http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
( Laura Amina Dahili ),( Endre Nagy ),( Tivadar Feczko ) 한국미생물 · 생명공학회 2017 Journal of microbiology and biotechnology Vol.27 No.4
Horseradish peroxidase (HRP) catalyzes the oxidation of aromatic compounds by hydrogen peroxide via insoluble polymer formation, which can be precipitated from the wastewater. For HRP immobilization, poly(lactic-co-glycolic acid) (PLGA) fine carrier supports were produced by using the Nano Spray Dryer B-90. Immobilized HRP was used to remove the persistent 2,4- dichlorophenol from model wastewater. Both extracted (9-16 U/g) and purified HRP (11- 25 U/g) retained their activity to a high extent after crosslinking to the PLGA particles. The immobilized enzyme activity was substantially higher in both the acidic and the alkaline pH regions compared with the free enzyme. Optimally, 98% of the 2,4-dichlorophenol could be eliminated using immobilized HRP due to catalytic removal and partly to adsorption on the carrier supports. Immobilized enzyme kinetics for 2,4-dichlorophenol elimination was studied for the first time, and it could be concluded that competitive product inhibition took place.
Programmed cell death in alcohol-associated liver disease
Tatsunori Miyata,Laura E. Nagy 대한간학회 2020 Clinical and Molecular Hepatology(대한간학회지) Vol.26 No.4
Alcohol-associated liver disease (ALD), which ranges from mild disease to alcohol-associated hepatitis and cirrhosis, is the most prevalent type of chronic liver disease and a leading cause of morbidity and mortality worldwide. Accumulating evidence reveals that programmed cell death (PCD) plays a crucial role in progression of ALD involving crosstalk between hepatocytes and immune cells. Multiple pathways of PCD, including apoptosis, necroptosis, autophagy, pyroptosis and ferroptosis, are reported in ALD. Interestingly, PCD pathways are intimately linked and interdependent, making it difficult to therapeutically target a single pathway. This review clarifies the multiple types of PCD occurring in liver and focuses on crosstalk between hepatocytes and innate immune cells in ALD.
Kim, Mi Jin,Nagy, Laura E.,Park, Pil-Hoon American Society for Pharmacology and Experimental 2014 Molecular pharmacology Vol.86 No.3
<P>Adiponectin, an adipokine predominantly secreted from adipocytes, has been shown to play protective roles against chronic alcohol consumption. Although excessive reactive oxygen species (ROS) production in macrophages is considered one of the critical events for ethanol-induced damage in various target tissues, the effect of adiponectin on ethanol-induced ROS production is not clearly understood. In the present study, we investigated the effect of globular adiponectin (gAcrp) on ethanol-induced ROS production and the potential mechanisms underlying these effects of gAcrp in macrophages. Here we demonstrated that gAcrp prevented ethanol-induced ROS production in both RAW 264.7 macrophages and primary murine peritoneal macrophages. Globular adiponectin also inhibited ethanol-induced activation of NADPH oxidase. In addition, gAcrp suppressed ethanol-induced increase in the expression of NADPH oxidase subunits, including Nox2 and p22<SUP>phox</SUP>, via modulation of nuclear factor-<I>κ</I>B pathway. Furthermore, pretreatment with compound C, a selective inhibitor of AMPK, or knockdown of AMPK by small interfering RNA restored suppression of ethanol-induced ROS production and Nox2 expression by gAcrp. Finally, we found that gAcrp treatment induced phosphorylation of liver kinase B1 (LKB1), an upstream signaling molecule mediating AMPK activation. Knockdown of LKB1 restored gAcrp-suppressed Nox2 expression, suggesting that LKB1/AMPK pathway plays a critical role in the suppression of ethanol-induced ROS production and activation of NADPH oxidase by gAcrp. Taken together, these results demonstrate that globular adiponectin prevents ethanol-induced ROS production, at least in part, via modulation of NADPH oxidase in macrophages. Further, LKB1/AMPK axis plays an important role in the suppression of ethanol-induced NADPH oxidase activation by gAcrp in macrophages.</P>
( Mi Jin Kim ),( Laura E. Nagy ),( Pil Hoon Park ) 영남대학교 약품개발연구소 2015 영남대학교 약품개발연구소 연구업적집 Vol.25 No.-
Adiponectin,an adipokine predominantly secreted from adipo-cytes,has been shiwn to play protective roles against chronic alcohol consumption. Although escessive oxygen species(ROS)production in macrophages is considered one of the critical events for ethanol-induced damage in various target tissues,the effect of adiponectin on ethanol-induced ROS production is not clearly understood. In the present study,we investigated the effect of globular adiponectin (gAcrp) on ethanol-induced ROS production and the potential mechanisms underlying these effects of gAcrp in macrophages. Here we demonstrated that gAcrp prevented ethanol-induced ROS production is not clearly understood.in the present study,we investigated the effect of globular adiponectin (gAcrp) on ethanol-induced ROS production and the potential mechanisms underlying these effects of gAcrp in macrophages.Here we demonstrated that gAcrp prevented ethanol-induced ROS production in both RAW 264.7 ,macrophages and primary murine peritoneal macrophages. Globular adiponectin also inhibited ethanol-induced activation df NADPH oxidase.In addition,gAcrp suppressed ethanol-induced increase in the expression of NADPH oxidase subunits,including Nox2 and P22phox,via modulation ofnuclear factor-kB pathway.Further-more,pretreatment with compound C,a selective inhibitor of AMPK,or knockdown of AMPK by small interfering PNA restored suppression of ethanol-induced ROS production and Nox2 espression by gAcrp. Finally,we found that gAcrp treatment induced phosphorylation of liver linase B1(LKB1),an upstream signaling molecule mediating AMPK actibation.Knockdown of LKB1 restored gAcrp-suppressed Nox2 expres-sion,suggesting that LKB1/AMPK pathway plays a critical role in the suppression of ethanol-induced ROS production and ctivation of NADPH oxidase by gAcrp. Taken together,these results demonstrate that globular adiponectin prevents ethanol-indyced ROS production,at least in part,via modulation of NADPH oxidase in macrophages.Further,LKB1/AMPK axis plays an important role in the suppression of ethanol-induced NADPH oxidase activation by gAcrp in macrophages.
Adiponectin as an Anti-fibrotic and Anti-inflammatory Adipokine in the Liver
( Pil Hoon Park ),( Carlos Sanz Garcia ),( Laura E Nagy ) 영남대학교 약품개발연구소 2016 영남대학교 약품개발연구소 연구업적집 Vol.26 No.-
Hepatic fibrosis is a dynamic process resulting from excessive deposition of extracellular matrix in the liver; uncontrolled progression of fibrosis can eventually lead to liver cirrhosis and/or hepatocellular carcinoma. The fibrogenic process is complex and modulated by a number of both hepatic and extra-hepatic biological factors. Growing evidence indicates that adipokines, a group of cytokines produced by adipose tissue, impart dynamic fibrosis. In particular, two key adipokines, adiponectin and leptin, directly regulate many biological responses closely associated with development and progression of hepatic fibrosis. Leptin acts as a pro-fibrogenic cytokine, while adiponectin possesses anti-fibrogenic and anti-inflamma-tory properties. Adiponectin, acting via its cognate recep-tors, adiponectin receptors 1 and 2, potently suppresses fibrosis and inflammation in liver via multiple mechanism. This review summarize recent findings concerning the role of adiponectin in fibrogenic process in liver and addresses the underlying molecular mechanisms in modu-lation of fibrosis.