연구논문(硏究論文) : 외식 소비자의 MSG 허용범위와 사용량 인식이 구매의도에 미치는 영향

소비자물가지수에 포함된 외식 메뉴를 중심으로 한국외식경영학회 2013 외식경영연구 Vol.16 No.1

본 연구는 국내의 주요 외식메뉴를 대상으로 각 메뉴별 MSG(monosodium glutamast) 허용수준, 사용량 인식, 구매의도를 조사함으로써 외식업체들이 MSG를 사용하는데 필요한 유의미한 정보를 제공하는데 목적이 있다. 이러한 목적을 달성하기 위하여 2013년 1월10일부터 2월10일까지 약 1달에 걸쳐서 서울 및 수도권 거주자 195명을 대상으로 설문조사를 실시하였으며, 충실하게 응답된 186부의 최종분석 결과를 정리하면 다음과 같다. 첫째, 요인분석 결과 외식메뉴는 ``한식 및 국수류``, ``회 및 고기류``, ``패스트푸드류``, ``돈가스 및 중식류``, ``비빔밥 및 찌개류``, ``단체급식``과 같이 총 6개로 분류되었다. 둘째, MSG의 허용수준은 모든 메뉴에서 평균값(3)보다 낮았으며, 사용량에 대한 인식은 모든 메뉴에서 평균값(3)보다 높은 것으로 나타났다. 셋째, MSG의 허용수준은 구매의도에 영향을 미치는 것으로 나타났으며, MSG사용량 인식은 구매의도에 영향을 미치지 않는 것으로 나타났다. This research has been conducted to provide useful information to restaurants that utilize MSG(monosodium glutamast), by inspecting major domestic menus in terms of the allowable range of the MSG, the awareness of its usage, and the intension of purchasing it. In order to accomplish this object, a survey has been conducted for 195 people living in and near Seoul from 2013. January 10th to February 10th. The following results stem from the 186 answers that were written well. First, factor analysis showed that restaurant menus were categorized into 6 menus; ``Korean foods and noodles``, ``sashimi and meat``, ``fast food``, ``pork cutlet and Chinese food``, ``bibimbap and stew``, and ``institutional food service.`` Second, the acceptable level of MSG was lower than the average rate(3) in every menus, and the awareness for its usage was higher than the average rate(3) in every menus. Third, the intension of purchasing MSG-contained products was influenced by the acceptable level of the MSG, while the awareness for its usage did not affect the purchase intention.

남은 밥을 이용한 개발메뉴

LG유통 메뉴개발실 대한영양사회 1998 國民營養 Vol.197 No.-

Suppression of Lipopolysaccharide-Induced Inflammatory and Oxidative Response by 5-Aminolevulinic Acid in RAW 264.7 Macrophages and Zebrafish Larvae

( Seon Yeong Ji ),( Hee-Jae Cha ),( Ilandarage Menu Neelaka Molagoda ),( Min Yeong Kim ),( So Young Kim ),( Hyun Hwangbo ),( Hyesook Lee ),( Gi-Young Kim ),( Do-Hyung Kim ),( Jin Won Hyun ),( Heui-Soo 한국응용약물학회 2021 Biomolecules & Therapeutics(구 응용약물학회지) Vol.29 No.6

In this study, we investigated the inhibitory effect of 5-aminolevulinic acid (ALA), a heme precursor, on inflammatory and oxidative stress activated by lipopolysaccharide (LPS) in RAW 264.7 macrophages by estimating nitric oxide (NO), prostaglandin E2 (PGE2), cytokines, and reactive oxygen species (ROS). We also evaluated the molecular mechanisms through analysis of the expression of their regulatory genes, and further evaluated the anti-inflammatory and antioxidant efficacy of ALA against LPS in the zebrafish model. Our results indicated that ALA treatment significantly attenuated the LPS-induced release of pro-inflammatory mediators including NO and PGE2, which was associated with decreased inducible NO synthase and cyclooxygenase-2 expression. ALA also inhibited the LPS-induced expression of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6, reducing their extracellular secretion. Additionally, ALA abolished ROS generation, improved the mitochondrial mass, and enhanced the expression of heme oxygenase-1 (HO-1) and the activation of nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2) in LPS-stimulated RAW 264.7 macrophages. However, zinc protoporphyrin, a specific inhibitor of HO-1, reversed the ALA-mediated inhibition of pro-inflammatory cytokines production and activation of mitochondrial function in LPS-treated RAW 264.7 macrophages. Furthermore, ALA significantly abolished the expression of LPS-induced pro-inflammatory mediators and cytokines, and showed strong protective effects against NO and ROS production in zebrafish larvae. In conclusion, our findings suggest that ALA exerts LPS-induced anti-inflammatory and antioxidant effects by upregulating the Nrf2/HO-1 signaling pathway, and that ALA can be a potential functional agent to prevent inflammatory and oxidative damage.

Apigenin promotes TRAIL-mediated apoptosis regardless of ROS generation

Kang, Chang-Hee,Molagoda, Ilandarage Menu Neelaka,Choi, Yung Hyun,Park, Cheol,Moon, Dong-Oh,Kim, Gi-Young Elsevier 2018 Food and chemical toxicology Vol.111 No.-

<P><B>Abstract</B></P> <P>Apigenin is a bioactive flavone in several herbs including parsley, thyme, and peppermint. Apigenin possesses anti-cancer and anti-inflammatory properties; however, whether apigenin enhances TRAIL-mediated apoptosis in cancer cells is unknown. In the current study, we found that apigenin enhanced TRAIL-induced apoptosis by promoting caspase activation and death receptor 5 (DR5) expression and a chimeric antibody against DR5 completely blocked the apoptosis. Apigenin also upregulated reactive oxygen species (ROS) generation; however, intriguingly, ROS inhibitors, glutathione (GSH) or N-acetyl-<SMALL>L</SMALL>-cysteine (NAC), moderately increased apigenin/TRAIL-induced apoptosis. Additional results showed that an autophagy inducer, rapamycin, enhanced apigenin/TRAIL-mediated apoptosis by a slight increase of ROS generation. Accordingly, NAC and GSH rather decreased apigenin-induced autophagy formation, suggesting that apigenin-induced ROS generation increased autophagy formation. However, autophagy inhibitors, bafilomycin (BAF) and 3-methyladenine (3-MA), showed different result in apigenin/TRAIL-mediated apoptosis without ROS generation. 3-MA upregulated the apoptosis but remained ROS levels; however, no changes on apoptosis and ROS generation were observed by BAF treatment. Taken together, these findings reveal that apigenin enhances TRAIL-induced apoptosis by activating apoptotic caspases by upregulating DR5 expression regardless of ROS generation, which may be a promising strategy for an adjuvant of TRAIL.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Apigenin sensitizes Hep3B and HepG2 cells to TRAIL-induced apoptosis. </LI> <LI> Apigenin activates caspases and apoptotic proteins during TRAIL sensitization. </LI> <LI> Apigenin induces DR5 expression and facilitates TRAIL-mediated apoptosis. </LI> <LI> Apigenin-induced ROS generation slightly hinders TRAIL-induced apoptosis. </LI> <LI> Apigenin transmits autophagy formation. </LI> </UL> </P>

Molecular chemotherapeutic potential of butein: A concise review

Jayasooriya, Rajapaksha Gedara Prasad Tharanga,Molagoda, Ilandarage Menu Neelaka,Park, Cheol,Jeong, Jin-Woo,Choi, Yung Hyun,Moon, Dong-Oh,Kim, Mun-Ock,Kim, Gi-Young Elsevier 2018 Food and chemical toxicology Vol.112 No.-

<P><B>Abstract</B></P> <P>Butein is a biologically active flavonoid isolated from the bark of <I>Rhus verniciflua</I> Stokes, which is known to have therapeutic potential against various cancers. Notably, butein inhibits cancer cell growth by inducing G<SUB>2</SUB>/M phase arrest and apoptosis. Butein-induced G<SUB>2</SUB>/M phase arrest is associated with increased phosphorylation of ataxia telangiectasia mutated (ATM) and Chk1/2, and consequently, with reduced cdc25C levels. In addition, butein-induced apoptosis is mediated through the activation of caspase-3, which is associated with changes in the expression of Bcl-2 and Bax proteins. Intriguingly, butein sensitizes cells to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis via ERK-mediated Sp1 activation, which promotes the transcription of specific death receptor 5. Butein also inhibits the migration and invasion of human cancer cells by suppressing nuclear factor-κB- and extracellular signal-regulated kinases 1/2-mediated expression of matrix metalloproteinase-9 and vascular endothelial growth factor. Additionally, butein downregulates the expression of human telomerase reverse transcriptase and causes a concomitant decrease in telomerase activity. These findings provide the basis for the pharmaceutical development of butein. The aim of this review is to provide an update on the mechanisms underlying the anticancer activity of butein, with a special focus on its effects on different cellular signaling cascades.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Butein induces apoptosis by activating Bax-caspase-3-PARP axis by PI3K/Akt-NF-κB axis through the inhibition of ROS generation. </LI> <LI> Butein induces G<SUB>2</SUB>/M phase cell cycle arrest by inhibiting ROS-mediated ATM-Chk1/2-Cdc25c-cdc2/cyclin B axis. </LI> <LI> Butein enhances TRAIL-mediated apoptosis by increasing DR5 expression through ERK-mediated Sp1 activation. </LI> <LI> Butein suppresses telomerase activity by inhibiting TERT expression and phosphorylation via c-Myc and PI3K/Akt. </LI> <LI> Butein attenuates angiogenesis, invasion/metastasis, and inflammation by suppressing the NF-κB signal pathway. </LI> </UL> </P>

TRAIL attenuates sulforaphane-mediated Nrf2 and sustains ROS generation, leading to apoptosis of TRAIL-resistant human bladder cancer cells

Jin, Cheng-Yun,Molagoda, Ilandarage Menu Neelaka,Karunarathne, Wisurumuni Arachchilage Hasitha Maduranga,Kang, Sang-Hyuck,Park, Cheol,Kim, Gi-Young,Choi, Yung Hyun Elsevier 2018 Toxicology and applied pharmacology Vol.352 No.-

<P><B>Abstract</B></P> <P>Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) can preferentially initiate apoptosis in malignant cells with minimal toxicity to normal cells. Unfortunately, many human cancer cells are refractory to TRAIL-induced apoptosis through many unknown mechanisms. Here, we report that TRAIL resistance can be reversed in human bladder cancer cell lines by treatment with sulforaphane (SFN), a well-known chemopreventive isothiocyanate in various cruciferous vegetables. Combined treatment with SFN and TRAIL (SFN/TRAIL) significantly induced apoptosis concomitant with activation of caspases, loss of mitochondrial membrane potential (MMP), Bid truncation, and induction of death receptor 5. Transient knockdown of <I>Bid</I> prevented collapse of MMP induced by SFN/TRAIL, consequently reducing apoptotic effects. Furthermore, SFN increased both the generation of reactive oxygen species (ROS) and the activation of nuclear factor erythroid 2-related factor 2 (Nrf2), which is an anti-oxidant enzyme. Interestingly, TRAIL effectively suppressed SFN-mediated nuclear translocation of Nrf2, and the period of ROS generation was more extended compared to that of treatment with SFN alone. In addition, silencing of <I>Nrf2</I> increased apoptosis in cells treated with SFN/TRAIL; however, blockade of ROS generation inhibited apoptotic activity. These data suggest that SFN-induced ROS generation promotes TRAIL sensitivity and SFN can be used for the management of TRAIL-resistant cancer.</P> <P><B>Highlights</B></P> <P> <UL> <LI> SFN sensitizes TRAIL-mediated apoptosis in TRAIL-resistant bladder cancer cells. </LI> <LI> SFN-mediated TRAIL sensitization requires Bid cleavage, leading to apoptosis. </LI> <LI> SFN enhances DR5 expression, resulting in cell death. </LI> <LI> SFN/TRAIL increases ROS generation in spite of Nrf2 activation. </LI> <LI> TRAIL helps to sustain SFN-mediated ROS generation. </LI> </UL> </P>

β-Hydroxyisovalerylshikonin promotes reactive oxygen species production in HCT116 colon cancer cells, leading to caspase-mediated apoptosis

Dilshara, Matharage Gayani,Karunarathne, Wisurumuni Arachchilage Hasitha Maduranga,Molagoda, Ilandarage Menu Neelaka,Kang, Chang-Hee,Jeong, Jin-Woo,Choi, Yung Hyun,Kim, Gi-Young Elsevier 2018 Revista brasileira de farmacognosia Vol.28 No.3

<P><B>Abstract</B></P> <P>Although β-hydroxyisovalerylshikonin is suggested as a potential therapeutic agent for preventing various cancers, the underlying molecular mechanisms are not completely understood. In the present study, we investigated whether β-hydroxyisovalerylshikonin enhances apoptosis by triggering reactive oxygen species production in colon cancer HCT116 cells. β-Hydroxyisovalerylshikonin significantly inhibited the viability of HCT116 cells with maximum inhibition at 4μM. Furthermore, treatment with β-hydroxyisovalerylshikonin subsequently increased sub-G<SUB>1</SUB> cells and annexin-V<SUP>+</SUP> cell population. Additionally, pretreatment with the caspase-8 inhibitor, z-IETD-fmk, and the caspase-9 inhibitor, z-LETD-fmk, significantly decreased β-hydroxyisovalerylshikonin-induced apoptosis, suggesting that β-hydroxyisovalerylshikonin promotes apoptosis through both the intrinsic and the extrinsic apoptotic pathways by activating caspase-8 and caspase-9. We also found that mitochondria played an important role in β-hydroxyisovalerylshikonin-mediated apoptosis via the intrinsic pathway. Accordingly, β-hydroxyisovalerylshikonin-induced reactive oxygen species production was evident after treatment with β-hydroxyisovalerylshikonin, and pretreatment with reactive oxygen species inhibitors, <I>N</I>-acetyl-<SMALL>L</SMALL>-cysteine and glutathione, significantly decreased β-hydroxyisovalerylshikonin-induced reactive oxygen species production, resulting in inhibition of apoptosis, which suggests that ROS generation is required for β-hydroxyisovalerylshikonin-mediated apoptosis. Taken together, these results demonstrated that the apoptotic effect of β-hydroxyisovalerylshikonin is enhanced in colon cancer HCT116 cells via reactive oxygen species generation and triggering of the caspase pathways, indicating that β-hydroxyisovalerylshikonin has potential as a therapeutic in the treatment of colon cancers.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

Camptothecin enhances c-Myc-mediated endoplasmic reticulum stress and leads to autophagy by activating Ca²⁺-mediated AMPK

Jayasooriya, Rajapaksha Gedara Prasad Tharanga,Dilshara, Matharage Gayani,Karunarathne, Wisurumuni Arachchilage Hasitha Maduranga,Molagoda, Ilandarage Menu Neelaka,Choi, Yung Hyun,Kim, Gi-Young Elsevier 2018 Food and chemical toxicology Vol.121 No.-

<P><B>Abstract</B></P> <P>Camptothecin (CPT) from <I>Camptotheca acuminate</I> was discovered for anticancer drugs, which targets topoisomease I. However, whether CPT regulates c-Myc expression has not been understood in endoplasmic reticulum (ER) stress and autophagy. In this study, we found that CPT enhanced c-Myc expression and that the transient knockdown of <I>c-Myc</I> abrogated reactive oxygen species (ROS) generation, which resulted in the accumulation of ER stress-regulating proteins, such as PERK, eIF2α, ATF4, and CHOP. Moreover, the transfection of <I>eIF2α</I>-targeted siRNA attenuated CPT-induced autophagy and decreased the levels of Beclin-1 and Atg7, which indicated that CPT upregulated ER stress-mediated autophagy. In addition, CPT phosphorylated AMPK in response to intracellular Ca<SUP>2+</SUP> release. Ca<SUP>2+</SUP> chelators, ethylene glycol tetraacetic acid and a CaMKII inhibitor, K252a, decreased CPT-induced Beclin-1 and Atg7, and downregulated AMPK phosphorylation, which suggested that CPT-induced Ca<SUP>2+</SUP> release leads to the activation of autophagy through CaMKII-mediated AMPK phosphorylation. CPT also phosphorylated JNK and activated the DNA-binding activity of AP-1; furthermore, knockdown of <I>JNK</I> abolished the expression level of Beclin-1 and Atg7, which implied that the JNK-AP-1 pathway was a potent mediator of CPT-induced autophagy. Our findings indicated that CPT promoted c-Myc-mediated ER stress and ROS generation, which enhances autophagy via the Ca<SUP>2+</SUP>-AMPK and JNK-AP-1 pathways.</P> <P><B>Highlights</B></P> <P> <UL> <LI> CPT induces c-Myc-mediated ROS formation, leading to CHOP expression. </LI> <LI> c-Myc positively regulates CPT-induced ER stress by increasing ROS generation. </LI> <LI> CPT promotes autophagy formation as a result of ER stress. </LI> <LI> CPT promotes autophagy through increased intracellular Ca2+ release. </LI> <LI> CPT induces JNK-mediated autophagy by enhancing AP-1 activity. </LI> </UL> </P>

Combined cerebral and somatic near-infrared spectroscopy oximetry monitoring during liver surgery: an observational and non-interventional study

Collin Yves,Hu Tina,Denault André,Fortier Annik,Beaubien-Souligny William,Lapointe Réal,Vandenbroucke-Menu Franck 대한마취통증의학회 2022 Korean Journal of Anesthesiology Vol.75 No.5

Background: Cerebral oximetry using near-infrared spectroscopy (NIRS) is used for monitoring cerebral oxygen saturation during cardiac surgery and is correlated with clinical outcomes. Our goal was to explore cerebral and somatic NIRS in liver resections as a predictor of post-operative complications. Methods: Prospective observational and non-interventional study from a tertiary care university hospital including adult patients undergoing liver resection monitored using NIRS at four sites before and during surgery. Those sites were: frontotemporal left and right zones, right thigh, and right arm. Anesthesiologists and surgeons were blinded to oximetry values. Correlations were assessed between baseline oximetry values and cerebro-somatic desaturation load (threshold of 80% from baseline) values with peri-operative events and complications. Results: Ninety patients were distributed equally among gender with a mean age of 59.7 ± 13.1 years. Lower baseline cerebral and/or somatic values were associated with increased risk of delirium, respiratory failure, surgical and renal complications, blood transfusions, and length of stay in the intensive care unit and in the hospital (P < 0.05). The severity of somatic desaturation below 80% was the only parameter associated with blood losses (P = 0.030) and length of hospital stay (P = 0.047). Conclusions: Cerebral and somatic desaturation does occur in liver resection and can be used simultaneously during liver surgery. Both baseline cerebral and somatic NIRS values are correlated with complications and outcomes. However, thigh desaturation appears more sensitive than cerebral NIRS values in predicting some of these complications.

Glutamine deprivation sensitizes human breast cancer MDA-MB-231 cells to TRIAL-mediated apoptosis

Dilshara, Matharage Gayani,Jeong, Jin-Woo,Prasad Tharanga Jayasooriya, Rajapaksha Gedara,Neelaka Molagoda, Ilandarage Menu,Lee, Seungheon,Park, Sang Rul,Choi, Yung Hyun,Kim, Gi-Young Elsevier 2017 Biochemical and biophysical research communication Vol. No.

<P><B>Abstract</B></P> <P>Tumor cell metabolism is a promising target for various cancer treatments. Apart from aerobic glycolysis, cancer cell growth is dependent on glutamine (Gln) supply, leading to their survival and differentiation. Therefore, we examined whether treatment with TNF-related apoptosis-inducing ligand (TRAIL) sensitizes MDA-MB-231 cells to apoptosis under Gln deprivation condition (TRAIL/Gln deprivation). Gln deprivation decreased cell proliferation as expected, but did not induce remarkable cell death. TRAIL/Gln deprivation, however, significantly increased growth inhibition and morphological shrinkage of MDA-MB-231 cells compared to those induced by treatment with either Gln deprivation or TRAIL alone. Moreover, TRAIL/Gln deprivation upregulated the apoptotic sub-G<SUB>1</SUB> phase accompanied with a remarkable decrease of pro-caspase-3, pro-caspase-9, and anti-apoptotic xIAP, and Bcl-2. Increased cleavage of PARP and pro-apoptotic Bid protein expression suggests that TRAIL/Gln deprivation triggers mitochondrion-mediated apoptosis in MDA-MB-231 cells. Additionally, TRAIL/Gln deprivation upregulated the expression of endoplasmic reticulum (ER) stress markers such as ATF4 and phosphorylated eIF2α, thereby enhancing the C/EBP homologous protein (CHOP) protein level. Transient knockdown of <I>CHOP</I> partically reversed TRAIL/Gln deprivation-mediated apoptosis. Accordingly, TRAIL/Gln deprivation enhanced the expression of death receptor 5 (DR5) and transient knockdown of <I>DR5</I> completely restored TRAIL/Gln deprivation-mediated apoptosis. Taken together, our results suggest that Gln deprivation conditions can be used for the development of new therapies for TRAIL-resistant cancers.</P>