机译:20-HETE,5,14-HEDGE的合成类似物通过增加20-HETE水平(与iNOS蛋白表达减少和大鼠血管扩张剂前列腺素生成有关)逆转内毒素诱导的低血压
Department of Pharmacology, Faculty of Pharmacy, Mersin University, Mersin, Turkey;
Department of Pharmacology, Faculty of Pharmacy, Mersin University, Mersin, Turkey;
Department of Pharmacology, Faculty of Pharmacy, Mersin University, Mersin, Turkey;
Department of Pharmacology, Faculty of Pharmacy, Mersin University, Mersin, Turkey;
Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX, USA;
Department of Pharmacology, College of Medicine, The University of Tennessee, Center for Health Sciences, Memphis, TN, USA;
Department of Pharmacology, Faculty of Pharmacy, Mersin University, Mersin, Turkey;
机译:20-HETE,5,14-HEDGE的合成类似物通过增加20-HETE水平(与大鼠iNOS蛋白表达降低和血管扩张性前列腺素生成相关)而逆转内毒素诱导的低血压。
机译:iNOS / sGC / PKG途径,COX-2,CYP4A1和gp91 phox对5型14-HEDGE(一种20-HETE模拟物)在败血性大鼠模型中对抗血管舒张,低血压,心动过速和炎症的保护作用休克
机译:5,14-HEDGE,一种20-HETE的模拟物,在败血性休克啮齿动物模型中逆转低血压并提高生存率:可溶性环氧化物水解酶,CYP2C23,MEK1 / ERK1 / 2 /IKKβ/IκB-α/NF-κB途径的贡献,和促炎细胞因子的形成
机译:改善异源蛋白表达和在微生物和哺乳动物细胞中产生的合成基因设计策略
机译:20-HETE的合成类似物514对冲逆转内毒素引起的低血压通过增加20-HETE水平相关与大鼠减少iNOs活性和血管扩张剂前列腺素生产
机译:iNOS / sGC / PKG途径,COX-2,CYP4A1和gp91phox对败血性休克大鼠模型中5,20-HEDGE,20-HETE模拟物的抗血管扩张,低血压,心动过速和炎症的保护作用