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RISS 인기검색어
- 검색키워드
- 저자 : Mei Xia Lv (검색결과 3 건)
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Yang Tao,Xiao-mei Bie,Feng-xia Lv,Hai-zhen Zhao,Zhao-xin Lu 한국미생물학회 2011 The journal of microbiology Vol.49 No.1
The antifungal activity and mechanism of fengycin in the presence and absence of commercial surfactin against Rhizopus stolonifer were investigated. The MIC (minimal inhibitory concentration) of fengycin without commercial surfactin added was 0.4 mg/ml while the MIC of fengycin with commercial surfactin added was 2.0 mg/ml. Fengycin acted on cell membrane and cellular organs and inhibited DNA synthesis. The antifungal effect of fengycin was reduced after commercial surfactin was added. All these results suggest that the fungal cell membrane may be the primary target of fengycin action and commercial surfactin may reduce the antifungal activity of fengycin.
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Jia Han,Rui Zhang,Dina Muheyati,Mei Xia Lv,Wubulikasimu Aikebaier,Bing Xin Peng 한국식품영양과학회 2021 Journal of medicinal food Vol.24 No.2
Hyperlipidemia is a metabolic disorder characterized by high lipid levels, which may lead to cardiovascular diseases. Evidence suggests that improving the gut microbiota homeostasis is of great importance in lipid metabolism. Dietary fiber may positively regulate blood lipid and intestinal microbiota, therefore, we have investigated the effect of chickpea dietary fiber (CDF) on high-fat diet (HFD)-induced hyperlipidemia and gut bacterial dysbiosis. Fifty male Sprague Dawley rats purchased for this study were randomly divided into 5 groups of 10 rats each. The control group was fed with normal diet (ND), while the other four groups were all fed with HFD for inducing hyperlipidemia. Then one of the four HFD groups continued to be fed with only HFD, and the other three groups were fed with CDF in different doses: high CDF (30 g CDF/kg of HFD), medium CDF (15 g CDF/kg of HFD), and low CDF (5 g CDF/kg of HFD). After CDF treatment, the lipid level in serum was determined through biochemical methods, and microbial content of the fecal sample was determined by 16S rDNA sequencing. We found that CDF could decrease the levels of total cholesterol, triglyceride, and low-density lipoprotein cholesterol and increase the level of high-density lipoprotein cholesterol significantly. The diversity of gut microbiota in the ND group and CDF-treated groups were higher than HFD group. The β-diversity analysis showed that there were significant differences in gut microbiota among HFD-, ND-, and CDF-treated groups. Rats in CDF groups tended to be similar and interactive. CDF can effectively increase the abundance of Bacteroides and Lactobacillus in rats and increase the level of propionic acid. These results indicated that CDF might affect serum lipid and gut bacterial ecosystem positively.
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Shi, Qing-Qiang,Zuo, Guo-Wei,Feng, Zi-Qiang,Zhao, Lv-Cui,Luo, Lian,You, Zhi-Mei,Li, Dang-Yang,Xia, Jing,Li, Jing,Chen, Di-Long Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.18
Purpose: To investigate the effect of deacetylase inhibitory trichostatin A (TSA) on anti HepG2 liver carcinoma cells and explore the underlying mechanisms. Materials and Methods: HepG2 cells exposed to different concentrations of TSA for 24, 48, or 72h were examined for cell growth inhibition using CCK8, changes in cell cycle distribution with flow cytometry, cell apoptosis with annexin V-FTIC/PI double staining, and cell morphology changes under an inverted microscope. Expression of ${\beta}$-catenin, HDAC1, HDAC3, H3K9, CyclinD1 and Bax proteins was tested by Western blotting. Gene expression for ${\beta}$-catenin, HDAC1and HDAC3 was tested by q-PCR. ${\beta}$-catenin and H3K9 proteins were also tested by immunofluorescence. Activity of Renilla luciferase (pTCF/LEF-luc) was assessed using the Luciferase Reporter Assay system reagent. The activity of total HDACs was detected with a HDACs colorimetric kit. Results: Exposure to TSA caused significant dose-and time-dependent inhibition of HepG2 cell proliferation (p<0.05) and resulted in increased cell percentages in G0/G1 and G2/M phases and decrease in the S phase. The apoptotic index in the control group was $6.22{\pm}0.25%$, which increased to $7.17{\pm}0.20%$ and $18.1{\pm}0.42%$ in the treatment group. Exposure to 250 and 500nmol/L TSA also caused cell morphology changes with numerous floating cells. Expression of ${\beta}$-catenin, H3K9and Bax proteins was significantly increased, expression levels of CyclinD1, HDAC1, HDAC3 were decreased. Expression of ${\beta}$-catenin at the genetic level was significantly increased, with no significant difference in HDAC1and HDAC3 genes. In the cytoplasm, expression of ${\beta}$-catenin fluorescence protein was not obvious changed and in the nucleus, small amounts of green fluorescence were observed. H3K9 fluorescence protein were increased. Expression levels of the transcription factor TCF werealso increased in HepG2 cells following induction by TSA, whikle the activity of total HDACs was decreased. Conclusions: TSA inhibits HDAC activity, promotes histone acetylation, and activates Wnt/${\beta}$-catenin signaling to inhibit proliferation of HepG2 cell, arrest cell cycling and induce apoptosis.
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