引用大鼠ELISA科研检测试剂盒的文献
引用大鼠elisa科研检测试剂盒的文献
文献收集：
epimedium aqueous extract ameliorates cerebral ischemia/reperfusion injury through inhibiting ros/nlrp3- mediated pyroptosis
引用试剂盒：
种属:大鼠
il-1β (rj15465), il-18 (rj15463),tnf-α (rj16622), il-6 (rj15478), il-10 (rj15453),inos(rj16565) , mda (rj15503), ros(rj15780) ,cat(rj15737),sod(rj16691) ,gshpx(rj25745) , ldh (rj16172)
if：7.675
abstract: cerebral ischemia/reperfusion causes exacerbated neuronal damage involving excessive neuroinflammation and oxidative stress. ros is considered a signal molecule to activate nlrp3; thus, the ros/nlrp3/pyroptosis axis plays a vital role in the pathogenesis of cerebral ischemia/reperfusion injury (ciri). therefore, targeting the inhibition of the ros/nlrp3/pyroptosis axis may be a promising therapeutic tactic for ciri. epimedium (ep) contains many active ingredients (ica, ics ii, and ict), which have a wide range of pharmacological activities. however, whether ep can protect against ciri remains unknown. thus, in this study, we designed to investigate the effect and possible underlying mechanism of ep on ciri. the results showed that treatment with ep dramatically mitigated brain damage in rats following ciri, which was achieved by suppressing mitochondrial oxidative stress and neuroinflammation. furthermore, we identified the ros/nlrp3/pyroptosis axis as a vital process and nlrp3 as a vital target in ep-mediated protection. most interestingly, the main compounds of ep directly bonded with nlrp3, as reflected by molecular docking, which indicated that nlrp3 might be a promising therapeutic target for ep-elicited cerebral protection. in conclusion, our findings illustrate that ics ii protects against neuron loss and neuroinflammation after ciri by inhibiting ros/nlrp3-mediated pyroptosis.
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引用大鼠ELISA科研检测试剂盒的文献
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文献收集：
epimedium aqueous extract ameliorates cerebral ischemia/reperfusion injury through inhibiting ros/nlrp3- mediated pyroptosis
引用试剂盒：
种属:大鼠
il-1β (rj15465), il-18 (rj15463),tnf-α (rj16622), il-6 (rj15478), il-10 (rj15453),inos(rj16565) , mda (rj15503), ros(rj15780) ,cat(rj15737),sod(rj16691) ,gshpx(rj25745) , ldh (rj16172)
if：7.675
abstract: cerebral ischemia/reperfusion causes exacerbated neuronal damage involving excessive neuroinflammation and oxidative stress. ros is considered a signal molecule to activate nlrp3; thus, the ros/nlrp3/pyroptosis axis plays a vital role in the pathogenesis of cerebral ischemia/reperfusion injury (ciri). therefore, targeting the inhibition of the ros/nlrp3/pyroptosis axis may be a promising therapeutic tactic for ciri. epimedium (ep) contains many active ingredients (ica, ics ii, and ict), which have a wide range of pharmacological activities. however, whether ep can protect against ciri remains unknown. thus, in this study, we designed to investigate the effect and possible underlying mechanism of ep on ciri. the results showed that treatment with ep dramatically mitigated brain damage in rats following ciri, which was achieved by suppressing mitochondrial oxidative stress and neuroinflammation. furthermore, we identified the ros/nlrp3/pyroptosis axis as a vital process and nlrp3 as a vital target in ep-mediated protection. most interestingly, the main compounds of ep directly bonded with nlrp3, as reflected by molecular docking, which indicated that nlrp3 might be a promising therapeutic target for ep-elicited cerebral protection. in conclusion, our findings illustrate that ics ii protects against neuron loss and neuroinflammation after ciri by inhibiting ros/nlrp3-mediated pyroptosis.
高通量组织研磨机在这几方面有些较好的优势
锂电标箔试验机：提升电池性能的关键设备
SUNDI密闭制冷加热控温系统产品特点
螺旋输送机如何清洁
海目星激光“闪电切割”功能篇
引用大鼠ELISA科研检测试剂盒的文献
2018年是物联网黄金时代or昙花一现？
CK-10系列裂缝测宽仪
PVH141R13AF30B252000001001AB010A*
跟随特斯拉脚步 Rimac也开始开发46毫米电池单元
大口径法兰在搬运和运输过程中是不允许磕碰的
酱菜杀菌设备选择微波设备的好处有哪些
喷雾加湿设备的使用常识
北京市PM2.5实现连续三年稳定达标 攻坚克难 全力稳固空气质量改善成果
带式干燥机工作的可靠性和操作条件的优化
矿用排污泵的安全操作规程
潜在我国干燥机械设备市场巨大有待发展
K&N隔离开关如何保障电力系统的安全运行？
浅析潜水推流器故障解除及日常保养
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