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정영표,이동렬,손용,김태요,윤재승,송윤강,김명선,박래길 圓光大學校 醫科學硏究所 1999 圓光醫科學 Vol.15 No.2
Background: The effect of opioids on nitric oxide (NO)- and peroxynitrite-induced neuronal cell death is largely unknown. In the present study, we examined the effect of morphine on NO- and peroxynitrite-induced cell death using a human neuroblastoma SH-SY5Y cell line, which abundantly expresses μ, δ, k-opioid receptors. Methods: The cultured cells were pretreated with morphine and exposed to 3-morpholinosydnonimine (SIN-1) that simultaneously generates NO and superoxide, thus possibly forming peroxynitrite. The cell damage was assessed by using MTT assay ana crystal violet staining. Exposure of the cells to SIN-1 for 24 hours induced apoptotic cell death, as evaluated by the occurrence of morphological nuclear changes characteristics of apoptosis using 4', 6-diamidino-2-phenylindole (DAPI) and measurement of pro-apoptotic protease, caspase-3, activity. Results: Pretreatment of SH-SY5Y with morphine, significantly inhibited the apoptotic cell death in a dose-dependent manner. Morphine also inhibited SIN-1-induced proapoptotic protease, caspase-3, activity in a dose-dependent manner. However, naloxone (20 μM) hardly antagonized the effect of morphine in SIN-1-induced cell death. The selective ligands for opioid receptor subtypes, [D-Ala^2, N-Me-Phe^4, Gly-ol^5]enkephalin (DAMGO, μ-opioid receptor agonist), [D-Pen^2.5]enkephalin (DPDPE, δ-opioid receptor agonist) and U-69593 (k-opioid receptor agonist) at the concentration of 10 μM did not prevent the cell death induced by SIN-1. PI3-kinase inhibitors, Wortmannin and LY294002, did not inhibit the action of morphine on apoptotic cell death. The neuroblastoma cells treated with morphine significantly elevated glutathione levels (GSH). Conclusions: The present study showed that morphine protected human neuroblastoma cell line, SH-SY45Y, from the peroxynitrite-induced apoptotic cell death through elevated GSH levels. However, it is suggested that the elevation of GSH by morphine is not via the activation of opioid receptors and/or PI3-kinase pathway but via other unknown mechanism.
Kim, Myung-Sunny,Kim, Soon-Hee,Park, Su-Jin,Sung, Mi Jung,Park, Jaeho,Hwang, Jin-Taek,Yang, Hye Jeong,Kim, Sunmi,Seo, Daebang,Shin, Song Seok,Hur, Haeng Jeon Elsevier 2017 Journal of Functional Foods Vol.35 No.-
<P><B>Abstract</B></P> <P>This study investigated the effect and the underlying mechanism of ginseng berry (GB) in a mouse model of type 2 diabetes, supplied with 0.05% or 0.1% dietary GB for 12weeks. GB significantly improved hyperglycemia and insulin resistance, as demonstrated by the blood glucose and insulin levels, HOMA-IR, and GTT. Moreover, the expression of gluconeogenic genes such as PEPCK and G6Pase and the hepatic metabolites involved in the pathway of gluconeogenesis, such as glucose-6-phosphate and dihydroxyacetone phosphate, were significantly reduced by GB. Hepatic steatosis was also significantly ameliorated; TG content and expression of lipogenic enzymes and transcriptional factors such as FAS, ACC, and SREBP1 were reduced by GB. Simultaneously, AMPK phosphorylation was increased both in fatty liver and in lipid-accumulated HepG2 cells by GB. In conclusion, GB improved hyperglycemia by downregulating hepatic glucose production and hepatic steatosis, and AMPK appeared to be an important regulator of these effects.</P> <P><B>Highlights</B></P> <P> <UL> <LI> GB significantly improves obesity-induced hyperglycemia and insulin resistance. </LI> <LI> Anti-diabetic effects of ginseng berry is mediated by downregulating hepatic glucose production and hepatic steatosis. </LI> <LI> AMPK may be an important contributing regulator in the GB-mediated suppression of hepatic glucose production. </LI> </UL> </P>
Ginseng for managing menopause symptoms
Myung-Sunny Kim,Hyun-Ja Lim,Hye Jeong Yang,Myeong Soo Lee,Byung-Cheul Shin,Edzard Ernst 고려인삼학회 2013 Journal of Ginseng Research Vol.37 No.1
The aim of this review was to assess the effectiveness of ginseng as a treatment option for managing menopause symptoms. We searched the literature using 11 databases from their inception to 26 September 2012 and included all randomised clinical trials (RCTs) that compared any type of ginseng to a placebo controls in postmenopausal women. The methodological quality of all studies was assessed using a Cochrane risk of bias tool. Four RCTs met our inclusion criteria. Most RCTs had high risk of bias. One RCT showed that Korean red ginseng (KRG) significantly improved sexual arousal and global health compared with placebo. Another RCT reported the superiority of KRG over placebo for treating menopause symptoms on Kupperman’s index and menopausal rating score. The third RCT failed to show a significant effect of KRG on hot flash frequency compared to placebo. The fourth RCT found beneficial effects of ginseng compared to placebo on depression and well-being. In conclusion, the evidence on ginseng as an effective treatment for managing menopause symptoms is limited. Most of the RCTs are burdened with a high risk of bias. Thus firm conclusions cannot be drawn. Rigorous studies seem warranted.
Kim, Do-Sung,Kwon, Dae-Young,Kim, Myung-Sunny,Kim, Hye Kyung,Lee, Yong Chul,Park, Seong Ju,Yoo, Wan Hee,Chae, Soo-Wan,Chung, Myoung-Ja,Kim, Hyung-Ryong,Chae, Han-Jung Pharmaceutical Society of Great Britain 2010 Journal of pharmacy and pharmacology Vol.62 No.2
<P>Objectives We have investigated whether endoplasmic reticulum stress and Bcl-2 proteins were linked to the protective effect exerted by flavonoids on ischaemia/reperfusion-induced cardiac damage. Methods Cell viability and immunoblotting were performed. Key findings H9c2 cardiac muscle cells were exposed to flavonoids such as biochanin A, daidzein, genistein, luteolin, quercetin and rutin, followed by ischaemia 12 h/reperfusion 4 h. The flavonoids protected against cell death induced by ischaemia/reperfusion. Flavonoid treatment significantly increased the expression level of the anti-apoptotic protein, Bcl-2, but decreased that of the proapoptotic protein, Bax. The flavonoids down-regulated the expression levels of endoplasmic reticulum stress proteins, glucose-regulated protein-78, activating transcription factor 6alpha, X-box binding protein 1, inositol-requiring protein-1, phosphor-eukaryotic initiation factor 2alpha, and C/EBP-homologous protein. Conclusions This study suggested that the protective mechanisms of flavonoids included regulation of Bcl-2/Bax proteins as well as the endoplasmic reticulum stress proteins.</P>
Kim, Sung Hee,Hur, Haeng Jeon,Yang, Hye Jeong,Kim, Hyun Jin,Kim, Min Jung,Park, Jae Ho,Sung, Mi Jeong,Kim, Myung Sunny,Kwon, Dae Young,Hwang, Jin-Taek Hindawi Publishing Corporation 2013 Evidence-based Complementary and Alternative Medic Vol.2013 No.-
<P>The antidiabetic effect of the <I>Citrus junos</I> Tanaka (also known as yuja or yuzu) was examined. Ethanol extract of yuja peel (YPEE) significantly stimulated 2-[<I>N</I>-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose (2-NBDG) uptake in C2C12 myotubes. However, ethanol extract of yuja pulp (YpEE) and water extract of yuja peel (YPWE) or pulp (YpWE) did not stimulate glucose uptake. In addition, peroxisome proliferator-activated receptor gamma (PPAR-<I>γ</I>) and AMP-activated protein kinase (AMPK) activities were increased by YPEE in a dose-dependent manner. Pretreatment of AMPK inhibitor decreased the glucose uptake stimulated by YPEE in C2C12 myotubes. We confirmed the anti-diabetic effect of YPEE in mice fed a high fat-diet (HFD). Compared with control mice on a normal diet (ND), these mice showed increased body weight, liver fat, insulin resistance, triacylglycerol (TG), and total cholesterol content. Addition of 5% YPEE significantly reduced the weight gain and rise in liver fat content, serum triacylglycerol (TG), total cholesterol, and insulin resistance found in mice fed a high-fat diet (HFD). Moreover, YPEE reduced the secretion of HFD-induced adipocytokines such as leptin and resistin. YPEE also resulted in increased phosphorylation of AMPK in muscle tissues. These results suggest that ethanol extract of yuja peel exerts anti-diabetic effects via AMPK and PPAR-<I>γ</I> in both cell culture and mouse models.</P>
Effects of Kimchi on human health : A protocol of systematic review of controlled clinical trials
Kim, Myung-Sunny,Yang, Hye Jeong,Kim, Soon-Hee,Lee, Hye Won,Lee, Myeong Soo Williams & Wilkins Co 2018 Medicine Vol.97 No.13
<P><B>Abstract</B></P><P><B>Background:</B></P><P>Kimchi, a traditional, fermented Korean food that is consumed daily, has been recognized as a health food due to its beneficial effects on human health. The aim of this overview is to critically evaluate all clinical trials of the use of Kimchi in the treatment of any condition or symptom.</P><P><B>Methods and analysis:</B></P><P>Eight databases will be searched from inception until March 2018. We will include all prospective trials, including randomized controlled trials (RCTs), non-RCTs, and uncontrolled trials. The methodological quality of the trials will be assessed using Cochrane risk of bias (ROB) assessment tool and ROB in nonrandomized studies-I for RCTs and non-RCTs, respectively.</P><P><B>Ethics and dissemination:</B></P><P>Ethical approval will not be required, given that this protocol is for a systematic review. The full systematic review will be published in a peer-reviewed journal. The review will also be disseminated electronically and in print. Updates of the review will be conducted to inform and guide health care practice and policy.</P><P><B>Trial registration number:</B></P><P>PROSPERO 2018 CRD42018087375</P>
Ginseng for managing menopause symptoms: a systematic review of randomized clinical trials
Kim, Myung-Sunny,Lim, Hyun-Ja,Yang, Hye Jeong,Lee, Myeong Soo,Shin, Byung-Cheul,Ernst, Edzard The Korean Society of Ginseng 2013 Journal of Ginseng Research Vol.37 No.1
The aim of this review was to assess the effectiveness of ginseng as a treatment option for managing menopause symptoms. We searched the literature using ll databases from their inception to 26 September 2012 and included all randomised clinical trials (RCTs) that compared any type of ginseng to a placebo controls in postmenopausal women. The methodological quality of all studies was assessed using a Cochrane risk of bias tool. Four RCTs met our inclusion criteria. Most RCTs had high risk of bias. One RCT showed that Korean red ginseng (KRG) significantly improved sexual arousal and global health compared with placebo. Another RCT reported the superiority of KRG over placebo for treating menopause symptoms on Kupperman's index and menopausal rating score. The third RCT failed to show a significant effect of KRG on hot flash frequency compared to placebo. The fourth RCT found beneficial effects of ginseng compared to placebo on depression and well-being. In conclusion, the evidence on ginseng as an effective treatment for managing menopause symptoms is limited. Most of the RCTs are burdened with a high risk of bias. Thus firm conclusions cannot be drawn. Rigorous studies seem warranted.