sybr-green-i and Reperfusion-Injury

sybr-green-i has been researched along with Reperfusion-Injury* in 2 studies

Other Studies

2 other study(ies) available for sybr-green-i and Reperfusion-Injury

ArticleYear
Epigallocatechin-3-gallate protects kidneys from ischemia reperfusion injury by HO-1 upregulation and inhibition of macrophage infiltration.
    Transplant international : official journal of the European Society for Organ Transplantation, 2011, Volume: 24, Issue:5

    Epigallocatechin-3-gallate (EGCG) shows diverse chemical and biological activities. We investigated the effects of EGCG in a rat renal ischemia reperfusion (I/R) injury model. Sprague-Dawley rats received intraperitoneal injection of 50 mg/kg EGCG 48 h, 24 h, and 30 min prior to I/R injury. The animals were subjected to left renal occlusion for 45 min. EGCG treatment suppressed the peak in serum creatinine. EGCG-treated kidneys showed significantly less tubular damage and a decreased number of apoptotic cells. The I/R-induced elevation in the renal MDA level was significantly decreased in the EGCG group. Reverse-transcriptase polymerase chain reaction showed that EGCG significantly decreased the expression of MHC class II, TLR2, TLR4, MCP-1, IL-18, TGF-β1, procollagen Ia1, TIMP-1, and Kim-1. ED-1 staining showed reduced macrophage infiltration and α-SMA staining revealed less interstitial expression. Heme oxygenase-1 (HO-1) expression in I/R kidneys was upregulated in the EGCG group based on the results of both RT-PCR and Western blotting analysis. Blockade of HO-1 gene induction by SnPP increased renal tubular damage and macrophage infiltration. These findings suggest that EGCG protects the kidneys against I/R injury by reducing macrophage infiltration and decreasing renal fibrosis. These beneficial effects may be mediated, in part, by augmentation of the HO-1 gene.

    Topics: Actins; Animals; Apoptosis; Benzothiazoles; Catechin; Diamines; Heme Oxygenase (Decyclizing); Kidney; Lipid Peroxidation; Macrophages; Malondialdehyde; Muscle, Smooth; Organic Chemicals; Quinolines; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Reverse Transcriptase Polymerase Chain Reaction; Up-Regulation

2011
Exogenous IL-6 inhibits acute inflammatory responses and prevents ischemia/reperfusion injury after intestinal transplantation.
    American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2004, Volume: 4, Issue:4

    Interleukin-6 (IL-6) is a pleiotropic acute reactant cytokine involved in inflammatory responses. To explore the role of IL-6 in inflammation, this study examined the efficacy of exogenous IL-6 in preventing intestinal ischemia/reperfusion (I/R) injury associated with small bowel transplantation (SBTx). Syngenic orthotopic SBTx was performed in Lewis rats after 6-h graft preservation in University of Wisconsin (UW) at 4 degrees C. IL-6 mutein (IL-6m, 500 microg/kg), a recombinant molecular variant of human IL-6, was subcutaneously given to donors 2 h before harvesting (IL-6mD) or to excised grafts by luminal infusion (IL-6mG). Animal survival was 100% and 75% in IL-6mD (p<0.05 vs. control) and IL-6mG groups, respectively, compared with 64.3% in untreated controls. The severity of I/R injury (e.g. epithelial denudation, villous congestion) was reduced with IL-6m, in addition to a striking increase in re-epithelization. With IL-6m, neutrophil extravasation was markedly reduced in intestinal grafts and in remote organs (e.g. lung). IL-6m mediated anti-inflammatory effects through the inhibition of I/R-induced up-regulation of intragraft and circulating IL-1-beta, tumor necrosis factor-alpha (TNF-alpha) and IL-6. IL-6m also increased intestinal graft tissue blood flow. These results show that IL-6 is effective in protecting the intestine from cold I/R injury by maintaining graft blood flow and reducing pro-inflammatory cytokine up-regulation and neutrophil infiltration.

    Topics: Acute Disease; Animals; Benzothiazoles; Blotting, Western; Cytokines; Diamines; Immunohistochemistry; Inflammation; Interleukin-1; Interleukin-6; Intestinal Mucosa; Intestines; Lung; Male; Mutation; Neutrophils; Organ Transplantation; Organic Chemicals; Peroxidase; Quinolines; Rats; Rats, Inbred Lew; Reperfusion Injury; Repressor Proteins; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Suppressor of Cytokine Signaling 3 Protein; Suppressor of Cytokine Signaling Proteins; Time Factors; Transcription Factors; Tumor Necrosis Factor-alpha; Up-Regulation

2004