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        Vanillin oxime inhibits lung cancer cell proliferation and activates apoptosis through JNK/ERK-CHOP pathway

        Jie Shen,Zhixiang Su 대한생리학회-대한약리학회 2021 The Korean Journal of Physiology & Pharmacology Vol.25 No.4

        Lung cancer despite advancement in the medical field continues to be a major threat to human lives and accounts for a high proportion of fatalities caused by cancers globally. The current study investigated vanillin oxime, a derivative of vanillin, against lung cancer cells for development of treatment and explored the mechanism. Cell viability changes by vanillin oxime were measured using MTT as-say. Vanillin oxime-mediated apoptosis was detected in A549 and NCI-H2170 cells at 48 h of exposure by flow cytometry. The CEBP homologous protein (CHOP) and death receptor 5 (DR5) levels were analysed by RT-PCR and protein levels by West-ern blotting. Vanillin oxime in concentration-dependent way suppressed A549 and NCI-H2170 cell viabilities. On exposure to 12.5 and 15 μM concentrations of vanillin oxime elevated Bax, caspase-3, and -9 levels in A549 and NCI-H2170 cells were ob-served. Vanillin oxime exposure suppressed levels of Bcl-2, survivin, Bcl-xL, cFLIP, and IAPs proteins in A549 and NCI-H2170 cells. It stimulated significant elevation in DR4 and DR5 levels in A549 and NCI-H2170 cells. In A549 and NCI-H2170 cells vanillin ox-ime exposure caused significant (p < 0.05) enhancement in CHOP and DR5 mRNA ex-pression. Vanillin oxime exposure of A549 and NCI-H2170 cells led to significant (p < 0.05) enhancement in levels of phosphorylated extracellular-signal-regulated kinase and c-Jun N-terminal kinase. Thus, vanillin oxime inhibits pulmonary cell proliferation via induction of apoptosis through tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mediated pathway. Therefore, vanillin oxime may be studied further to develop a treatment for lung cancer.

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        Chlorogenic acid accumulation and related gene expression in peach fruit

        Yan Juan,Su Ziwen,Guo Shaolei,Zhang Minghao,Zhang Binbin,Cai Zhixiang,Shen Zhijun,Ma Ruijuan,Yu Mingliang 한국원예학회 2022 Horticulture, Environment, and Biotechnology Vol.63 No.3

        To reveal the molecular mechanism in the accumulation of chlorogenic acids (CGAs) in peach (Prunus persica) fruit during growth and development, CGA contents in the flesh of the three peach cultivars ‘Ruiguang 18’, ‘Heiyoutao’, and ‘Beijingyixianhong’ were determined. The expression levels of CGA metabolism-related genes were analyzed based on transcriptome data (RNA-seq). These candidate genes were then screened and real-time fluorescent quantitative PCR (qRT-PCR) was performed to verify their expression. The results showed that the content of total CGAs, 5-O-caffeoylquinic acid and 3-O-caffeoylquinic acid, in the flesh of ‘Ruiguang 18’ exhibited a decreasing trend during fruit development, and there was a great drop at maturity stage (P < 0.05). The three contents in ‘Heiyoutao’ increased first at stage S2 (P < 0.05) and then decreased significantly (P < 0.05). In ‘Beijingyixianhong’, they stayed stable in the early stages, then total CGAs and 3-O-caffeoylquinic acid decreased significantly at the maturity stage (P < 0.05). RNA-seq transcriptome data analysis and qRT-PCR expression analysis showed that the accumulation of CGAs in fruit flesh was mainly affected by the expression of Prupe.3G100800 (PpHCT) and Prupe.3G107300 (Pp4CL), and their expression levels were highly consistent with total CGA content. Thus, we concluded that Prupe.3G100800 (PpHCT) and Prupe.3G107300 (Pp4CL) are the key genes for CGAs synthesis in peach flesh.

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