wei WANG Yuan FENG Gao-jie ZHANG Qin-feng BAI Rui QIN Wei-wei LI Hong SONG Xiao-su 《园艺学报》2019,35(2):212-217
AIM:To study whether homocysteine (Hcy) inhibits the expression of ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette transporter G1 (ABCG1) by microRNA-33 (miRNA-33) signaling, and reduces the efficiency of reverse cholesterol transport (RCT).METHODS:RAW264.7 macrophages were induced by oxidized low-density lipoprotein (ox-LDL) to establish foam cell model. Oil red O staining was used to determine whether the model was established successfully. miRNA-33 mimics and miRNA-33 inhibitor were transfected into the cells by Lipofectamine 2000, and the cells were exposed to Hcy at concentration of 5 mmol/L for 24 h. The intracellular lipid droplets were observed by Oil red O staining. The expression of ABCA1 and ABCG1 at mRNA and protein levels was determined by real-time PCR and Western blot. The cellular cholesterol content was analyzed by HPLC, and effluent rate of cholesterol was detected by the method of liquid scintillation counting.RESULTS:Compared with blank control group, the lipid content in miRNA-33 mimics group was increased, and the expression of ABCA1 and ABCG1 at mRNA and protein levels was decreased (P<0.05). The intracellular cholesterol content was increased gradually (P<0.05), and the cellular cholesterol efflux rate was gradually decreased (P<0.05) in miRNA-33 mimics group. Compared with blank control group, the testing results in miRNA-33 inhibitor group were the opposition of those in miRNA-33 mimics group (P<0.05). No diffe-rence of the above indexes among blank control group, miRNA-33 mimics-NC group and miRNA-33 inhibitor-NC group was observed.CONCLUSION:Hcy inhibits the mRNA and protein expression of ABCA1 and ABCG1 through miRNA-33 signaling, and reduces the efficiency of RCT in RAW264.7 macrophage-derived foam cells. 相似文献
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AIM To investigate the effect of F-box and WD repeat domain containing protein 7 （FBW7） on the injury of granulosa cells （GCs） induced by oxidized low-density lipopretion （ox-LDL） stimulation and its potential mechanism. METHODS The GCs isolated from women of reproductive age with different obesity levels, the GCs isolated from high fatty diet （HFD）-fed rats, and the ox-LDL-treated rat GCs were collected, and the expression of FBW7 was detected by Western blot. After the rat GCs were infected with adenovirus encoding FBW7 （Ad-FBW7）, the cells were treated with ox-LDL （80 mg/L） for 48 h, and then the cell viability, apoptosis, NADPH oxidase （NOX） activity and the key subunit proteins of NOX were detected by CCK-8 assay, Annexin V/PI staining, lucigenin chemiluminescence and Western blot, respectively. The effect of FBW7 over-expression on NOX1 degradation was evaluated by cycloheximide （CHX） chase assay. RESULTS The expression of FBW7 was lower in the GCs isolated from obese women of reproductive age, the GCs isolated from HFD-fed rats, and the ox-LDL-treated rat GCs （P <0.05）. Over-expression of FBW7 inhibited ox-LDL-induced injury of GCs, NOX activity, and NOX1 expression （P <0.05）. The results of CHX chase assay showed that over-expression of FBW7 accelerated the degradation of NOX1 protein under ox-LDL condition （P <0.05）. CONCLUSION Over-expression of FBW7 reduces ox-LDL-induced injury of GCs by accelerating NOX1 degradation and then weakening NOX activity. 相似文献
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ZHENG Hao-long SONG Nan CAO Hui-min CHEN Si WANG Jie Lü Xiao-ming JIA Lian-qun 《园艺学报》2020,36(4):713-718
AIM To investigate the effects of different components of Gynostemma pentaphyllum ［gypenosides (Gps), gypenoside XLIX (GpXLIX) and ginsenoside Rb3 (GRb3)］ on mitochondrial energy metabolism-related proteins in endothelial cells induced by oxidized low-density lipoprotein (ox-LDL). METHODS EA.hy926 cells were divided into control group, model group, Gps group, GpXLIX group and GRb3 group. The cells in control group were cultured only in DMEM complete medium. The cells in model group were treated with 100 mg/L ox-LDL for 48 h. The cells in Gps group, GpXLIX group and GRb3 group were treated with 100 mg/L ox-LDL for 24 h, and then treated with Gps, GpXLIX and GRb3 at 100 mg/L for another 24 h, respectively. The ATP content in each group was detected by ELISA. The expression levels of mitochondrial energy metabolism-related proteins, cytochrome C oxidase subunit 5a （Cox5a）, NADH:ubiquinone oxidoreductase core subunit S1 （Ndufs1）, ATP synthase F1 subunit alpha (ATP5a) and cytochrome C (Cyt C）, were determined by Wes automatic Western blot quantitative analysis system and Western blot. RESULTS Compared with control group, the ATP content in model group was decreased (P <0.01). After drug intervention, the ATP content increased to different degrees in Gps group, GpXLIX group and GRb3 group (P <0.01). The results of Wes automatic Western blot quantitative analysis system were consistent with those of Western blot. These results showed that compared with control group, the protein expression of Cox5a, Ndufs1 and ATP5a in model group was decreased, and the protein expression of Cyt C was increased (P <0.01). After intervention, the protein expression of Cox5a, Ndufs1 and ATP5a was increased and the protein expression of Cyt C was decreased in Gps group, GpXLIX group and GRb3 group (P <0.05 or P <0.01). Among them, the effect of Gps on the protein expression of Cox5a, Ndufs1 and Cyt C was significantly stronger than those of the 2 monomer components, and the effect of GRb3 was found to be superior in the 2 monomer components. The effect of GpXLIX on ATP5a protein was superior to the other 2 components. CONCLUSION Gynostemma total saponins and related active ingredients protect ox-LDL-induced endothelial cells by affecting mitochondrial energy metabolism-related proteins, thereby preventing and treating atherosclerosis. 相似文献
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AIM To investigate the effect of microRNA-22 (miR-22) secreted by macrophage exosomes on the autophagy of H9c2 cardiomyocytes under uremic toxin stimulation. METHODS The macrophage-derived exosomes stimulated by indoxyl sulfate (IS) were collected and co-cultured with H9c2 cells. The levels of miR-22 in the macrophages， macrophage-derived exosomes and H9c2 cells were detected by RT-qPCR. The viability of H9c2 cells was measured by CCK-8 assay. The expression of exosome surface marker protein CD63 and autophagy-related proteins LC3 and P62 was determined by Western blot. RESULTS Under IS stimulation, the expression of exosome surface marker protein CD63 in the macrophages was significantly higher than that in control group (P <0.05), and the levels of miR-22 in the macrophages and macrophage-derived exosomes were significantly increased (P <0.01). With the increase in macrophage exosome concentration, the viability of H9c2 cells was decreased gradually (P <0.05), and the stimulation of macrophage exosomes reduced P62 expression and promoted the conversion of LC3-I to LC3-II in a dose-dependent manner (P <0.05). Macrophage-derived exosomes increased the ratio of LC3-II to LC3-I but decreased P62 protein expression in the H9c2 cells transfected with miR-22 mimic compared with the cells transfected with corresponding negative control miRNAs (P <0.05). However, miR-22 inhibitor yielded contrasting results. CONCLUSION IS-stimulated macrophages increase expression of miR-22 in cardiomyocytes through exosomes, and promote autophagy of the cardiomyocytes. 相似文献