The precipitation behaviors of an A1-Cu-Li-Mn-Zr alloy at different ageing temperatures （120, 160 and 200 ~C） were investigated using Vickers hardness measurements and transmission electron microscopy （TEM） charac...The precipitation behaviors of an A1-Cu-Li-Mn-Zr alloy at different ageing temperatures （120, 160 and 200 ~C） were investigated using Vickers hardness measurements and transmission electron microscopy （TEM） characterization. Age hardening curves show an increase in precipitation kinetics with increasing ageing temperature. The results of TEM show that for the samples peak aged at 120 ~C, the amount of g＇ （A13Li）, GP zones/0＇ （A12Cu） and Z （A15Cu6Li2） phases is obviously higher than that of T1 （A12CuLi） precipitates; while the samples peak aged at 160 and 200 ~C are usually dominated by T1 phase with a minor fraction of GP zones/0＇ and g＇, and the Z phase almost does not form. In addition, quantitative analysis on the T1 platelets demonstrates that the samples peak aged at 200 ~C have larger plate diameter and smaller area fraction of T1, as compared to the samples peak aged at 160 ~C. Correspondingly, the possible reasons for such phenomena are discussed.展开更多
Our previous study has revealed that procyanidin A_(1)(A_(1))and its simulated digestive product(D-A,)can alleviate acrylamide(ACR)-induced intestine cell damage.However,the underlying mechanism remains unknown.In thi...Our previous study has revealed that procyanidin A_(1)(A_(1))and its simulated digestive product(D-A,)can alleviate acrylamide(ACR)-induced intestine cell damage.However,the underlying mechanism remains unknown.In this study,we elucidated the molecular mechanism for and D-A_(1) to alleviate ACR-stimulated IPEC-J2 cell damage.ACR slightly activated nuclear factor erythroid 2-related factor 2(Nrf2)signaling and its target genes,but this activation could not reduce intestine cell damage.A_(1) and D-A_(1) could alleviate ACR-induced cell damage,but the effect was abrogated in cells transiently transfected with Nrf2 small interfering RNA(siRNA).Further investigation confirmed that A_(1) and D-A_(1) interacted with Ketch-like ECH-associated protein 1(Keapl),which boosted the stabilization of Nrf2,subsequently promoted the translocation of Nrf2 into the nucleus,and further increased the expression of antioxidant proteins,thereby inhibiting glutathione(GSH)consumption,maintaining redox balance and eventually alleviating ACR-induced cell damage.Importantly,there was no difference between A_(1) and D-A_(1) treated groups,indicating that A_(1) can tolerate gastrointestinal digestion and may be a potential compound to limit the toxicity of ACR.展开更多
基金Project（2016YFB0300901） supported by the National Key R＆D Program of China Project（51421001） supported by the National Natural Science Foundation of China Project（2018CDJDCL0019） supported by the Fundamental Research Funds for the Central Universities, China
文摘The precipitation behaviors of an A1-Cu-Li-Mn-Zr alloy at different ageing temperatures （120, 160 and 200 ~C） were investigated using Vickers hardness measurements and transmission electron microscopy （TEM） characterization. Age hardening curves show an increase in precipitation kinetics with increasing ageing temperature. The results of TEM show that for the samples peak aged at 120 ~C, the amount of g＇ （A13Li）, GP zones/0＇ （A12Cu） and Z （A15Cu6Li2） phases is obviously higher than that of T1 （A12CuLi） precipitates; while the samples peak aged at 160 and 200 ~C are usually dominated by T1 phase with a minor fraction of GP zones/0＇ and g＇, and the Z phase almost does not form. In addition, quantitative analysis on the T1 platelets demonstrates that the samples peak aged at 200 ~C have larger plate diameter and smaller area fraction of T1, as compared to the samples peak aged at 160 ~C. Correspondingly, the possible reasons for such phenomena are discussed.
基金supported by the project from National Natural Science Foundation of China (31671962)Fundamental Research Funds for the Central Universities (2662019PY034)。
文摘Our previous study has revealed that procyanidin A_(1)(A_(1))and its simulated digestive product(D-A,)can alleviate acrylamide(ACR)-induced intestine cell damage.However,the underlying mechanism remains unknown.In this study,we elucidated the molecular mechanism for and D-A_(1) to alleviate ACR-stimulated IPEC-J2 cell damage.ACR slightly activated nuclear factor erythroid 2-related factor 2(Nrf2)signaling and its target genes,but this activation could not reduce intestine cell damage.A_(1) and D-A_(1) could alleviate ACR-induced cell damage,but the effect was abrogated in cells transiently transfected with Nrf2 small interfering RNA(siRNA).Further investigation confirmed that A_(1) and D-A_(1) interacted with Ketch-like ECH-associated protein 1(Keapl),which boosted the stabilization of Nrf2,subsequently promoted the translocation of Nrf2 into the nucleus,and further increased the expression of antioxidant proteins,thereby inhibiting glutathione(GSH)consumption,maintaining redox balance and eventually alleviating ACR-induced cell damage.Importantly,there was no difference between A_(1) and D-A_(1) treated groups,indicating that A_(1) can tolerate gastrointestinal digestion and may be a potential compound to limit the toxicity of ACR.
