17β-Estradiol: a novel hormone for improving immune and cardiovascular responses following trauma-hemorrhage
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چکیده
منابع مشابه
17 -Estradiol inhibits keratinocyte-derived chemokine production following trauma-hemorrhage
Frink M, Thobe BM, Hsieh Y-C, Choudhry MA, Schwacha MG, Bland KI, Chaudry IH. 17 -Estradiol inhibits keratinocytederived chemokine production following trauma-hemorrhage. Am J Physiol Lung Cell Mol Physiol 292: L585–L591, 2007. First published November 3, 2006; doi:10.1152/ajplung.00364.2006.—Neutrophil infiltration is a key step in the development of organ dysfunction following trauma-hemorrha...
متن کامل17beta-Estradiol inhibits keratinocyte-derived chemokine production following trauma-hemorrhage.
Neutrophil infiltration is a key step in the development of organ dysfunction following trauma-hemorrhage (T-H). Although we have previously shown that 17beta-estradiol (E2) prevents neutrophil infiltration and organ damage following T-H, the mechanism by which E2 inhibits neutrophil transmigration remains unknown. We hypothesized that E2 prevents neutrophil infiltration via modulation of kerat...
متن کاملLidocaine depresses splenocyte immune functions following trauma-hemorrhage in mice.
Traumatic and/or surgical injury as well as hemorrhage induces profound suppression of cellular immunity. Although local anesthetics have been shown to impair immune responses, it remains unclear whether lidocaine affects lymphocyte functions following trauma-hemorrhage (T-H). We hypothesized that lidocaine will potentiate the suppression of lymphocyte functions after T-H. To test this, we rand...
متن کاملp38 MAPK-dependent eNOS upregulation is critical for 17beta-estradiol-mediated cardioprotection following trauma-hemorrhage.
Studies have shown that p38 MAPK and nitric oxide (NO), generated by endothelial NO synthase (eNOS), play key roles under physiological and pathophysiological conditions. Although administration of 17beta-estradiol (E2) protects cardiovascular injury from trauma-hemorrhage, the mechanism by which E2 produces those effects remains unknown. Our objective was to determine whether the E2-mediated a...
متن کاملp38 MAPK-dependent eNOS upregulation is critical for 17 -estradiol-mediated cardioprotection following trauma-hemorrhage
Kan WH, Hsu JT, Ba ZF, Schwacha MG, Chen JG, Choudhry MA, Bland KI, Chaudry IH. p38 MAPK-dependent eNOS upregulation is critical for 17 -estradiol-mediated cardioprotection following trauma-hemorrhage. Am J Physiol Heart Circ Physiol 294: H2627–H2636, 2008. First published April 11, 2008; doi:10.1152/ajpheart.91444.2007.—Studies have shown that p38 MAPK and nitric oxide (NO), generated by endot...
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ژورنال
عنوان ژورنال: Journal of Leukocyte Biology
سال: 2007
ISSN: 0741-5400
DOI: 10.1189/jlb.0607369