Fluvastatin ameliorates endotoxin induced multiple organ failure in conscious rats

Chen, Chung Hua; Lee, Ru Ping; Wu, Weiliang; Liao, Kuang‐Wen; Hsu, Nanly; Hsu, Bang Gee

doi:10.1016/j.resuscitation.2006.12.002

Cited by 33 publications

(27 citation statements)

References 27 publications

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“…To examine the effects of statin treatment on clinical outcome in experimental cerebral malaria, simvastatin was administered once a day beginning one day prior to inoculation with P. berghei at a dose (2 mg/kg/day) based on previous studies in which statins improved outcome in both the CLP and systemic LPS mouse models of experimental sepsis. 13,14,26 Treatment with simvastatin was continued until mice died or recovered from cerebral malaria. Simvastatin failed to improve survival compared with vehicle-treated C57BL/6 mice ( P = 0.61), and no mice survived past day 7 post-infection ( Figure 1A ).…”

Section: Resultsmentioning

confidence: 99%

“…[6][7][8][9] Therapeutic statin-mediated immunomodulatory activity has been demonstrated in animal models of asthma and sepsis. [10][11][12][13][14][15][16][17] Specifically, statins have been reported to improve survival in the cecal-ligation and puncture (CLP) and lipopolysaccharide (LPS)-injection models of sepsis. [10][11][12][13][14] Based on clinical similarities between sepsis and cerebral malaria, the objective of this study was to examine the impact of statins on the innate immune response and clinical outcome in experimental cerebral malaria.…”

Section: Introductonmentioning

confidence: 99%

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Statins Fail to Improve Outcome in Experimental Cerebral Malaria and Potentiate Toll-Like Receptor-Mediated Cytokine Production by Murine Macrophages

Helmers

Gowda²,

Kain

et al. 2009

The American Journal of Tropical Medicine and Hygiene

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Abstract. Cerebral malaria is responsible for a large proportion of the estimated one million deaths caused by Plasmodium falciparum malaria annually. This disease is associated with excessive pro-inflammatory cytokine production resulting from dysregulated host responses to infection. On the basis of reports indicating potent activity against host-mediated inflammatory disorders such as sepsis, we examined the activity of statins (3-hydroxy-3-methylglutarylcoenzyme A reductase inhibitors) on malaria-associated inflammation in vivo and in vitro . Simvastatin failed to improve survival or alter parasitemia in C57BL/6 mice infected with Plasmodium berghei ANKA, an experimental model of cerebral malaria. In vitro statin treatment potentiated production of tumor necrosis factor and interleukin-6 by murine peritoneal macrophages in response to P. falciparum glycosylphosphatidyl inositol, a Toll-like receptor 2 (TLR2) ligand. Statin treatment also potentiated pro-inflammatory cytokine production stimulated by a panel of TLR2 and TLR4 ligands. Our results indicate that statins fail to confer protection in experimental cerebral malaria and potentiate TLR-mediated proinflammatory cytokine production by primary murine macrophages.

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Section: Resultsmentioning

confidence: 99%

Section: Introductonmentioning

confidence: 99%

Statins Fail to Improve Outcome in Experimental Cerebral Malaria and Potentiate Toll-Like Receptor-Mediated Cytokine Production by Murine Macrophages

Helmers

Gowda²,

Kain

et al. 2009

The American Journal of Tropical Medicine and Hygiene

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“…TNF-a and IL-6 measured by ELISA TNF-a and IL-6 concentrations in blood samples were measured separately by antibody enzyme-linked immunosorbent assay (ELISA) with the commercial antibody pair, the recombinant standard and the biotin-streptavidin-peroxidase detection system (Endogen, Rockford, IL, USA) as described previously (Chen et al 2007). Blood samples were collected in serum-separated tubes.…”

Section: Blood Sample Analysesmentioning

confidence: 99%

Single dose intravenous thioacetamide administration as a model of acute liver damage in rats

Chen

Subeq

Lee

et al. 2008

Int J Experimental Path

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1Contributed equally to this study. SummaryThioacetamide (TAA) has been used extensively in the development of animal models of acute liver injury. Frequently, TAA is administered intraperitoneally to induce liver damage under anaesthesia. However, it is rarely administered by intravenous injection in conscious rats. The experiments in this study were designed to induce acute liver damage by single intravenous injection of TAA (0, 70 and 280 mg ⁄ kg) in unrestrained rats. Biochemical parameters and cytokines measured during the 60-h period following TAA administration, included white blood cells (WBC), haemoglobulin (Hb), platelet, aspartate transferase (GOT), alanine transferase (GPT), total bilirubin (TBIL), direct bilirubin (DBI), albumin, ammonia (NH3), r-glutamyl transpeptidase (r-GT), tumour necrosis factor-a (TNF-a) and interleukin-6 (IL-6). Rats were sacrificed by decapitation 60 h after TAA administration and livers were removed immediately for pathology and immunohistochemical (IHC) examination. Another group of rats were sacrificed by decapitation 1, 6 and 24 h after TAA administration and livers were removed immediately for time course change of pathology and IHC examination. TAA significantly increased blood WBC, GOT, GPT, TBIL, DBIL, NH3, r-GT, TNF-a and IL-6 levels but decreased the blood Hb, platelet and albumin level. The levels of histopathological damage in the liver after intravenous TAA administration were also increased with a dose-dependent trend and more increased at 60 h after TAA administration. The levels of inducible nitric oxide synthase (iNOS) and nuclear factor-jB (NF-jB) detected by IHC in the liver after intravenous TAA administration were also increased with a dose-dependent trend and more increased at 1 h after TAA administration. Single intravenous TAA administration without anaesthesia is a restorable animal model which may be used to investigate acute liver damage.

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“…[17] All reagents, samples, and working standards were brought to room temperature and prepared according to the manufacturer's directions. The quantification of the reactions was determined by optical density using an automated ELISA reader (Sunrise; Tecan Co., Grödingen, Austria) at 450/540 nm.…”

Section: Elisa Measurement For Tnf-a and Il-10mentioning

confidence: 99%

IntravenousN-acetylcysteine with Saline Hydration Improves Renal Function and Ameliorates Plasma Total Homocysteine in Patients Undergoing Cardiac Angiography

et al. 2008

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Proinflammatory cytokines and hyperhomocysteinemia are associated with clinically relevant restenosis in coronary artery disease. N-acetylcysteine (NAC) can decrease proinflammatory cytokines and plasma homocystine as well as reduce contrastinduced nephropathy. The aim of this study, therefore, was to compare normal saline hydration with and without intravenous NAC in terms of changes in renal function, proinflammatory cytokines, inflammatory markers, and plasma total homocysteine during coronary angiography. Forty-six patients who underwent coronary angiography and/or stent implantation for unstable angina were enrolled and assigned to NAC or NS treatment groups based on normal saline hydration with or without intravenous NAC, respectively. The NS group had lower serum creatinine (Cre: p = 0.02) and plasma total homocysteine (tHcy; p < 0.001) and increased glomerular filtration rate (GFR; p = 0.003) after angiography. In the NAC group, the serum blood urea nitrogen (BUN; p = 0.001), Cre (p < 0.001), and plasma tHcy (p < 0.001) were lower, and the GFR (P = 0.013) was increased after angiography. There were no statistically significant differences in serum high-sensitivity C reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), or interleukin-10 (IL-10) before and after angiography in the NS and NAC groups. Intergroup comparison revealed that plasma tHcy level was lower for the NAC-treated patients (p = 0.002), with lower plasma tHcy level before and after treatment in this group (p < 0.001). Normal saline hydration can improve renal function and decrease plasma tHcy after coronary angiography with or without NAC; however, the combination of the two decreases plasma tHcy more than normal saline hydration alone.

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Fluvastatin ameliorates endotoxin induced multiple organ failure in conscious rats

Cited by 33 publications

References 27 publications

Statins Fail to Improve Outcome in Experimental Cerebral Malaria and Potentiate Toll-Like Receptor-Mediated Cytokine Production by Murine Macrophages

Statins Fail to Improve Outcome in Experimental Cerebral Malaria and Potentiate Toll-Like Receptor-Mediated Cytokine Production by Murine Macrophages

Single dose intravenous thioacetamide administration as a model of acute liver damage in rats

IntravenousN-acetylcysteine with Saline Hydration Improves Renal Function and Ameliorates Plasma Total Homocysteine in Patients Undergoing Cardiac Angiography

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