Ginsenoside Rg1 activates ligand-independent estrogenic effects via rapid estrogen receptor signaling pathway

Quan-Gui Gao,Li-Ping Zhou,Vien Hoi-Yi Lee,Hoi-Yi Chan,Cornelia Wing-Yin Man,Man-Sau Wong 고려인삼학회 2019 Journal of Ginseng Research Vol.43 No.4

Background: Ginsenoside Rg1 was shown to exert ligand-independent activation of estrogen receptor(ER) via mitogen-activated protein kinaseemediated pathway. Our study aimed to delineate themechanisms by which Rg1 activates the rapid ER signaling pathways. Methods: ER-positive human breast cancer MCF-7 cells and ER-negative human embryonic kidneyHEK293 cells were treated with Rg1 (10 12M, 10 8M), 17ß-estradiol (10 8M), or vehicle. Immunoprecipitationwas conducted to investigate the interactions between signaling protein and ER in MCF-7 cells. To determine the roles of these signaling proteins in the actions of Rg1, small interfering RNA or theirinhibitors were applied. Results: Rg1 rapidly induced ERa translocation to plasma membrane via caveolin-1 and the formation ofsignaling complex involving linker protein (Shc), insulin-like growth factor-I receptor, modulator ofnongenomic activity of ER (MNAR), ERa, and cellular nonreceptor tyrosine kinase (c-Src) in MCF-7 cells. The induction of extracellular signal-regulated protein kinase and mitogen-activated protein kinase kinase(MEK) phosphorylation in MCF-7 cells by Rg1 was suppressed by cotreatment with small interferingRNA against these signaling proteins. The stimulatory effects of Rg1 on MEK phosphorylation in thesecells were suppressed by both PP2 (Src kinase inhibitor) and AG1478 [epidermal growth factor receptor(EGFR) inhibitor]. In addition, Rg1-induced estrogenic activities, EGFR and MEK phosphorylation in MCF-7 cells were abolished by cotreatment with G15 (G protein-coupled estrogen receptor-1 antagonist). Theincrease in intracellular cyclic AMP accumulation, but not Ca mobilization, in MCF-7 cells by Rg1 could beabolished by G15. Conclusion: Ginsenoside Rg1 exerted estrogenic actions by rapidly inducing the formation of ER containingsignalosome in MCF-7 cells. Additionally, Rg1 could activate EGFR and c-Src ER-independentlyand exert estrogenic effects via rapid activation of membrane-associated ER and G protein-coupled estrogenreceptor.

The therapeutic efficacy of water-soluble coenzyme Q10 in an experimental model of tacrolimus-induced diabetes mellitus

Yi Quan,Kang Luo,Sheng Cui,Sun Woo Lim,신유진,Eun Jeong Ko,Ju Hwan Kim,Sang J. Chung,Soo Kyung Bae,Byung Ha Chung,Chul Woo Yang 대한내과학회 2020 The Korean Journal of Internal Medicine Vol.35 No.6

Background/Aims: Coenzyme Q10 (CoQ10) has antioxidant effects and is commercially available and marketed extensively. However, due to its low bioavailability, its effects are still controversial. We developed a water-soluble CoQ10-based micelle formulation (CoQ10-W) and tested it in an experimental model of tacrolimus (TAC)-induced diabetes mellitus (DM). Methods: We developed CoQ10-W from a glycyrrhizic-carnitine mixed layer CoQ10 micelle preparation based on acyltransferases. TAC-induced DM rats were treated with either lipid-soluble CoQ10 (CoQ10-L) or CoQ10-W for 4 weeks. Their plasma and pancreatic CoQ10 concentrations were measured using liquid chromatography- tandem mass spectrometry. The therapeutic efficacies of CoQ10-W and CoQ10-L on TAC-induced DM were compared using functional and morphological parameters and their effects on cell viability and reactive oxygen species (ROS) production were also evaluated in cultured rat insulinoma cells. Results: The plasma CoQ10 level was significantly increased in the CoQ10-W group compared to that in the CoQ10-L group. Intraperitoneal glucose tolerance tests and glucose-stimulated insulin secretion revealed that CoQ10-W controlled hyperglycemia and restored insulin secretion significantly better than CoQ10-L. The TAC-mediated decrease in pancreatic islet size was significantly attenuated by CoQ10-W but not by CoQ10-L. TAC-induced oxidative stress and apoptosis were significantly more reduced by CoQ10-W than CoQ10-L. Electron microscopy revealed that CoQ10-W restored TAC-induced attenuation in the number of insulin granules and the average mitochondrial area, unlike CoQ10-L. In vitro studies showed that CoQ10-L and CoQ10-W both improved cell viability and reduced ROS production in TAC-treated islet cells to a similar extent. Conclusions: CoQ10-W has better therapeutic efficacy than CoQ10-L in TAC-induced DM.

Assessment of nephrotoxicity of herbal medicine containing aristolochic acid in mice

Yi Quan,Long Jin,Kang Luo,Jian Jin,Sun Woo Lim,신유진,Eun Jeong Ko,Byung Ha Chung,Chul Woo Yang 대한내과학회 2020 The Korean Journal of Internal Medicine Vol.35 No.2

Background/Aims: It is undetermined if herbal medicines (HM) containing aristolochic acid (AA)-containing have similar nephrotoxicity to AA itself. Methods: We administered HM containing a high concentration of AA for 5 days (short-term study) or a low concentration of AA for 30 days (long-term study) to C57BL/6 mice; for comparison, same dose of AA compound was used as controls. Results: The nephrotoxicity in the HM- and AA-treated mice was compared in terms of renal function, histopathology, oxidative stress, apoptotic cell death, and mitochondrial damage. Short-term HM treatment resulted in acute kidney injury (marked renal dysfunction, acute tubular necrosis, and neutrophil gelatinase-associated lipocalin [NGAL] expression) in which the severity of renal dysfunction and histopathology was comparable with that induced by the administration of AA alone. Long-term HM treatment resulted in features of chronic kidney disease (CKD, mild renal dysfunction and tubular atrophy and dilatation). No significant differences in these parameters were observed between the HM- and AA-treated mice. HM-induced oxidative stress (8-hydroxy-2’-deoxyguanosine and manganese- dependent superoxide dismutase expression) and apoptotic cell death (terminal deoxynucleotidyl transferase dUTP nick end labelling [TUNEL]-positive cells and active caspase-3 expression) were similar in HM- and AA-treated mice in the short-term and long-term studies. Mitochondrial injury, evaluated by electron microscopy, was also similar in HM- and AA-treated mice in the short-term and long-term studies. Conclusions: The nephrotoxic potential of HM containing AA was similar to that of AA itself.

Ginsenoside Rg1 activates ligand-independent estrogenic effects via rapid estrogen receptor signaling pathway

Gao, Quan-Gui,Zhou, Li-Ping,Lee, Vien Hoi-Yi,Chan, Hoi-Yi,Man, Cornelia Wing-Yin,Wong, Man-Sau The Korean Society of Ginseng 2019 Journal of Ginseng Research Vol.43 No.4

Background: Ginsenoside Rg1 was shown to exert ligand-independent activation of estrogen receptor (ER) via mitogen-activated protein kinase-mediated pathway. Our study aimed to delineate the mechanisms by which Rg1 activates the rapid ER signaling pathways. Methods: ER-positive human breast cancer MCF-7 cells and ER-negative human embryonic kidney HEK293 cells were treated with Rg1 ($10^{-12}M$, $10^{-8}M$), $17{\beta}$-estradiol ($10^{-8}M$), or vehicle. Immunoprecipitation was conducted to investigate the interactions between signaling protein and ER in MCF-7 cells. To determine the roles of these signaling proteins in the actions of Rg1, small interfering RNA or their inhibitors were applied. Results: Rg1 rapidly induced $ER{\alpha}$ translocation to plasma membrane via caveolin-1 and the formation of signaling complex involving linker protein (Shc), insulin-like growth factor-I receptor, modulator of nongenomic activity of ER (MNAR), $ER{\alpha}$, and cellular nonreceptor tyrosine kinase (c-Src) in MCF-7 cells. The induction of extracellular signal-regulated protein kinase and mitogen-activated protein kinase kinase (MEK) phosphorylation in MCF-7 cells by Rg1 was suppressed by cotreatment with small interfering RNA against these signaling proteins. The stimulatory effects of Rg1 on MEK phosphorylation in these cells were suppressed by both PP2 (Src kinase inhibitor) and AG1478 [epidermal growth factor receptor (EGFR) inhibitor]. In addition, Rg1-induced estrogenic activities, EGFR and MEK phosphorylation in MCF-7 cells were abolished by cotreatment with G15 (G protein-coupled estrogen receptor-1 antagonist). The increase in intracellular cyclic AMP accumulation, but not Ca mobilization, in MCF-7 cells by Rg1 could be abolished by G15. Conclusion: Ginsenoside Rg1 exerted estrogenic actions by rapidly inducing the formation of ER containing signalosome in MCF-7 cells. Additionally, Rg1 could activate EGFR and c-Src ER-independently and exert estrogenic effects via rapid activation of membrane-associated ER and G protein-coupled estrogen receptor.

CONTINUOUS HOPFIELD NEURAL NETWORK FOR OFDM SIGNAL DETECTION UNDER PHASE NOISE

Qing-Yi Quan,Jung-Gon Kim 대한전자공학회 2006 ITC-CSCC :International Technical Conference on Ci Vol.2006 No.3

A Novel Multi-User Signal Detector with Neural Computing

Quing Yi Quan,Jian Dong Hu 대한전자공학회 1998 CDMA International Conference and Exhibition Vol.- No.-

中國 會計制度의 發展史的 接近

權藝卿(Quan Yi-qing),崔震賢(Choi Jin-hyeon) 한국국제회계학회 2007 국제회계연구 Vol.0 No.17

중국의 회계는 그 어원으로 보아 요순시대(BC 2000경)로부터 발전된 것으로 보이나 부기가 일반화된 것은 BC475년경 춘추전국시대의 종료 이후 성립된 봉건사회라고 할 수 있다. 중국에서 복식주기에 의한 회계의 시초는 청나라 말기 해외 유학생의 귀국으로 전파된 것으로 보인다. 현재의 중국회계는 러시아 회계의 발전과 약간의 시차를 두고 봉건자본주의회계-사회주의계획경제회계-사회주의시장경제회계의 순서로 변화ㆍ발전되어 왔다. 공산주의 정권의 초기에는 봉건자본주의회계를 원용했기 때문에 사회주의 개조과정에 적합하지 못했다. 따라서 1953년으로부터 1978년까지 형성된 통일회계제도는 중국의 특수한 역사조건하에서 고도로 집중된 계획경제모형아래 건립하였다. 당시 중국의 경제규모가 크지 않고, 그 구조가 간단하여 중앙 집중ㆍ통일의 회계관리 방식에 특별한 결점이 나타나지 않았지만 경제규모의 확대에 따라 과거 회계제도의 부적응이라는 문제점이 부각되었다. 1978년 대외개방이후 주로 중국 영내에 해외직접투자가 급증하면서 이런 기업들을 위해 기업의 입장에서 미시적 차원의 영미식 회계를 필요로 하였다. 이러한 필요성 때문에 도입된 것이 1985년도의 「중화인민공화국회계법」 및 「중외합작경영기업회계제도」이다. 특히 「중외합작경영기업회계제도」는 영미식 회계에 의한 국제적 회계관례에 접근하기 시작한 최초의 회계제도이다. 2000년에 중국이 회계제도를 개혁한 이유는 1998년의 기업회계준칙과 주식유한회사회계제도 중 구체회계준칙 사이의 모순점에 대하여 비록 일부의 보충 규정을 공포하여 조정하였지만 구체적 집행과정에서 일부 주식유한회사의 재무상태와 경영성과 및 현금흐름을 허위로 보고할 수 있는 여지가 남아 있었다. 따라서 2006년의 제2차 회계제도의 개혁은 한마디로 세계화와 개방경제에 알맞은 회계제도의 도입이후 국제회계기준에 근접하는 중국 회계기준의 마련을 위해서 「실질주의」와 「공시의 확대」를 위한 개혁을 단행했다. 한마디로 말하면 2006년 2월의 회계제도개혁은 업종별회계제도의 보류와 회계제도의 국제화라고 요약해 말할 수 있다. 현재 중국의 회계제도 개혁은 대외적 개방에 박차를 가하면서 경제개발을 꾀하고 내부적으로 빈부격차의 문제를 완화시켜야 하는 과제를 안고 있기 때문에 중국의 경제발전단계나 사회주의시장경제라는 중국적 특성과 경제의 국제화 관계를 고려하여 중국내회계제도와 국제회계기준 간의 상호관계를 규정하여 병존시키거나 통일시켜야 할 것이다. The Chinese accounting existed as early as 2000 B.C accompanied by audit function and independent public officials. But Chinese accounting of the double-entry system was adopted in Qing-dynasty. The Chinese accounting based on the private ownership at the first stage of socialism in China existed. The origin of Chinese accounting for social-planning established at year 1953. Which was modified Soviet accounting system. Chinese accounting for social-planning was applied at all economic sectors. After adopting market-based socialism. the revolution of Chinese accounting was changed at, year 1985. 1992, 2000, 2006. The Modern Chinese accounting standards is similar to International Accounting standards. But it is necessary to consider problems of the individual income gap in domestic and globalism of Chinese economy in the revolution of Chinese accounting. So, the Chinese accounting standards changed by fitting to International Accounting standards is not so good all aspects.

동반성장 우수 대기업의 재무적 특성에 관한 연구

권예경(Quan Yi-qing) 한국국제회계학회 2015 국제회계연구 Vol.0 No.61

중국회계준칙의 제정규범과 국제재무보고기준과의 비교

권예경(Quan, Yi Qing) 한국국제회계학회 2013 국제회계연구 Vol.0 No.49

중국의 국제회계기준과의 수렴에 있어서도 정치경제적 차원에서 보면 65개 다민족 국가로 사회주의 시장경제라는 특성을 갖고 있다. 또 한편으로는 세계의 중심이라는 중화사상의 자긍심을 갖고 있다. 이러한 정치경제적 상황과 자긍심은 1개의 규율, 2개 원칙, 3개의 이념에 의해서 회계기준의 설정에서도 그대로 반영되어 있다. 예컨대, 준칙의 내용에서 뿐만 아니라 회계용어(자산부채표, 권익, 권채발생주의, 지속경영가설)에서도 이런 규범에 입각해서 중국의 경제사정과 고유의 자긍심을 반영하고 있다. 국제회계기준과 비교해보면 중국의 기업회계준칙은 부문규칙의 범주에 속하여 재정부의 법률 규범이기 때문에 법률적 강제력을 갖고 있다. 이러한 중국 회계준칙에서 ‘재무보고를 위한 개념체계’를 기본준칙으로 하고 ‘기준서’에 해당하는 부분을 구체준칙이라 한다. 기본준칙의 면에서 보면, 중국의 경우에 회계의 수탁책임을 국제회계기준에서 보다 더 중요시 하고 다음과 같은 점에서도 차이가 있다. 첫째, 국제회계기준위원회의 체계가 재무제표의 목표, 기본가정 부분을 단독으로 열거하지만 중국의 기본준칙이 총칙부분에서 재무제표의 목표와 기본 가정을 규정하고 있다. 둘째, 국제회계기준위원회의 체계는 재무제표의 요소가 전체로서 그것의 정의, 인식, 측정을 규범에 맞도록 하고 있지만 중국기업회계준칙은 각 요소을 단독으로 열거하여 규범에 맞도록 하고 있다. 셋째, 국제회계기준위원회의 체계는 자본과 자본유지개념을 일개 부분으로 간주하지만 중국기업회계준칙은 그것을 언급하지 않고 있다. 구체준칙의 면에서 중국회계준칙을 국제회계기준과 비교해 보면, 중국에서는 공정가치모형을 일정 조건을 만족하는 경우에만 적용할 수 있고, 대손충당금、단기투자감가충당금、재고자산감가충당금、장기투자감가충당금고정자산감가충당금、무형자산간가충당금、건설중인자산감가충당금과 위탁차관감가충당금의 설정으로 일단 손실로 인식하면 이후에 이득으로 환수된다고 하더라도 충당금환입(이득)으로 인식하지 못하도록 규정하고 있다. 그 외에도 고정자산과 무형자산에 재평가모형과 관련이 있는 규정이 없으며 현금선택권이 있는 주식기준 보상 규정이 없다. 또, 현금흐름표의 작성에 직접법만을 허용하고 있는 차이점이 있다. The Chinese Accounting Standard are similar to International Financial Reporting Standard altogether. Nevertheless, Chinese Accounting Standard is not different from IFRS so much. I found a few differentia between IFRS and CAS. That are stewardship emphasized, monetary assumption in CAS. I found some different image from the same english words such as going concerns postulate(繼續經營), accounting entity(經營實體),owners`right(所有者權益), balance sheet(資産負債表), income statement(利潤表), revenues(收入), accrual basis(權債發生主義), measuring(計量), recognition(確認) and so on in CAS. The objectives of financial statements in IFRS is to provide useful information about economic entities that is intended to be useful in making economic decisions. but the objectives of financial accounting in Chinese Accounting Standard are to provide useful information about economic entities and to ensure the stewardship responsibilities of management. The differentia of accounting standard and terms" nuance are based on their own culture. Nevertheless, Chinese Accounting Standard and International Accounting Standard will be astringent in future. there are not capital maintenance concept in CAS and revaluation model is not applied in measuring fixed asset and intangible asset. Fair value measurement can be applied under a few conditions strictly and direct method can be applied only on cash-flow statement in CAS.

Role of hypothalamic proopiomelanocortin neuron autophagy in the control of appetite and leptin response.

Quan, Wenying,Kim, Hyun-Kyong,Moon, Eun-Yi,Kim, Su Sung,Choi, Cheol Soo,Komatsu, Masaaki,Jeong, Yeon Taek,Lee, Moon-Kyu,Kim, Kwang-Won,Kim, Min-Seon,Lee, Myung-Shik Association for the Study of Internal Secretions 2012 Endocrinology Vol.153 No.4

<P>Autophagy is a catabolic cellular process involving the degradation of the cell's own components. Although the role of autophagy of diverse tissues in body metabolism has been investigated, the importance of autophagy in hypothalamic proopiomelanocortin (POMC) neurons, key regulators of energy balance, has not been addressed. The role of autophagy in leptin sensitivity that is critical for the control of body weight and appetite has also not been investigated. We produced mice with specific deletion of autophagy-related 7 (Atg7), an essential autophagy gene, in hypothalamic POMC neurons (Atg7(δPOMC) mice). Atg7 expression was deficient in the arcuate nucleus of the hypothalamus of Atg7(δPOMC) mice. p62, a specific substrate of autophagy, accumulated in the hypothalamus of Atg7(δPOMC) mice, which colocalized with ubiquitin. Atg7(δPOMC) mice had increased body weight due to increased food intake and decreased energy expenditure. Atg7(δPOMC) mice were not more prone to diet-induced obesity compared with control mice but more susceptible to hyperglycemia after high-fat diet. The ability of leptin to suppress fasting-elicited hyperphagia and weight gain during refeeding was attenuated in Atg7(δPOMC) mice. Deficient autophagy did not significantly affect POMC neuron number but impaired leptin-induced signal transducer and activation of transcription 3 activation. Our findings indicate a critical role for autophagy of POMC neurons in the control of energy homeostasis and leptin signaling.</P>