benzyloxycarbonylleucyl-leucyl-leucine-aldehyde and helenalin
benzyloxycarbonylleucyl-leucyl-leucine-aldehyde has been researched along with helenalin* in 1 studies
Other Studies
1 other study(ies) available for benzyloxycarbonylleucyl-leucyl-leucine-aldehyde and helenalin
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Nuclear factor-kappaB p65 and upregulation of interleukin-6 in retinal ischemia/reperfusion injury in rats.
We previously demonstrated that endogenous interleukin-6 (IL-6) is upregulated and may be neuroprotective after retinal ischemia. The purpose of this study is to investigate the role of nuclear factor kappa-B (NF-kappaB) in regulating IL-6 expression after ischemia. NF-kappaB p65 mRNA levels were significantly elevated between 2 and 12 h after the insult. A high number of NF-kappaB p65 positive cells were detected in the inner retina at 12 h after ischemia. Activated nuclear NF-kappaB p65 and IL-6 were colocalized in cells, which were also marked by a microglial/phagocytic cell marker (ED1) in the inner retina. Carbobenzoxy-L-leucyl-L-leucyl-L-leucinal (MG-132, a proteasome inhibitor, which inhibits IkappaB degradation and hence prevents the activation and translocation of NF-kappaB into the nucleus) abolished the increase in NF-kappaB p65 mRNA levels after the insult, while there was no effect by helenalin (an inhibitor which inhibits NF-kappaB activity by alkylation of the p65 subunit, thereby blocking its binding to the target DNA). However, MG-132 and/or helenalin significantly diminished the increase in IL-6 mRNA levels after the insult. Small interfering RNAs (siRNAs, inhibit target gene expression through the sequence-specific destruction of the target messenger RNA) against NF-kappaB p65 significantly reduced the increase in NF-kappaB p65 mRNA levels as well as IL-6 mRNA levels after ischemia. The number of retinal ganglion cells (RGCs) was also significantly decreased using the inhibitors of NF-kappaB compared with those of the controls after ischemia. These findings support the hypothesis that upregulation of endogenous retinal IL-6 in retinal I/R injury in microglial/phagocytic cells is controlled predominantly by NF-kappaB p65. Topics: Analysis of Variance; Animals; Anti-Inflammatory Agents, Non-Steroidal; Cell Count; Cysteine Proteinase Inhibitors; Drug Interactions; Gene Expression Regulation; Immunohistochemistry; Interleukin-6; Leupeptins; Male; NF-kappa B; Rats; Rats, Inbred Lew; Reperfusion Injury; Retina; Retinal Ganglion Cells; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; RNA, Small Interfering; Sesquiterpenes; Sesquiterpenes, Guaiane; Time Factors | 2006 |