Heat Shock Protein 72 Expressing Stress in Sepsis: Unbridgeable Gap between Animal and Human Studies—A Hypothetical “Comparative” Study
Table 1
(a) Results of animal in vivo studies examining the preventive role of intra- or extracellular Hsp72 (Hsp70) expression and Hsp72 (Hsp70) expression in experimental sepsis or sepsis-related pathophysiology. (b) Results of animal in vitro studies examining the preventive role of intracellular Hsp72 (Hsp70) expression in experimental sepsis or sepsis-related pathophysiology. (c) Results of genetic animal studies examining the preventive role of intracellular Hsp72 (Hsp70) expression in experimental sepsis or sepsis-related pathophysiology.
Blood samples: increased Hsp72 only after coadministration of Gln and ciprofloxacin [26]
Quercetin blocked Gln-mediated enhancement of Hsp and HSF-1-p expressions and survival benefit (2) LD75 dose of P. aeruginosa and ciprofloxacin in combinations (1)
Prevented ARDS (2) arterial pressure, cardiac contractility restored in the Gln than in the LPS shock (2) Quercetin prevented Gln protection (1) No difference in hemodynamic parameters (1)
Inhibited activation, translocation of NF-κB to the nucleus degradation of IKBalpha, phosphorylation of p38 MAPK, ERK, increased MKP-1 (1) lung HMGB-1 expression NF-κB DNA-binding activity suppressed (1) Reduced peroxide biosynthesis (1)
iNOS mRNA completely abolished by HS-Hsp70–transfected cells (1) HS inhibited LPS-induced NF-κB and HSF-1 activity (1) increases both cellular SK1 mRNA and protein levels (1)
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Enhanced (2)
CLP rats, murine lung epithelial-12 cells in culture [47] Murine macrophage-like RAW 264.7 cells [12]
Exogenous Hsp72
Lungs (1) Macrophages (1)
Overexpression of Hsp72 in RAW/Hsp72 cells (1) —
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Limited nuclear translocation of NF-κB, phosphorylation of IkappaBalpha (2) Inhibition of the MAP kinases (p38, JNK, and ERK) (1)
Inhibition of the NF-κB - HMGB1-induced release of TNF-, IL-1 (1)