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Park Yeong-Ju,Hwang Unsik,Park Suyeon,Sim Sol,Jeong Soyeon,Park Misun,Kang Minji,Lee Youngsoo,Song Youngju,Park Hoon,Suh Hee-Jae 한국응용생명화학회 2021 Applied Biological Chemistry (Appl Biol Chem) Vol.64 No.1
Compound K (CK; 20-O-β-(d-glucopyranosyl)-20(S)-protopanaxadiol) is one of the metabolites of ginsenosides contained in red ginseng (RG) and is known to have high bioavailability. This study aimed to establish the optimal conditions for enzyme treatment to convert ginsenosides from RG extract to CK, and to prove the characteristics of bioconverted red ginseng (BRG) extract. CK was not detected in unenzyme-treated RG extract, and in the single-step enzyme treatment, it was produced at less than 4.58 mg/g only in treatment group with Pyr-flo or Sumizyme AC (at 50 °C for 48 h). The highest yield of CK (14.32 mg/g) was obtained by Ultimase MFC treatment at 50 °C for 48 h after treatment with a mixture of Pyr-flo and Rapidase at 50 °C for 24 h. Total polyphenol, 2,2-diphenyl-1-picrylhydrazyl (DPPH), and 2,2-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid)) (ABTS) radical scavenging activity were higher in BRG than in RG (p < 0.5). High-fat diet (HD) rat fed 1% BRG had significantly lower body weight, heart weight, fat pads (periosteal fat, epididymal fat), serum glucose levels, and hepatic triglyceride levels than those HD rat fed 1% RG (p < 0.05). In conclusion, the sequential enzymatic bioconversion was produces higher CK in RG root extract than single-step enzyme treatment.
Park, Min Hee,Lee, Misun,Nam, Geewoo,Kim, Mingeun,Kang, Juhye,Choi, Byung Jo,Jeong, Min Seock,Park, Kang Ho,Han, Wan Hui,Tak, Eunyoung,Kim, Min Sun,Lee, Juri,Lin, Yuxi,Lee, Young-Ho,Song, Im-Sook,Choi National Academy of Sciences 2019 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.116 No.47
<P><B>Significance</B></P><P>Microglial dysfunction accompanying the loss of phagocytic ability and the overexpression of neurotoxic factors presents a positive-feedback loop that contributes to the rapid progression of neurodegeneration. Termination of this cycle is considered a promising strategy to halt the progression of neurodegenerative diseases, including Alzheimer’s disease; however, effective chemical reagents for this purpose have been very limited. Herein, we report a compact synthetic molecule capable of restoring microglial dysfunction and improving cognitive function. Our in-depth studies of such a molecular entity could be beneficial toward the urgent global search for a new and effective treatment of neurodegenerative disorders.</P><P>As a central feature of neuroinflammation, microglial dysfunction has been increasingly considered a causative factor of neurodegeneration implicating an intertwined pathology with amyloidogenic proteins. Herein, we report the smallest synthetic molecule (<I>N</I>,<I>N</I>′-diacetyl-<I>p</I>-phenylenediamine [DAPPD]), simply composed of a benzene ring with 2 acetamide groups at the <I>para</I> position, known to date as a chemical reagent that is able to promote the phagocytic aptitude of microglia and subsequently ameliorate cognitive defects. Based on our mechanistic investigations in vitro and in vivo, 1) the capability of DAPPD to restore microglial phagocytosis is responsible for diminishing the accumulation of amyloid-β (Aβ) species and significantly improving cognitive function in the brains of 2 types of Alzheimer’s disease (AD) transgenic mice, and 2) the rectification of microglial function by DAPPD is a result of its ability to suppress the expression of NLRP3 inflammasome-associated proteins through its impact on the NF-κB pathway. Overall, our in vitro and in vivo investigations on efficacies and molecular-level mechanisms demonstrate the ability of DAPPD to regulate microglial function, suppress neuroinflammation, foster cerebral Aβ clearance, and attenuate cognitive deficits in AD transgenic mouse models. Discovery of such antineuroinflammatory compounds signifies the potential in discovering effective therapeutic molecules against AD-associated neurodegeneration.</P>
Doping effects of multiferroic manganitesYMn0.9X0.1O3(X=Al, Ru, and Zn)
Park, Junghwan,Kang, Misun,Kim, Jiyeon,Lee, Seongsu,Jang, Kwang-Hyun,Pirogov, A.,Park, J.-G.,Lee, Changhee,Park, S.-H.,Kim, Hyoung Chan American Physical Society 2009 Physical review. B, Condensed matter and materials Vol.79 No.6
PTK7 regulates radioresistance through nuclear factor-kappa B in esophageal squamous cell carcinoma
Park, Misun,Yoon, Hyeon-joon,Kang, Moon Chul,Kwon, Junhye,Lee, Hae Won Springer-Verlag 2016 TUMOR BIOLOGY Vol.37 No.10
<P>Tumor radioresistance is a major reason for decreased efficiency of cancer radiation therapy. Although a number of factors involved in radioresistance have been identified, the molecular mechanisms underlying radioresistance of esophageal squamous cell carcinoma (ESCC) have not been elucidated. In this study, we investigated the role of oncogenic protein tyrosine kinase 7 (PTK7) in the resistance of ESCC to radiation therapy. ESCC cell lines with high PTK7 expression were more refractive to radiation than those with low PTK7 levels. In radioresistant ESCC cells, PTK7 knockdown by specific siRNAs decreased the survival of irradiated cells and increased radiation-induced apoptosis, while in radiosensitive ESCC cells, PTK7 overexpression promoted cell survival and inhibited radiation-induced apoptosis. We hypothesized that PTK7 could regulate the activation of transcription factor NF-kB known for its role in cancer radioresistance. Our results indicated that the inhibition of PTK7 suppressed nuclear translocation of NF-kB subunit p65 induced by radiation, suggesting relevance of PTK7 expression with NF-kB activation in radioresistant ESCC. Furthermore, the levels of inhibitor of apoptosis proteins (IAPs), XIAP, and survivin, encoded by NF-kB-regulated genes, were induced in irradiated radioresistant cells but not in radiosensitive cells, while PTK7 knockdown downregulated IAP expression. Our findings revealed a novel mechanism underlying radioresistance in ESCC, which is associated with PTK7 and NF-kB-dependent apoptosis. These results suggest that the manipulation of PTK7 expression can be instrumental in enhancing ESCC response to radiotherapy. This study demonstrates that PTK7 plays a significant role in ESCC radioresistance via the NF-kB pathway.</P>