[1]
Li W, Wang Y, Wang X, et al. Esculin attenuates endotoxin shock induced by lipopolysaccharide in mouse and NO production in vitro through inhibition of NF-kappaB activation. Eur J Pharmacol 2016; 791: 726-34.
[2]
Chaudhry H, Zhou J, Zhong Y, et al. Role of cytokines as a double-edged sword in sepsis. In Vivo 2013; 27: 669-84.
[3]
Akira S, Uematsu S, Takeuchi O. Pathogen recognition and innate immunity. Cell 2006; 124: 783-801.
[4]
Wiersinga WJ, Leopold SJ, Cranendonk DR, van der Poll T. Host innate immune responses to sepsis. Virulence 2014; 5: 36-44.
[5]
Laurent-Rolle M, Morrison J, Rajsbaum R, et al. The interferon signaling antagonist function of yellow fever virus NS5 protein is activated by type I interferon. Cell Host Microbe 2014; 16: 314-27.
[6]
Stearns-Kurosawa DJ, Osuchowski MF, Valentine C, Kurosawa S, Remick DG. The pathogenesis of sepsis. Annu Rev Pathol 2011; 6: 19-48.
[7]
Seeley EJ, Matthay MA, Wolters PJ. Inflection points in sepsis biology: from local defense to systemic organ injury. Am J Physiol Lung Cell Mol Physiol 2012; 303: L355-63.
[8]
Ferrer R, Artigas A, Suarez D, et al. Effectiveness of treatments for severe sepsis: A prospective, multicenter, observational study. Am J Physiol Lung Cell Mol Physiol 2009; 180: 861-6.
[9]
Stone R. Search for sepsis drugs goes on despite failures. Science 1994; 264: 365-8.
[10]
Cohen J, Guyatt G, Bernard GR, et al. New strategies for clinical trials in patients with sepsis and septic shock. Crit Care Med 2001; 29: 880-6.
[11]
Opal SM, Dellinger RP, Vincent J-L, Masur H, Angus DC. The next generation of sepsis trials: What’s next after the demise of recombinant human activated Protein C? Crit Care Med 2014; 42: 1714-23.
[12]
Kellum JA, Kong L, Fink MP, et al. Understanding the inflammatory cytokine response in pneumonia and sepsis: Results of the Genetic and Inflammatory Markers of Sepsis (GenIMS) Study. Arch Intern Med 2007; 167: 1655-63.
[13]
Calvano SE, Xiao W, Richards DR, et al. A network-based analysis of systemic inflammation in humans. Nature 2005; 437: 1032-7.
[14]
Maslove DM, Wong HR. Gene expression profiling in sepsis: Timing, tissue, and translational considerations. Trends Mol Med 2014; 20: 204-13.
[15]
Tang BM, McLean AS, Dawes IW, Huang SJ, Lin RC. The use of gene-expression profiling to identify candidate genes in human sepsis. Am J Respir Crit Care Med 2007; 176: 676-84.
[16]
Kouzine F, Levens D, Baranello L. DNA topology and transcrip-tion. Nucleus 2014; 5: 195-202.
[17]
Rialdi A, Campisi L, Zhao N, et al. Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation. Science 2016; 352: 1-35.
[18]
Hoesel B, Schmid JA. The complexity of NF-κB signaling in inflammation and cancer. Mol Cancer 2013; 12: 1-15.
[19]
McKay LI, Cidlowski JA. Cross-talk between nuclear factor-κB and the steroid hormone receptors: Mechanisms of mutual antagonism. J Mol Endocrinol 1998; 12: 45-56.
[20]
Lawrence T. The nuclear factor NF-κB pathway in inflammation. Cold Spring Harb Perspect Biol 2009; 1: a001651-62.
[21]
Niu X, Yao H, Li W, et al. Delta-Amyrone inhibits lipopolysaccharide-induced inflammatory cytokines and protects against endotoxic shock in mice. Chem Biol Interact 2015; 240: 354-61.
[22]
Zhai J, Guo Y. Paeoniflorin attenuates cardiac dysfunction in endotoxemic mice via the inhibition of nuclear factor-kappaB. Biomed Pharmacother 2016; 80: 200-6.
[23]
Hung Y-L, Fang S-H, Wang S-C, et al. Corylin protects LPS-induced sepsis and attenuates LPS-induced inflammatory response. Sci Rep 2017; 7: 462-99.
[24]
Huang S-S, Deng J-S, Lin J-G, Lee C-Y, Huang G-J. Anti-inflammatory effects of trilinolein from Panax notoginseng through the suppression of NF-κB and MAPK expression and proinflammatory cytokine expression. Am J Chin Med 2014; 42: 1485-506.
[25]
Joyce DE, Gelbert L, Ciaccia A, DeHoff B, Grinnell BW. Gene expression profile of antithrombotic protein C defines new mechanisms modulating inflammation and apoptosis. J Biol Chem 2001; 276: 11199-203.
[26]
Niu X, Mu Q, Li W, et al. Protective effects of esculentic acid against endotoxic shock in Kunming mice. Int Immunopharmacol 2014; 23: 229-35.
[27]
Wang N, Huang Y, Li A, et al. Hydrostatin-TL1, an Anti-Inflammatory Active Peptide from the Venom Gland of Hydrophis cyanocinctus in the South China Sea. Int J Mol Sci 2016; 17(11): E1940.
[28]
Zheng X, Wang N, Yang Y, Chen Y, Liu X, Zheng J. Insight into the inhibition mechanism of kukoamine B against CpG DNA via binding and molecular docking analysis. RSC Advances 2016; 6: 85756-62.
[29]
Liu X, Zheng X, Wang N, et al. a novel dual inhibitor of LPS and CpG DNA, is a potential candidate for sepsis treatment. Br J Pharmacol 2011; 162: 1274-90.
[30]
Lecker SH, Goldberg AL, Mitch WE. Protein degradation by the ubiquitin–proteasome pathway in normal and disease states. J Am Soc Nephrol 2006; 17: 1807-19.
[31]
Zhang R, Li R, Liu Y, Tang Y. 1449: Bortezomib Protects Endothelial Barrier Disruption In Acute Inflammation. Crit Care Med 2018; 46: 708-11.
[32]
Leng L, Bucala R. Insight into the biology of macrophage Migration Inhibitory Factor (MIF) revealed by the cloning of its cell surface receptor. Cell Res 2006; 16: 162-8.
[33]
Calandra T, Roger T. Macrophage migration inhibitory factor: A regulator of innate immunity. Nat Rev Immunol 2003; 3: 791-800.
[34]
Grieb G, Merk M, Bernhagen J, Bucala R. Macrophage Migration Inhibitory Factor (MIF): a promising biomarker. Drug News Perspect 2010; 23: 257-66.
[35]
Dabideen DR, Cheng KF, Aljabari B, Miller EJ, Pavlov VA, Al-Abed Y. Phenolic hydrazones are potent inhibitors of macrophage migration inhibitory factor proinflammatory activity and survival improving agents in sepsis. J Med Chem 2007; 50: 1993-7.
[36]
Cvetkovic I, Al-Abed Y, Miljkovic D, et al. Stosic-Grujicic, Critical role of macrophage migration inhibitory factor activity in experimental autoimmune diabetes. Endocrinology 2005; 146: 2942-51.
[37]
Opal SM, Cross AS. Clinical trials for severe sepsis. Past failures, and future hopes. Infect Dis Clin North Am 1999; 13: 285-97.
[38]
Greisman SE, Johnston CA. Failure of antisera to J5 and R595 rough mutants to reduce endotoxemic lethality. J Infect Dis 1988; 157: 54-64.
[39]
Vincent J-L, Sun Q, Dubois M-J. Clinical trials of immunomodulatory therapies in severe sepsis and septic shock. Clin Infect Dis 2002; 34: 1084-93.
[40]
Bone RC, Fisher CJ Jr, Clemmer TP, et al. A controlled clinical trial of high-dose methylprednisolone in the treatment of severe sepsis and septic shock. N Engl J Med 1987; 317: 653-8.
[41]
Luce JM, Montgomery AB, Marks JD, Turner J, Metz CA, Murray JF. Ineffectiveness of high-dose methylprednisolone in preventing parenchymal lung injury and improving mortality in patients with septic shock. Am Rev Respir Dis 1988; 138: 62-8.
[42]
Balk RA. Steroids for septic shock*: Back from the dead?(Pro). Chest 2003; 123: 490S-9S.
[43]
Venkatesh B, Finfer S, Cohen J, et al. Adjunctive glucocorticoid therapy in patients with septic shock. N Engl J Med 2018.; [Epub ahead of print]
[44]
Toner P, McAuley DF, Shyamsundar M. Aspirin as a potential treatment in sepsis or acute respiratory distress syndrome. Crit Care 2015; 19: 374-84.
[45]
U.S.N.L.O. Medicine. Aspirin for Treatment of Severe Sepsis Clinicaltrialsgov
[46]
Laterre P-F. Clinical trials in severe sepsis with drotrecogin alfa (activated). Crit Care 2007; 11: 1-7.
[47]
Iskander KN, Osuchowski MF, Stearns-Kurosawa DJ, et al. Sepsis: Multiple abnormalities, heterogeneous responses, and evolving understanding. Physiol Rev 2013; 93: 1247-88.
[48]
Wang N, Huang Y, Li A, et al. Hydrostatin-TL1, an Anti-Inflammatory Active Peptide from the Venom Gland of Hydrophis cyanocinctus in the South China Sea. Int J Mol Sci 2016; 17: 1-15.
[49]
Šafránek R, Ishibashi N, Oka Y, Ozasa H, Shirouzu K, Holeček M. Modulation of inflammatory response in sepsis by proteasome inhibition. Int J Exp Pathol 2006; 87: 369-72.
[50]
Shih M, Chen L, Tsai P, Cherng J. In vitro and in vivo therapeutics of β-thujaplicin on LPS-induced inflammation in macrophages and septic shock in mice. Int J Immunopathol Pharmacol 2012; 25: 39-48.
[51]
Rim H-K, Cho W, Sung SH, Lee K-T. Nodakenin suppresses lipopolysaccharide-induced inflammatory responses in macrophage cells by inhibiting tumor necrosis factor receptor-associated factor 6 and nuclear factor-κB pathways and protects mice from lethal endotoxin shock. J Pharmacol Exp Ther 2012; 342: 654-64.
[52]
D’Acquisto F, May MJ, Ghosh S. Inhibition of nuclear factor kappa B (NF-B). Mol Interv 2002; 2: 22-33.
[53]
Chao W-W, Kuo Y-H, Lin B-F. Anti-inflammatory activity of new compounds from Andrographis paniculata by NF-κB transactivation inhibition. J Agric Food Chem 2010; 58: 2505-12.
[54]
O’Neil J, Ammit A, Clark A. MAPK p38 regulates inflammatory gene expression via tristetraprolin: Doing good by stealth. Int J Biochem Cell Biol 2018; 94: 6-9.
[55]
Mongardon N, Dyson A, Singer M. Pharmacological optimization of tissue perfusion. Br J Anaesth 2009; 103(1): 82-8.
[56]
Singer M, De Santis V, Vitale D, Jeffcoate W. Multiorgan failure is an adaptive, endocrine-mediated, metabolic response to overwhelming systemic inflammation. Lancet 2004; 364: 545-8.
[57]
Conway-Morris A, Wilson J, Shankar-Hari M. Immune Activation in Sepsis. Crit Care Clin 2018; 34: 29-42.
[58]
Abraham E. Nuclear Factor-κB and Its role in sepsis-associated organ failure. J Infect Dis 2003; 187: S364-9.
[59]
Aimbire F, Santos F, Albertini R, Castro-Faria-Neto H, Mittmann J, Pacheco-Soares C. Low-level laser therapy decreases levels of lung neutrophils anti-apoptotic factors by a NF-κB dependent mechanism. Int Immunopharmacol 2008; 8: 603-5.
[60]
Ross J, Elliott P. The proteasome: A new target for novel drug therapies. Am J Clin Pathol 2015; 1: 637-46.
[61]
Bleicher KH, Böhm H-J, Müller K, Alanine AI. A guide to drug discovery: Hit and lead generation: Beyond high-throughput screening. Nat Rev Drug Discov 2003; 2: 369.
[62]
Decque A, Joffre O, Magalhaes JG, et al. Sumoylation coordinates the repression of inflammatory and anti-viral gene-expression programs during innate sensing. Nat Immunol 2016; 17: 140-9.
[63]
Padhy B, Gupta Y. Drug repositioning: Re-investigating existing drugs for new therapeutic indications. J Postgrad Med 2011; 57: 153-64.
[64]
Lee CH. Resolvins as new fascinating drug candidates for inflammatory diseases. Arch Pharm Res 2012; 35: 3-7.
[65]
Spite M, Norling LV, Summers L, et al. Resolvin D2 is a potent regulator of leukocytes and controls microbial sepsis. Nature 2009; 461: 1287-91.
[66]
Chen F, Fan X, Wu Y, et al. Resolvin D1 improves survival in experimental sepsis through reducing bacterial load and preventing excessive activation of inflammatory response. Eur J Clin Microbiol Infect Dis 2014; 33: 457-64.
[67]
Mittur A. A Simultaneous Mixed-Effects Pharmacokinetic Model for Nefopam, N-desmethylnefopam, and Nefopam N-Oxide in Human Plasma and Urine. Eur J Drug Metab Pharmacokinet 2018; 43(4): 391-404.
[68]
Hobai IA, Edgecomb J, LaBarge K, Colucci WS. Dysregulation of intracellular calcium transporters in animal models of sepsis induced cardiomyopathy. Shock (Augusta, Ga) 2015; 43: 3-15.
[69]
Novak KR, Nardelli P, Cope TC, et al. Inactivation of sodium channels underlies reversible neuropathy during critical illness in rats. J Clin Invest 2009; 119: 1150-8.
[70]
Pasparakis M, Vandenabeele P. Necroptosis and its role in inflammation. Nature 2015; 517: 311-20.
[71]
N.C. Institue, Sorafenib Tosylate NIH. NIH Cancer Institute.
[72]
Martens S, Jeong M, Tonnus W, et al. Sorafenib tosylate inhibits directly necrosome complex formation and protects in mouse models of inflammation and tissue injury. Cell Death Dis 2017; 8: e2904.
[73]
Kwak S, Ku S-K, Kang H, Baek M-C, Bae J-S. Methylthiouracil, a new treatment option for sepsis. Vascul Pharmacol 2017; 88: 1-10.
[74]
Rudis MI, Basha MA, Zarowitz BJ. Is it time to reposition vasopressors and inotropes in sepsis? Crit Care Med 1996; 24: 525-37.
[75]
Jung B, Kim J, Bae J-S. Dabrafenib, as a novel insight into drug repositioning against secretory group IIa phospholipase A2. Int J Immunopathol Pharmacol 2016; 12: 415-21.