AIM: To explore the role and potential mechanism of miR-30 b regulation of autophagy in hepatic ischemiareperfusion injury(IRI).METHODS: An animal model of hepatic IRI was generated in C57BL/6 mice. For in vitro studi...AIM: To explore the role and potential mechanism of miR-30 b regulation of autophagy in hepatic ischemiareperfusion injury(IRI).METHODS: An animal model of hepatic IRI was generated in C57BL/6 mice. For in vitro studies, AML12 cells were immersed in mineral oil for 1 h and then cultured in complete Dulbecco's Modified Eagle's Medium(DMEM)/F12 to simulate IRI. Mice and cells were transfected with miR-30 b agomir/mimics or antagomir/inhibitor to examine the effect of miR-30 b on autophagy to promote hepatic IRI. The expression of miR-30 b was measured by real-time polymerase chain reaction. Apoptotic cells were detected by terminal uridine nickend labeling(TUNEL) staining, and cell viability was detected by methylthiazole tetrazolium assay. The expression of light chain 3, autophagy-related gene(Atg)12, Atg5, P62, and caspase-3 were detected by western blotting analysis.RESULTS: miR-30 b levels were significantly downregulated after hepatic IRI, and the numbers of autophagosomes were increased in response to IRI both in vivo and in vitro. These findings demonstrate that low levels of miR-30 b could promote hepatic IRI. Furthermore, we found that miR-30 b interacted with Atg12-Atg5 conjugate by binding to Atg12. Overexpression of miR-30 b diminished Atg12 and Atg12-Atg5 conjugate levels, which promoted autophagy in response to IR. In contrast, downregulation of miR-30 b was associated with increased Atg12-Atg5 conjugate levels and increased autophagy.CONCLUSION: miR-30 b inhibited autophagy to alleviate hepatic ischemia-reperfusion injury via decreasing the Atg12-Atg5 conjugate.展开更多
对30Ni Cr Mo V12钢不同热处理工艺后的力学性能和组织进行研究。结果表明,回火温度对调质后力学性能影响较大,但是对晶粒度和组织几乎无影响。最佳热处理工艺为900℃奥氏体化,双液淬火冷却后590℃回火。该车轴热处理后淬透性较好,整体...对30Ni Cr Mo V12钢不同热处理工艺后的力学性能和组织进行研究。结果表明,回火温度对调质后力学性能影响较大,但是对晶粒度和组织几乎无影响。最佳热处理工艺为900℃奥氏体化,双液淬火冷却后590℃回火。该车轴热处理后淬透性较好,整体性能基本一致,各项性能合格并稳定,说明该热处理工艺合理。展开更多
A new triterpenoid. 3 beta. 4 beta. 23-trihydroxy-24, 30-dinorolean-12. 20(29)-dien-28-oic acid. together with five known compounds. 2 alpha. 3 beta. 23-trihydroxy-12-oleanen-28-oic acid-beta -D-glucose glucopyranosyl...A new triterpenoid. 3 beta. 4 beta. 23-trihydroxy-24, 30-dinorolean-12. 20(29)-dien-28-oic acid. together with five known compounds. 2 alpha. 3 beta. 23-trihydroxy-12-oleanen-28-oic acid-beta -D-glucose glucopyranosyl ester. palbinone. 2-hydroxy-benzoic acid, vanillic acid. syringic acid. were isolated from the roots of Paeonia delavayi Franch. Their structures were characterized by spectral analysis.展开更多
基金Supported by National High Technology Research and Development Program(863)of China,No.2012AA021001National Natural Science Foundation of China,No.81270554+1 种基金Special Fund for Health Research in the Public Interest of China,No.201302009National Key Specialty Construction of Clinical Projects,No.201354409
文摘AIM: To explore the role and potential mechanism of miR-30 b regulation of autophagy in hepatic ischemiareperfusion injury(IRI).METHODS: An animal model of hepatic IRI was generated in C57BL/6 mice. For in vitro studies, AML12 cells were immersed in mineral oil for 1 h and then cultured in complete Dulbecco's Modified Eagle's Medium(DMEM)/F12 to simulate IRI. Mice and cells were transfected with miR-30 b agomir/mimics or antagomir/inhibitor to examine the effect of miR-30 b on autophagy to promote hepatic IRI. The expression of miR-30 b was measured by real-time polymerase chain reaction. Apoptotic cells were detected by terminal uridine nickend labeling(TUNEL) staining, and cell viability was detected by methylthiazole tetrazolium assay. The expression of light chain 3, autophagy-related gene(Atg)12, Atg5, P62, and caspase-3 were detected by western blotting analysis.RESULTS: miR-30 b levels were significantly downregulated after hepatic IRI, and the numbers of autophagosomes were increased in response to IRI both in vivo and in vitro. These findings demonstrate that low levels of miR-30 b could promote hepatic IRI. Furthermore, we found that miR-30 b interacted with Atg12-Atg5 conjugate by binding to Atg12. Overexpression of miR-30 b diminished Atg12 and Atg12-Atg5 conjugate levels, which promoted autophagy in response to IR. In contrast, downregulation of miR-30 b was associated with increased Atg12-Atg5 conjugate levels and increased autophagy.CONCLUSION: miR-30 b inhibited autophagy to alleviate hepatic ischemia-reperfusion injury via decreasing the Atg12-Atg5 conjugate.
文摘A new triterpenoid. 3 beta. 4 beta. 23-trihydroxy-24, 30-dinorolean-12. 20(29)-dien-28-oic acid. together with five known compounds. 2 alpha. 3 beta. 23-trihydroxy-12-oleanen-28-oic acid-beta -D-glucose glucopyranosyl ester. palbinone. 2-hydroxy-benzoic acid, vanillic acid. syringic acid. were isolated from the roots of Paeonia delavayi Franch. Their structures were characterized by spectral analysis.
