Abstract
Parthenolide (PTN), a selective nuclear factor kappa B (NF-κB) inhibitor, has been used extensively to inhibit NF-κB activation. The duration of the inhibitory effect of PTN on NF-κB in vivo remains unclear. This study was to determine whether a lipopolysaccharide (LPS) challenge 6, 12 and 24 h after the administration of PTN could activate NF-κB. Rats were devided into five groups. The rats in the PTN, PTN+LPS and DMSO groups were injected intraperitoneally with PTN or DMSO. After 6, 12 or 24 h, LPS was administered in LPS and PTN+LPS groups. The expressions of NF-κB p50, IκBα and p-IκBα were inhibited in both PTN and PTN+LPS group at end of 6 and 12 h and no effects at 24 h. In summary, myocardial NF-κB expression occurs 1 h after the administration of LPS. PTN blocks this effect given at 6 h and no inhibitory effect 24 h after administration in vivo.
Highlights
NF-κB as a central event leading to the activation of sepsis and septic shock can be activated by a variety of pathogens known to cause septic shock syndrome[2]
We investigated the specific role of NF-κB translocation in rat myocardium after an LPS challenge and determined whether the administration of PTN as a NF-κB inhibitor 6, 12 and 24 h prior could inhibit this effect
The NF-κB p50 protein at 6 h was up-regulated in the LPS group [(97±10)%, P < 0.05] in comparison with the CON group [(36±11)%], but there was no significant difference in the expression of NF-κB p50 in the PTN, DMSO and PTN+LPS groups [(32±9)%, (37±12)% and (41±13)%, respectively] compared to the CON group (Fig. 2A)
Summary
Parthenolide (PTN), an NF-κB inhibitor, is responsible for many anti-inflammatory effects and has been used extensively in previous studies[3,4,5,6,7,8]. In vitro study has suggested that PTN can inhibit IKK and directly inactivate NF-κB[4]. Other studies have reported that PTN inhibits NF-κB activation in cultured cells and experimental models[5,6,7,8]. Evidence supports the concept that PTN can inhibit NF-κB activation by selective inhibition of IKK activation and IκBα degradation; data regarding effectiveness of PTN duration in vivo are currently unavailable. Treating cells with lipopolysaccharide (LPS) results in the dissociation of cytoplasmic complexes containing NF-κB and the translocation of free NF-
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