Hualien District Agricultural Research and Extension Station

Hualian, Taiwan

Hualien District Agricultural Research and Extension Station

Hualian, Taiwan
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Lu Y.-L.,Taipei Medical University | Liu Y.-H.,Shin Kong Wu Ho Su Memorial Hospital | Liu Y.-H.,Taipei Medical University | Chyuan J.-H.,Hualien District Agricultural Research and Extension Station | And 4 more authors.
Botanical Studies | Year: 2012

Antioxidant activity assays were conducted using water (H) and methanolic (M) extracts of sixteen cultivars from indigenous wild bitter gourd (Momordica charantia L. var. abbreviata Seringe, MCA) in Taiwan. The scavenging activities against 2,2-diphenyl-1-picrylhydrazyl (DPPH) and hydroxyl radicals were different among MCA cultivars and the concentrations of 50% scavenging activity (IC50) for the effective cultivar was 181 μg/mL (H) and 246 μg/mL (M) in the former extract and 148 μg/mL (H) and 37 μg/mL (M) in the latter. For inhibitory activities against Cu2+-induced low-density-lipoprotein peroxidation, most MCA cultivars at 4000 μg/mL (especially for M extracts) showed protective activities and were equivalent to 0.8 mM Trolox by thiobarbituric acid reactive substance assays. These useful data may help promote the use and further research of MCA as an antioxidant in the health food industry.

Lu K.-H.,National Taiwan University of Science and Technology | Tseng H.-C.,National Taiwan University of Science and Technology | Liu C.-T.,National Taiwan University of Science and Technology | Huang C.-J.,National Taiwan University of Science and Technology | And 3 more authors.
Food and Function | Year: 2014

Bitter gourd (Momordica charantia L.) is a common vegetable grown widely in Asia that is used as a traditional medicine. The objective of this study was to investigate whether wild bitter gourd possessed protective effects against chronic alcohol-induced liver injury in mice. C57BL/6 mice were fed an alcohol-containing liquid diet for 4 weeks to induce alcoholic fatty liver. Meanwhile, mice were treated with ethanol extracts from four different wild bitter gourd cultivars: Hualien No. 1′, Hualien No. 2′, Hualien No. 3′ and Hualien No. 4′. The results indicated that the daily administration of 500 mg kg body weight-1 of a Hualien No. 3′ extract (H3E) or a Hualien No. 4′ extract (H4E) markedly reduced the steatotic alternation of liver histopathology. In addition, the activation of serum aminotransferases (AST and ALT) and the accumulation of hepatic TG content caused by alcohol were ameliorated. The hepatoprotective effects of H3E and H4E involved the enhancement of the antioxidant defence system (GSH, GPx, GRd, CAT and SOD), inhibition of lipid peroxidation (MDA) and reduction of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) in the liver. Moreover, H3E and H4E supplementation suppressed the alcohol-induced elevation of CYP2E1, SREBP-1, FAS and ACC protein expression. These results demonstrated that ethanol extracts of Hualien No. 3′ and Hualien No. 4′ have beneficial effects against alcoholic fatty liver, in which they attenuate oxidative stress and inflammatory responses. © 2014 the Partner Organisations.

Chou Y.-C.,National Taiwan University | Chou Y.-C.,China Medical University at Taichung | Su H.-M.,National Taiwan University | Lai T.-W.,China Medical University at Taichung | And 2 more authors.
Nutrition | Year: 2012

Objective: The aim of this study was to investigate the adipogenic effect of cis-9, trans-11, trans-13-conjugated linolenic acid (c9, t11, t13-CLN), a fatty acid naturally present in bitter melon. Methods: The 3T3-L1 murine preadipocyte cell line was used to test the effect of saponifiables from whole bitter melon and of commercially prepared pure c9, t11, t13-CLN on adipocyte differentiation. The effect of c9, t11, t13. -CLN on 3T3-L1 cell viability was also tested at proliferation, mitotic clonal expansion, and terminal differentiation stages. Results: Compared to the free fatty acid control mixture, the proadipogenic effect on 3T3-L1 was less potent using saponifiables obtained from bitter melon. C9, t11, t13-CLN, unlike its non-conjugated counterpart linolenic acid (LN) or other common fatty acids such as oleic acid or linoleic acid, exerted no proadipogenic effect on 3T3-L1. In contrast to LN displaying no cytotoxic effect at a concentration ≤100 μM, c9, t11, t13-CLN caused a dose-dependent reduction in the viability of pre- and postconfluent preadipocytes associated with apoptosis. Sustained ERK/MAPK activation, accompanied by increased peroxisome proliferator-activated receptor γ phosphorylation, was seen in c9, t11, t13-CLN-treated cells at initiation of differentiation. Conclusion: C9, t11, t13-CLN is less adipogenic for 3T3-L1 cells than LN and this is partly due to its apoptotic effect on proliferating preadipocytes and to the sustained ERK phosphorylation seen during mitotic clonal expansion. © 2012 Elsevier Inc.

Chang T.-W.,National Taiwan University | Chang T.-W.,Hualien District Agricultural Research and Extension Station | Lin C.-Y.,Tzu Chi University | Tzeng Y.-J.,Tzu Chi University | Lur H.-S.,National Taiwan University
Anticancer Research | Year: 2014

Aim: To determine the combinative effects of tanshinone IIA (Tan IIA) and trans-resveratrol (Resv) on cytotoxicity, apoptosis, cell-cycle arrest and DNA fragmentation in HepG2 human liver cancer cells. Materials and Methods: Cytotoxicity was detected by the cell proliferation and cytotoxicity WST-1 assay. Cell-cycle arrest and apoptosis were determined using flow cytometry analysis. DNA fragments were separated by gel electrophoresis. Results: Tan IIA and Resv at mixture ratios of 1/2:1/2 and 1/3:2/3 exerted synergistic cytotoxicity comparable to that of cisplatin. Elevated proportions of sub-G1 and apoptotic cells were respectively found in the combinative treatments in comparison with hypothetic values of additive effects. Moreover, a more intensive pattern of apoptotic DNA fragmentation was visualized in combined treatments than in individual ones. Conclusion: Combining Tan IIA and Resv causes synergistic cisplatin-comparable, cytotoxicity and robustly induces apoptosis, sub-G1 cell cycle arrest and DNA fragmentation. This study provides evidence supporting further pre-clinical investigations of the combinational synergism. © 2014, International Institute of Anticancer Research. All rights reserved.

PubMed | China Medical University at Taichung, Hualien District Agricultural Research and Extension Station and National Taiwan University
Type: | Journal: The Journal of nutritional biochemistry | Year: 2016

-Eleostearic acid (-ESA), or the cis-9, trans-11, trans-13 isomer of conjugated linolenic acid, is a special fatty acid present at high levels in bitter melon seed oil. The aim of this study was to examine the effect of -ESA on hepatic lipid metabolism. Using H4IIEC3 hepatoma cell line, we showed that -ESA significantly lowered intracellular triglyceride accumulation compared to -linolenic acid (LN), used as a fatty acid control, in a dose- and time-dependent manner. The effects of -ESA on enzyme activities and mRNA profiles in H4IIEC3 cells suggested that enhanced fatty acid oxidation and lowered lipogenesis were involved in -ESA-mediated triglyceride lowering effects. In addition, -ESA triggered AMP-activated protein kinase (AMPK) activation without altering sirtuin 1 (SIRT1) protein levels. When cells were treated with vehicle control (VC), LN alone (LN; 100mol/L) or in combination with -ESA (LN+-ESA; 75+25mol/L) for 24h, acetylation of forkhead box protein O1 was decreased, while the NAD(+)/NADH ratio, mRNA levels of NAMPT and PTGR1 and enzyme activity of nicotinamide phosphoribosyltransferase were increased by LN+-ESA treatment compared to treatment with LN alone, suggesting that -ESA activates SIRT1 by increasing NAD(+) synthesis and NAD(P)H consumption. The antisteatosis effect of -ESA was confirmed in mice treated with a high-sucrose diet supplemented with 1% -ESA for 5weeks. We conclude that -ESA favorably affects hepatic lipid metabolism by increasing cellular NAD(+)/NADH ratio and activating PPAR, AMPK and SIRT1 signaling pathways.

PubMed | China Medical University at Taichung, Hualien District Agricultural Research and Extension Station and National Taiwan University
Type: Journal Article | Journal: Nutrients | Year: 2016

We previously reported that bitter melon seed oil (BMSO) was an effective anti-steatosis and antiobesity agent. Since the major fatty acid -eleostearic acid (-ESA) in BMSO is a peroxisome proliferator-activated receptor (PPAR) activator, the objective was to investigate the role of PPAR in BMSO-modulated lipid disorders and -ESA metabolism. C57BL/6J wild (WD) and PPAR knockout (KO) mice were fed a high-fat diet containing BMSO (15% soybean oil + 15% BMSO, HB) or not (30% soybean oil, HS) for 5 weeks. The HB diet significantly reduced hepatic triglyceride concentrations and increased acyl-CoA oxidase activity in WD, but not in KO mice. However, regardless of genotype, body fat percentage was lowered along with upregulated protein levels of uncoupling protein 1 (UCP1) and tyrosine hydroxylase, as well as signaling pathway of cAMP-dependent protein kinase and AMP-activated protein kinase in the white adipose tissue of HB-treated groups compared to HS cohorts. In WD-HB and KO-HB groups, white adipose tissue had autophagy, apoptosis, inflammation, and browning characteristics. Without PPAR, in vivo reduction of -ESA into rumenic acid was slightly but significantly lowered, along with remarkable reduction of hepatic retinol saturase (

Kou M.-C.,Chia Nan University of Pharmacy and Science | Chiou S.-Y.,Hualien District Agricultural Research and Extension Station | Weng C.-Y.,Chia Nan University of Pharmacy and Science | Wang L.,Chia Nan University of Pharmacy and Science | And 2 more authors.
Molecular Nutrition and Food Research | Year: 2013

Scope: Curcumin (CUR), demethoxycurcumin (DMC), and bisdemethoxycurcumin (BDMC) have been demonstrated as having antioxidant, anticarcinogenic, and hypocholesterolemic activities. We report the diverse antiatherogenic effects and mechanisms of curcuminoids. Methods and results: We found that CUR was the most potent antioxidant against copper-mediated LDL oxidation as measured by thiobarbituric acid-reactive substances assay, oxidized LDL (oxLDL) ELISA, and electrophoretic mobility. CUR upregulated heme oxygenase-1, modifier subunit of glutamate-cysteine ligase (GCLM), and CD36 expression in undifferentiated THP-1 cells, supporting the possible involvement of Nrf2 pathway in CD36 expression. Monocyte-to-macrophage differentiation plays a vital role in early atherogenesis. BDMC reduced oxLDL uptake most effectively, while CUR was the best inhibitor for CD36, scavenger receptor A, and lectin-like oxidized LDL receptor-1 expression during phorbol 12-myristate 13-acetate (PMA)-induced THP-1 differentiation. In PMA-differentiated THP-1 macrophages, CUR and DMC effectively induced heme oxygenase-1 expression, but attenuated oxLDL-induced CD36 expression, leading to decreased oxLDL uptake. Conclusion: This result indicates curcuminoids, despite structural similarities, exert different atheroprotective effects. Curcuminoids, especially CUR and DMC, are hormetic compounds, which induce Phase II enzyme expression and confer resistance to PMA- and oxLDL-induced scavenger receptor expression and activity. © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Weng C.-Y.,Chia Nan University of Pharmacy and Science | Chiou S.-Y.,Hualien District Agricultural Research and Extension Station | Wang L.,Chia Nan University of Pharmacy and Science | Kou M.-C.,Chia Nan University of Pharmacy and Science | And 2 more authors.
Archives of Toxicology | Year: 2014

Chronic arsenic exposure has been linked to endothelial dysfunction and apoptosis. We investigate the involvement of unfolded protein response (UPR) signaling in the arsenic-mediated cytotoxicity of the SVEC4-10 mouse endothelial cells. The SVEC4-10 cells underwent apoptosis in response to As 2O3 dose- and time-dependently, accompanied by increased accumulation of calcium, and activation of caspase-3. These phenomena were completely inhibited by α-lipoic acid (LA), which did not scavenge ROS over-production, but were only partially or not ameliorated by tiron, a potent superoxide scavenger. Moreover, arsenic activated UPR, leading to phosphorylation of eukaryotic translation initiation factor 2 subunit α (eIF2α), induction of ATF4, and processing of ATF6. Treatment with arsenic also triggered the expression of endoplasmic reticulum (ER) stress markers, GRP78 (glucose-regulated protein), and CHOP (C/EBP homologous protein). The activation of eIF2α, ATF4 and ATF6 and expression of GRP78 and CHOP are repressed by both LA and tiron, indicating arsenic-induced UPR is mediated through ROS-dependent and ROS-independent pathways. Arsenic also induced ER stress-inducible genes, BAX, PUMA (p53 upregulated modulator of apoptosis), TRB3 (tribbles-related protein 3), and SNAT2 (sodium-dependent neutral amino acid transporter 2). Consistent with intracellular calcium and cell viability data, ROS may not be important in arsenic-induced death, because tiron did not affect the expression of these pro-apoptotic genes. In addition, pretreatment with salubrinal, a selective inhibitor of eIF2α dephosphorylation, enhanced arsenic-induced GRP78 and CHOP expression and partially prevented arsenic cytotoxicity in SVEC4-10 cells. Taken together, these results suggest that arsenic-induced endothelial cytotoxicity is associated with ER stress, which is mediated by ROS-dependent and ROS-independent signaling. © 2013 Springer-Verlag Berlin Heidelberg.

Chen P.-H.,China Medical University at Taichung | Chen G.-C.,China Medical University at Taichung | Yang M.-F.,China Medical University at Taichung | Hsieh C.-H.,China Medical University at Taichung | And 5 more authors.
Journal of Nutrition | Year: 2012

The aim of this study was to investigate the antiadiposity effect of bitter melon seed oil (BMSO), which is rich in the cis-9, trans-11, trans-13 isomer of conjugated linolenic acid. In Expt. 1, C57BL/6J mice were fed a butter-based, high-fat diet [HB; 29% butter + 1% soybean oil (SBO)] for 10 wk to induce obesity. They then continued to receive that diet or were switched to an SBO-based, high-fat diet alone (HS; 30%SBO) or containing bitter melon seed oil (BMSO) (HBM; 15%SBO+ 15% BMSO) for 5 wk. The body fat percentage was significantly lower in mice fed the HBM diet (21%), but not the HS diet, compared with mice fed the HB diet. In Expt. 2, mice were fed an SBO-based, high-fat diet containing 0 (HS), 5 (LBM), 10 (MBM), or 15% (HBM) BMSO for 10 wk. In the LBM, MBM, and HBM groups, the body fat percentage was significantly lower by 32, 35, and 65%, respectively, compared with the HS control. The reduction in the HBM group was significantly greater than that in the LBM or MBM group. BMSO administration increased phosphorylation of acetyl-CoA carboxylase, cAMP-activated protein kinase (PKA), and signal transducer and activator of transcription 3 in the white adipose tissue (WAT), suggesting that PKA and leptin signaling might be involved in the BMSO-mediated reduction in lipogenesis and increase in thermogenesis and lipolysis. However, compared with the HS control, the HBM group had a significantly higher TNFa concentration in the WAT accompanied by TUNEL-positive nuclei. We conclude that BMSO is effective in attenuating body fat accumulation through mechanisms associated with PKA activation and programmed cell death in the WAT, but safety concerns need to be carefully addressed. © 2012 American Society for Nutrition.

Li C.-J.,Tzu Chi University | Tsang S.-F.,Tzu Chi University | Tsai C.-H.,Tzu Chi University | Tsai H.-Y.,Tzu Chi University | And 2 more authors.
Evidence-based Complementary and Alternative Medicine | Year: 2012

Plants are an invaluable source of potential new anti-cancer drugs. Momordica charantia is one of these plants with both edible and medical value and reported to exhibit anticancer activity. To explore the potential effectiveness of Momordica charantia, methanol extract of Momordica charantia (MCME) was used to evaluate the cytotoxic activity on four human cancer cell lines, Hone-1 nasopharyngeal carcinoma cells, AGS gastric adenocarcinoma cells, HCT-116 colorectal carcinoma cells, and CL1-0 lung adenocarcinoma cells, in this study. MCME showed cytotoxic activity towards all cancer cells tested, with the approximate ICranging from 0.25 to 0.35 mg/mL at 24 h. MCME induced cell death was found to be time-dependent in these cells. Apoptosis was demonstrated by DAPI staining and DNA fragmentation analysis using agarose gel electrophoresis. MCME activated caspase-3 and enhanced the cleavage of downstream DFF45 and PARP, subsequently leading to DNA fragmentation and nuclear condensation. The apoptogenic protein, Bax, was increased, whereas Bcl-2 was decreased after treating for 24 h in all cancer cells, indicating the involvement of mitochondrial pathway in MCME-induced cell death. These findings indicate that MCME has cytotoxic effects on human cancer cells and exhibits promising anti-cancer activity by triggering apoptosis through the regulation of caspases and mitochondria. © 2012 Chia-Jung Li et al.

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