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#28481295   2017/05/08 Save this To Up

Inhibiting HDAC1 Enhances the Anti-Cancer Effects of Statins through Downregulation of GGTase-Iβ Expression.

Hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors, namely statins, are potential anti-tumor agents. Previously, we showed that a pan-histone deacetylase (HDAC) inhibitor enhances the anti-tumor effects of the HMG-CoA inhibitor. However, the underlying mechanisms were not fully understood. Cancer cell lines (CAL-27 and SACC-83) were exposed to pan-HDAC inhibitor, or HDAC1 inhibitor, or geranylgeranyl transferase type I (GGTase-I) inhibitor alone or in combination with statin. Cell viability, apoptosis, migration, and invasion were assessed by Cell Count Kit-8, 4',6-diamidino-2-phenylindole staining, and transwell assay, respectively. A xenograft model was used for assessing tumor growth in vivo. Western blot and real-time PCR were used to assess the expression of genes. We observed that inhibiting HDAC1 could enhance the anti-tumor effects of statins both in vitro and in vivo. Inhibiting HDAC1 blocked the statin-induced upregulation of geranylgeranyl transferase type Iβ subunit (GGTase-Iβ), resulting in an enhancement of the anti-cancer effects of statin. Overexpression of GGTase-Iβ or constitutively active RhoA abolished the enhancement by inhibiting HDAC1 on anti-tumor effects of statins. The HDAC1 inhibitor failed to enhance cytotoxicity in non-tumor primary cells treated with statin. Inhibiting HDAC1 enhanced the anti-cancer effects of statins through downregulation of GGTase-Iβ expression, and thus further inactivation of RhoA. A combination of statin with HDAC1 or GGTase-I inhibitor would be a new strategy for cancer chemotherapy.

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#28462132   2017/05/02 Save this To Up

Spirogyra neglecta inhibits the absorption and synthesis of cholesterol in vitro.

Spirogyra neglecta (SN) has many nutritional benefits and it is commonly used to ameliorate different human conditions including inflammation, gastric ulcer, hyperglycemia, and hyperlipidemia. However, the mechanism of the hypocholesterolemic effect of SN still remains unclear. Therefore, the present study was aimed to evaluate the effect of SN extract particularly on cholesterol absorption and synthesis mechanisms.

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#27023504   2016/03/30 Save this To Up

The Chemical Composition of Achillea wilhelmsii C. Koch and Its Desirable Effects on Hyperglycemia, Inflammatory Mediators and Hypercholesterolemia as Risk Factors for Cardiometabolic Disease.

This study was done to identify the content compounds of Achillea wilhelmsii (A. wilhelmsii) and to evaluate its hypoglycemic and anti-hypercholesterolemic activity and effect on inflammatory mediators. The extracts and fractions of A. wilhelmsii were thoroughly analyzed using high performance liquid chromatography (HPLC), and the total content of phenols and flavonoids was determined. The hypoglycemic activity was evaluated in vivo using alloxan-induced diabetic mice. The effect upon inflammatory mediators was evaluated in vitro using the human monocytic leukemia cell line (THP-1). The anti-hypercholesterolemic activity was evaluated in vitro using the 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase assay kit. The water extract (WE)-treated group showed the highest reduction in the fasting blood glucose levels (FBGL). The chloroform fraction (CF) and ethyl acetate fraction (EAF) both showed a significant ability to reduce the secretion of tumor necrosis factor alpha (TNF-α). The EAF, however, also attenuated the levels of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9). The CF showed the most significant 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) inhibition activity. The five main compounds in the CF were isolated and identified. Out of the five compounds in the CF, 1β,10β-epoxydesacetoxymatricarin (CP1) and leucodin (CP2) showed the highest anti-hypercholesterolemic potential. A molecular docking study provided corresponding results.

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#26509687   2015/10/29 Save this To Up

Clinical Characteristics of Anti-3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Antibodies in Chinese Patients with Idiopathic Inflammatory Myopathies.

The objective of this study was to detect the prevalence of anti-3-hydroxyl-3- methylglutaryl coenzyme A reductase (anti-HMGCR) antibodies in Chinese patients with idiopathic inflammatory myopathies (IIMs), and to analyze the clinical features of the antibody-positive IIM patients.

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#23978306   2013/09/30 Save this To Up

Use of enoyl coenzyme A hydratase of Mycobacterium avium subsp. paratuberculosis for the serological diagnosis of Johne's disease.

Johne's disease (JD), caused by Mycobacterium avium subspecies paratuberculosis (MAP), remains difficult to control because of the lack of specific and sensitive diagnostic tests. In order to improve the specificity of sero-diagnosis for JD, the phage display library derived from genomic DNA of MAP was immunoscreened to identify novel antigenic targets. We selected a clone using antibodies from MAP experimentally infected cattle, and annotated its coding sequence as MAP1197 in the MAP genome, which encoded "echA12_2" in the MAP protein (Map-echA) belonging to Enoyl-CoA hydratase, known as a crotonase enzyme. The Map-echA was expressed in Esherichia coli and purified as a histidine-tag recombinant protein (rMap-echA), and the diagnostic potential of the protein was further evaluated by enzyme-linked immunosorbent assays (ELISA). Antibody responses to rMap-echA were higher in MAP-infected cattle than in uninfected cattle. The specificity of the Map-echA ELISA was also confirmed by evaluation with hyper-immune sera against various kinds of Mycobacterium species. Furthermore, in all experimentally infected cattle the antibody against rMap-echA was detected 2-7months earlier than by a commercially available ELISA kit. These results suggested that Map-echA can be used as a specific and sensitive serological diagnostic antigen for the detection of MAP infection.

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#23899453   2013/08/27 Save this To Up

Berberine metabolites exhibit triglyceride-lowering effects via activation of AMP-activated protein kinase in Hep G2 cells.

Rhizoma coptidis (Huanglian in Chinese) is commonly used in Chinese folk medicine to treat diarrhea, diabetes, hypertension, hyperlipidemia and tumors. This herb has increasingly gained attention because of its use as a hypolipidemic herb. Berberine (BBR) is the most important constituent of R. coptidis that contribute to the pharmacological efficacy of the herb.

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#22495376   2012/06/18 Save this To Up

Nephrogenic adenoma: an immunohistochemical analysis using biotin-free methods.

Nephrogenic adenoma (NA) has been considered as a metaplastic process of the urothelium. It has been suggested that this lesion is of renal tubular cell origin or differentiation. Immunohistochemical studies of NA emphasize its staining with α-methylacyl-coenzyme A racemase (AMACR), and prostatic adenocarcinoma may be a possible differential diagnosis. This reactivity was recently discussed as an artifact due to endogenous biotin. Kidney-specific cadherin (Ksp-cad) is a marker of distal nephron. CD10 and KIT are also expressed in the kidney. We studied the immunohistochemical expression of AMACR, p63, Ksp-cad, CD10, and KIT in 9 cases of NA (forming a total of 12 lesions). Practically all of the lesions stained for AMACR with 2 different antibodies and 2 high-sensitivity (multimer or polymer based) biotin-free methods (83% and 100%). The staining was similar for both methods in 9 of these 12 lesions. All of the NAs were negative for p63 and KIT, except 1 case, with focal reactivity for KIT. CD10 was expressed very focally in 4 of the 12 lesions (33%). We observed weak staining for Ksp-cad in 6 lesions (50%) and 3 (25%) showed a moderate positivity in 15% to 50% of the cells. In conclusion, positivity of NA for AMACR is not an artifact, as we confirmed using 2 different methods. Besides, p63, a basal cell marker, is usually negative. Immunoreactivity for Ksp-cad seems to support the differentiation of NA to distal nephron cells, at least in some of the cases. Other markers expressed by the nephron, such as CD10 and KIT, are usually negative in NA.

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#20467885   2011/08/24 Save this To Up

Simvastatin enhances irinotecan-induced apoptosis in human non-small cell lung cancer cells by inhibition of proteasome activity.

Simvastatin, a potent inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA) is known to stimulate apoptotic cell death and induce cell cycle arrest through inhibition of proteasome. The purpose of this study is to investigate whether simvastatin would be synergistic with irinotecan against human non-small cell lung cancer (NSCLC) cells. Antitumor effect was measured by growth inhibition of cells and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The cytotoxic interaction between irinotecan and simvastatin was assessed using the combination index. Effects on cell cycle distribution and apoptosis were determined by flow cytometry and DNA fragmentation. Proteasome activity was measured by ELISA quantification of 20S proteasome. NF-κB activation was determined using TransAM™ NF-κB p65 Transcription Factor Assay Kit. IκB-α was measured by immunoblot. A combination of irinotecan with simvastatin showed significantly enhanced cell growth inhibition compared with irinotecan alone, which resulted in a synergistic cytotoxicity. Irinotecan and simvastatin combination treatment of A549 and H460 cells increased G(1) phase arrest, which was associated with up-regulation of p21(WAF1/CIP) and p53 compared with irinotecan alone. In addition, simvastatin combination treatment increased irinotecan-related apoptosis as determined by fluorescence microscopy and flow cytometric analysis. We also found that combination therapy showed superior proteasome inhibitory activity leading to effectively suppress NF-κB transcription factor activation. Consistently, this effect was associated with up-regulation of IκB-α. These findings suggest that simvastatin enhances irinotecan-induced apoptosis in human NSCLC cells through inhibition of proteasome activity.

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#19730362   2009/10/28 Save this To Up

Revisiting the immunophenotype of nephrogenic adenoma.

Nephrogenic adenoma (NA) is a rare benign lesion of the urinary tract. Although its histogenesis is still debated, several reports suggest that the lesion has a renal tubular cell origin or differentiation. As NA can be difficult to distinguish from malignant conditions such as prostate cancer, there is a need for reliable markers. Unfortunately, it has been reported that NA cells also stained positive for the prostate cancer marker alpha-methylacyl-coenzyme A racemase (AMACR). Because all the previous studies have used an avidin-biotin (AB) detection procedure, and because cells with tubular renal differentiation are likely to contain a high level of endogenous biotin, we investigated in NA the expression of several markers including AMACR, using both AB and biotin-free detection systems. We assessed the expression of p63, cytokeratins 7 and 20, CD10 (proximal tubule marker), MUC1 (distal tubule marker), PAX2, and AMACR on 14 NAs (from 6 patients) grouped on a tissue microarray. The tissue microarray also included renal, urothelial, and prostate tissues. Staining was detected using both AB and biotin-free Envision systems. Detection with the AB procedure leads to nonspecific staining in kidney samples and NA. More specific expression was obtained by using the Envision kit, and only CK7, PAX2, and MUC1 remained positive in NA, without any AMACR staining. These findings provide supporting evidence that NA has the differentiation of distal renal tubules, and strongly suggest that AMACR, when detected with a biotin-free procedure, can be used as a reliable marker for distinguishing NA from prostate cancer.

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#17536189   2007/06/25 Save this To Up

Conjugated linoleic acid reduces adipose depots without reduction of stearoyl coenzyme A desaturase 1 gene expression.

This study investigated the effects of conjugated linoleic acid (CLA) on the body weight, fat deposition and the expression of stearoyl coenzyme A desaturase 1 (SCD1) in the livers of male ICR mice that were fed with either beef tallow (BT) or fish oil (FO) supplemented with CLA. Mice weighing 25-30 g were divided into four groups, BT and BT supplemented with 0.5% CLA (BTC), FO and FO supplemented with 0.5% CLA (FOC). Each group consisted of 8 mice, and they were fed the experimental diets for 4 weeks. The experimental diets were composed of 59.18% carbohydrates, 19.73% proteins and 21.09% fat in terms of their contributions to total calories, and other nutrients were identical. CLA was added to the diets of the CLA supplementation groups at 0.5% (w/w). The measurement of triglyceride (TG) was done by using a kit. Fatty acid compositions were analyzed in both the plasma and the liver using a gas chromatograph. The levels of SCD1 expression were analyzed by RT-PCR in the liver.

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