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Preparation of T-2-glucoronide with Rat Hepatic Microsomes and Its Use along with T-2 for Activation of the JAK/STAT Signaling Pathway in RAW264.7 Cells  ( SCI-EXPANDED收录 EI收录)   被引量:4

文献类型:期刊文献

英文题名:Preparation of T-2-glucoronide with Rat Hepatic Microsomes and Its Use along with T-2 for Activation of the JAK/STAT Signaling Pathway in RAW264.7 Cells

作者:Wang, Xing[1];Wang, Yaling[1];Wang, Yapei[1];Sun, Lijun[1];Gooneratne, Ravi[2]

机构:[1]Guangdong Ocean Univ, Coll Food Sci & Technol, Guangdong Prov Key Lab Aquat Prod Proc & Safety, Key Lab Adv Proc Aquat Prod,Guangdong Higher Educ, Zhanjiang 524088, Peoples R China;[2]Lincoln Univ, Fac Agr & Life Sci, Dept Wine Food & Mol Biosci, POB 85084, Lincoln 7647, New Zealand

年份:2017

卷号:65

期号:23

起止页码:4811

外文期刊名:JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY

收录:SCI-EXPANDED(收录号:WOS:000403631100032)、、EI(收录号:20172503796089)、Scopus(收录号:2-s2.0-85020833594)、WOS

基金:This work was funded by the National Natural Science Foundation of China (NSFC No. 31171634 and No. 31371777).

语种:英文

外文关键词:T-2-glucuronide; T-2 toxin; liver microsomes; UDPGT; immune-toxicity

外文摘要:T-2 toxin (T-2), one of the most toxic trichothecene A-type mycotoxins, is biotransformed in animal tissues to modified T-2s (mT-2s) including T-2-glucuronide (T-2-GlcA). In this study, the optimal conditions for T-2-GlcA synthesis were established, and the JAK/STAT pathway in RAW264.7 cells was used to study the toxicity of T-2-GlcA. Because many mT-2 standards are not readily available, optimal conditions for T-2-GlcA synthesis in vitro were established by incubating T-2 with rat liver microsomes, UDPGA, and 0.2% Triton X-100 for 90 min. qRT-PCR and Western blot results showed 21- and 760-fold increases in IL-6 mRNA expression induced by T-2-GlcA and T-2, respectively. Similar differences were observed in JAK3, SOCS2/3, and CIS mRNA expression. T-2-GlcA induced a dose-responsive decrease in STAT1 mRNA expression, whereas the result with T-2 was the opposite. Moreover, the phosphorylation of STAT3 induced by T-2-GlcA was higher than that by T-2, whereas the phosphorylation of STAT1 was to the contrary. Overall, the results show that T-2-GlcA was somewhat toxic, but activation of the JAK/STAT pathway in RAW264.7 was higher by T-2.

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