RISS 학술연구정보서비스

검색
다국어 입력

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      검색결과 좁혀 보기

      선택해제

      오늘 본 자료

      • 오늘 본 자료가 없습니다.
      더보기
      • 무료
      • 기관 내 무료
      • 유료
      • KCI등재

        Effects of Gyeongshingangjeehwan 18 on Pancreatic Fibroinflammation in High-Fat Diet-Fed Obese C57BL/6J Mice

        Joonseong Jang,Younghyun Park,Michung Yoon 대한의생명과학회 2018 Biomedical Science Letters Vol.24 No.4

        The polyherbal drug Gyeongshingangjeehwan 18 (GGEx18) from Rheum palmatum L. (Polygonaceae), Laminaria japonica Aresch (Laminariaceae), and Ephedra sinica Stapf (Ephedraceae) has traditionally been used as an antiobesity drug in Korean local clinics. This study investigates the effects of GGEx18 on pancreatic fibroinflammation in high-fat diet (HFD)-fed obese C57BL/6J mice and the molecular mechanism involved in this process. After HFD-fed obese C57BL/6J mice were treated with GGEx18 (125, 250, and 500 mg/kg) for 12 weeks, variables and determinants of obesity, pancreatic inflammation, and fibrosis were measured using histology, immunohistochemistry, and real-time polymerase chain reaction. Administration of GGEx18 at 500 mg/kg/day to obese mice decreased body weight gain, mesenteric adipose tissue mass, and adipocyte size. GGEx18 treatment not only reduced mast cells and CD68-immunoreactive cells, but also decreased collagen levels and α-smooth muscle actin-positive cells in the pancreas of HFD-fed mice. Concomitantly, GGEx18 decreased the expression of genes for inflammation (i.e., CD68 and tumor necrosis factor α) and fibrosis (i.e., collagen α1 and transforming growth factor β) in the pancreas of obese mice. These results suggest that GGEx18 may inhibit visceral obesity and related pancreatic fibroinflammation in HFD-fed obese mice.

      • KCI등재

        Vitamin C Inhibits Visceral Adipocyte Hypertrophy and Lowers Blood Glucose Levels in High-Fat-Diet-Induced Obese C57BL/6J Mice

        Younghyun Park,Joonseong Jang,Dongju Lee,Michung Yoon 대한의생명과학회 2018 Biomedical Science Letters Vol.24 No.4

        Vitamin C (ascorbic acid) supplementation has been suggested to negatively correlate with obesity in humans and other animals. Previous studies, including ours, have demonstrated that a high-fat diet (HFD) induces obesity and related diseases such as hyperlipidemia, hyperglycemia, insulin resistance, and nonalcoholic fatty liver disease. Here, we investigated the effects of vitamin C on visceral adipocyte hypertrophy and glucose intolerance in C57BL/6J mice. Mice received a low-fat diet (LFD, 10% kcal fat), HFD (45% kcal fat), or the same HFD supplemented with vitamin C (HFD-VC, 1% w/w) for 15 weeks. Visceral adiposity and glucose intolerance were examined using metabolic measurements, histology, and gene expression analyses. Mice in the HFD-VC supplementation group had reduced body weight, mesenteric fat mass, and mesenteric adipocyte size compared with HFD-fed mice. Vitamin C intake in obese mice also decreased the mRNA levels of lipogenesis-related genes (i.e., stearoyl-CoA desaturase 1 and sterol regulatory element-binding protein 1c) in mesenteric adipose tissues, inhibited hyperglycemia, and improved glucose tolerance. In addition, vitamin C attenuated the HFD-induced increase in the size of pancreatic islets. These results suggest that vitamin C suppresses HFD-induced visceral adipocyte hypertrophy and glucose intolerance in part by decreasing the visceral adipose expression of genes involved in lipogenesis.

      • Total synthesis of (+)-brasilenyne <i>via</i> concise construction of an oxonane framework containing a 1,3-<i>cis</i>,<i>cis</i>-diene

        Lim, Changjin,Ahn, Jungmin,Sim, Jaehoon,Yun, Hwayoung,Hur, Joonseong,An, Hongchan,Jang, Jaebong,Lee, Seungbeom,Suh, Young-Ger The Royal Society of Chemistry 2018 Chemical communications Vol.54 No.5

        <P>The enantioselective total synthesis of (+)-brasilenyne has been accomplished. The key features of the synthesis include the convergent preparation of a highly functionalized endocyclization precursor <I>via</I> selective epoxide opening, the construction of an oxonene skeleton through perfect regioselective Pd(0)-catalyzed endocyclization, and the installation of a 1,3-<I>cis</I>,<I>cis</I>-diene unit <I>via</I> a decarboxylative photophenylselenylation and site-selective selenoxide elimination sequence.</P>

      • The polyherbal drug GGEx18 from <i>Laminaria japonica, Rheum palmatum</i>, and <i>Ephedra sinica</i> inhibits hepatic steatosis and fibroinflammtion in high-fat diet-induced obese mice

        Lim, Jonghoon,Lee, Haerim,Ahn, Jiwon,Kim, Jeongjun,Jang, Joonseong,Park, Yonghyun,Jeong, Birang,Yang, Heejung,Shin, Soon Shik,Yoon, Michung Elsevier 2018 Journal of Ethnopharmacology Vol.225 No.-

        <P><B>Abstract</B></P> <P><B>Ethnopharmacological relevance</B></P> <P>The herbal composition Gyeongshingangjeehwan 18 (GGEx18), composed of <I>Rheum palmatum</I> L. (Polygonaceae), <I>Laminaria japonica</I> Aresch (Laminariaceae), and <I>Ephedra sinica</I> Stapf (Ephedraceae), is used as an antiobesity drug in Korean clinics. The constituents of GGEx18 have traditionally been reported to inhibit obesity and related metabolic diseases such as insulin resistance and dyslipidemia.</P> <P><B>Objective</B></P> <P>This study investigated the effects of GGEx18 on nonalcoholic fatty liver disease (NAFLD) in mice fed a high-fat diet (HFD) and the underlying cellular and molecular mechanisms involved.</P> <P><B>Methods</B></P> <P>C57BL/6 J mice were fed either a low-fat diet (LFD), an HFD, or an HFD supplemented with GGEx18 (125, 250, or 500 mg/kg of body weight/day). After 13 weeks, blood analyses, histology, immunohistochemistry, and real-time PCR were performed to assess NAFLD development in these mice.</P> <P><B>Results</B></P> <P>Mice fed an HFD had increases in body weight, epididymal adipose tissue mass, adipocyte size, and adipose expression of inflammation-related genes compared with those fed an LFD. These increases were ameliorated in mice treated with 500 mg/kg/day GGEx18 without affecting food consumption profiles. GGEx18 not only decreased serum levels of triglycerides, free fatty acids, and alanine aminotransferase, but also decreased hepatic lipid accumulation, numbers of mast cells and α-smooth muscle actin-positive cells, and collagen levels induced by an HFD. Consistent with the histological data, the hepatic expression of lipogenesis-, inflammation-, and fibrosis-related genes was lower, while hepatic fatty acid β-oxidation-related gene expression was higher, in mice receiving GGEx18 compared to mice fed only the HFD.</P> <P><B>Discussion and conclusion</B></P> <P>These results indicate that GGEx18 attenuates visceral obesity and NAFLD, in part by altering the expression of genes involved in hepatic steatosis and fibroinflammation in HFD-induced obese mice. These findings suggest that GGEx18 may be effective for preventing and treating NAFLD associated with visceral obesity.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

      연관 검색어 추천

      이 검색어로 많이 본 자료

      활용도 높은 자료

      해외이동버튼