Table 1.
Approaches to therapeutic interventions in sepsis
S. No. | Approach | Class/Drug | Mechanism of action | References |
---|---|---|---|---|
1 | Experimental | LPS sequestrants | Neutralize LPS activity | Burns et al., 2005; Puddu et al., 2010; Vicent et al., 2010; Zheng et al., 2010 |
2 | HMGB-1 inhibitors | Block HMGB-1 activity | Ulloa et al., 2002; Matthay and Ware, 2004; Chen et al., 2005; Tang et al., 2008; 2009 | |
3 | MIF inhibitors | Act against MIF | Tohyama et al., 2008 | |
4 | Antimicrobial peptides | Antibacterial and LPS-neutralizing activity | Yibin et al., 2005; Shai et al., 2006 | |
5 | Curcumin | Inhibits the transcriptional activity of NF-κB | Kang et al., 2004 | |
6 | Diacerhein | Attenuates the synthesis and activity of pro-inflammatory cytokines | Calisto et al., 2012 | |
7 | Andrographolide sulfonate | Suppresses the expression of TNF-α, IL-1β, IL-6 | Guo et al., 2012 | |
8 | Clinical | Recombinant activated protein C | Blocks factors Va and VIIIa, inhibits cytokine production | Matthay, 2001 |
9 | TLR4 antagonists | Block TLR4 | Sha et al., 2007; Opal et al., 2013 | |
10 | C5a receptor (C5aR) antagonists and C1 inhibitors | Prevent activation of complement system | Strachan et al., 2000; Charchaflieh et al., 2012 | |
11 | Endotoxin removal devices | Bind and neutralize LPS activity | Davies and Cohen, 2011 | |
12 | Caspase inhibitors | Anti-apoptic activity | Weber et al., 2009 | |
13 | Oestrogen receptor-β agonists | Suppress transcription of pro-inflammatory genes | Cristofaro et al., 2006 | |
14 | Statins | Inhibit LPS-induced activation of NF-κB and antioxidant | Fraunberger et al., 2009 |