http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Kenichi Ikejima,Kazuyoshi Kon,Shunhei Yamashina 대한간학회 2020 Clinical and Molecular Hepatology(대한간학회지) Vol.26 No.4
Two major causes of steatohepatitis are alcohol and metabolic syndrome. Although the underlying causes of alcoholrelated liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH) differ, there are certain similarities in terms of the mode of disease progression and underlying pathophysiological mechanisms. Further, excessive alcohol consumption is often seen in patients with metabolic syndrome, and alcoholic hepatitis exacerbation by comorbidity with metabolic syndrome is an emerging clinical problem. There are certain ethnic differences in the development of both NAFLD and ALD. Especially, Asian populations tend to be more susceptible to NAFLD, and genetic polymorphisms in patatin-like phospholipase domain-containing 3 (PNPLA3) play a key role in both NAFLD and ALD. From the viewpoint of pathophysiology, cellular stress responses, including autophagy and endoplasmic reticulum (ER) stress, are involved in the development of cellular injury in steatohepatitis. Further, gutderived bacterial products and innate immune responses in the liver most likely play a profound role in the pathogenesis of both ALD and NASH. Though the recent progress in the treatment of viral hepatitis has reduced the prevalence of viral-related development of hepatocellular carcinoma (HCC), non-viral HCC is increasing. Alcohol and metabolic syndrome synergistically exacerbate progression of steatohepatitis, resulting in carcinogenesis. The gut-liver axis is a potential therapeutic and prophylactic target for steatohepatitis and subsequent carcinogenesis.
Tetsuo Gotoh,Tomoko Korenaga,Satomi Ikejima,Tsutomu Hoshino 한국응용곤충학회 2008 한국응용곤충학회 학술대회논문집 Vol.2008 No.10
Population density of the citrus red mite, Panonychus citri (McGregor), in Japanese pear orchards remained low until mid-August, even after inoculation of pear leaves with a considerable number of adult female P. citri from May onwards. This raised the possibility that pear leaves contain a natural compound that suppresses an increase of P. citri populations. The rate of development from larva to adult was significantly lower on leaves collected in July than on leaves collected earlier or later, in several years. The population suppression was caused by molting inhibition and ovicidal activity, according to our close observation in the laboratory [Gotoh and Kubota (1997) Exp. Appl. Acarol. 21: 343-356]. To clarify whether a natural pear compound caused this molting inhibition, a methanol crude extract of pear leaves was isolated and added to a newly developed artificial diet, consisting of sodium caseinate, sucrose, levulose, glucose and inositol. The compound extracted from pear leaves resulted in the molting inhibition as observed on pear leaves. Based on infrared and NMR spectral analysis, the compound extracted from pear leaves closely resembled the synthetic acaricide hexythiazox. Furthermore, the LC50-values of the compound extracted from pear leaves for ovicidal activity of P. citri eggs and for inhibition of molting to protonymphs were similar to those of hexythiazox. These results strongly suggest that the molting deterrent extracted from pear leaves was in fact hexythiazox, an acaricide in use on pear trees, rather than a natural product. This suggestion becomes even stronger, considering that the molting inhibition was observed in a hexythiazox-spray year, but not in a non-spray year.
Huang, Jian,Tang, Xiao-Hui,Ikejima, Takashi,Sun, Xiu-Jia,Wang, Xiao-Bo,Xi, Rong-Gang,Wu, Li-Jun 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.3
A new triterpenoid, 20(R),22$({\zeta})$,24(S)-dammar-25(26)-ene-$3{\beta},6{\alpha},12{\beta}$,20,22,24-hexanol (1), and three known triterpenoids, ${\beta}$-D-glucopyranoside,($3{\beta},12{\beta}$)-12,20-dihydroxydammar-24-en-3-yl,6-acetate (2), 20(R)-ginsenoside $Rg_3$ (3), and 20(R)-ginsenoside $Rg_2$ (4), were isolated from the leaves of Panax ginseng. Their structures were determined by chemical analysis and spectral methods (IR, 1D and 2D NMR, HR-ESI-MS). Compounds 1-4 were exhibited various degrees of cytotoxicity in the human hepatoma cell line, HepG2. Compound 1 had the highest cytotoxic Potency, with an $IC_{50}$ value of 20.1 ${\mu}M$, by stimulating p53-mediated cell cycle arrest at the G1 to S phase transition, leading to apoptosis via activation of the caspase signaling pathway.
Jian Huang,Xiao-hui Tang,Takashi Ikejima,Xiu-jia Sun,Xiao-bo Wang,Rong-gang X,Li-jun Wu 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.3
A new triterpenoid, 20(R),22( ξ),24(S)-dammar-25(26)-ene-3 β,6 α,12 β,20,22,24-hexanol (1), and three known triterpenoids, β-D-glucopyranoside,(3 β,12 β)-12,20-dihydroxydammar-24-en- 3-yl,6-acetate (2), 20(R)-ginsenoside Rg3 (3), and 20(R)-ginsenoside Rh2 (4), were isolated from the leaves of Panax ginseng. Their structures were determined by chemical analysis and spectral methods (IR, 1D and 2D NMR, HR-ESI-MS). Compounds 1-4 were exhibited various degrees of cytotoxicity in the human hepatoma cell line, HepG2. Compound 1 had the highest cytotoxic potency, with an IC50 value of 20.1 µM, by stimulating p53-mediated cell cycle arrest at the G1 to S phase transition, leading to apoptosis via activation of the caspase signaling pathway.
Xian-Feng Gong,Min-Wei Wang,Shin-Ichi Tashiro,Satoshi Onodera,Takashi Ikejima 대한약학회 2005 Archives of Pharmacal Research Vol.28 No.1
Pseudolaric acid B is a major compound found in the bark of Pseudolarix kaempferi Gordon. In our study, pseudolaric acid B inhibited growth of human melanoma cells, A375-S2 in a timeand dose-dependent manner. A375-S2 cells treated with pseudolaric acid B showed typical characteristics of apoptosis including morphologic changes, DNA fragmentation, sub-diploid peak in flow cytometry, cleavage of poly-ADP ribose polymerase (PARP) and degradation of inhibitor of caspase-activated DNase (ICAD). P53 protein expression was upregulated while cells were arrested at the G2/M phase of the cell cycle. There was a decrease in the expression of anti-apoptotic Bcl-2 and Bcl-xL proteins, whereas pro-apoptotic Bax was increased. The two classical caspase substrates, PARP and ICAD, were both decreased in a time-dependent manner, indicating the activation of downstream caspases.
Gong Xian-Feng,Wang Min-Wei,Tashiro Shin-Ichi,Onodera Satoshi,Ikejima Takashi The Pharmaceutical Society of Korea 2005 Archives of Pharmacal Research Vol.28 No.1
Pseudolaric acid B is a major compound found in the bark of Pseudolarix kaempferi Gordon. In our study, pseudolaric acid B inhibited growth of human melanoma cells, A375-S2 in a time and dose-dependent manner. A375-S2 cells treated with pseudolaric acid B showed typical characteristics of apoptosis including morphologic changes, DNA fragmentation, sub-diploid peak in flow cytometry, cleavage of poly-ADP ribose polymerase (PARP) and degradation of inhibitor of caspase-activated DNase (ICAD). P53 protein expression was upregulated while cells were arrested at the $G_2/M$ phase of the cell cycle. There was a decrease in the expression of anti-apoptotic Bcl-2 and Bcl-xL proteins, whereas pro-apoptotic Bax was increased. The two classical caspase substrates, PARP and ICAD, were both decreased in a time-dependent manner, indicating the activation of downstream caspases.
Xianfeng Gong,Minwei Wang,Shin-ichi Tashiro,Satoshi Onodera,Takashi Ikejima 생화학분자생물학회 2006 Experimental and molecular medicine Vol.38 No.4
A terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay was used to determine that apoptosis causes HeLa cell death induced by pseudolaric acid B. The c-Jun N-terminal kinase (JNK) inhibitor SP600125 decreased p53 protein expression during exposure to pseudolaric acid B. SP600125 decreased the phosphorylation of p53 during pseudolaric acid B exposure, indicating that JNK mediates phosphorylation of p53 during the response to pseudolaric acid B. SP600125 reversed pseudolaric acid B-induced down-regulation of phosphorylated extracellular signal-regulated pro-tein kinase (ERK), and protein kinase C (PKC) was activated by pseudolaric acid B, whereas stau-rosporine, calphostin C, and H7 partly blocked this effect. These results indicate that p53 is partially regulated by JNK in pseudolaric acid B-induced HeLa cell death and that PKC participates in pseudolaric acid B-induced HeLa cell death.