[1] 赵雷,钱风华,丁纯蕾,等.升降散对脓毒症大鼠心肌p38MAPK 蛋白磷酸化水平的影响[J].中国临床医学, 2017, 24(1):6-11.
[2] 周雄根,朱亮,钱风华,等.升降散对脓毒症瘀毒内阻证患者心肌肌钙蛋白I及一氧化氮的影响[J].中国临床医学, 2011, 18(3):287-289.
[3] 钱义明,朱亮,高斌,等.升降散对全身炎症反应综合征患者血清IL-2、IL-4、IL-6干预的影响[J].中外医疗, 2008, 27(10):34-35.
[4] 朱亮,赵雷,钱风华,等.升降散对脓毒症小鼠细胞炎症因子抑制作用的研究[J].中国中医急症, 2015, 24(3):384-386,460.
[5] 胡才宝,严静,李莉,等.脓毒症大鼠不同时期炎症因子水平与心功能关系的研究[J].中华危重症医学杂志(电子版), 2014, 7(3):166-171.
[6] Yang M, Wu J, Martin CM, et al. Important role of p38MAP kinase/NF-kappaB signaling pathway in the sepsis induced conversion of cardiac myocytes to a proinflammatory phenotype[J]. Am J Physiol Heart Circ Physiol, 2008, 294(2):994-1001.
[7] Koch L, Frommhold D, Buschmann K, et al. LPS-and LTA-induced expression of IL-6 and TNF-α in neonatal and adult blood: role of MAPKs and NF-κB[J]. Mediators Inflamm, 2014, 2014: 283 126.
[8] Yego EC, Dillman JF. Cytokine regulation by MAPK activated kinase 2 in keratinocytes exposed to sulfur mustard[J]. Toxicol In Vitro, 2013, 27(7): 2067-2075.
[9] Luo Y, Che W, Zhao M. Ulinastatin post-treatment attenuates lipopolysaccharide-induced acute lung injury in rats and human alveolar epithelial cells[J]. Int J Mol Med, 2017, 39(2): 297-306.
|