Antithrombin reduces ischemia/reperfusion-induced renal injury in rats by inhibiting leukocyte activation through promotion of prostacyclin production

Mizutani, Akio; Okajima, Kenji; Uchiba, Mitsuhiro; Isobe, Hirotaka; Harada, Naoaki; Mizutani, Sachiko; Noguchi, Takayuki

doi:10.1182/blood-2002-08-2406

Cited by 120 publications

(123 citation statements)

References 39 publications

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“…Renal dysfunction was evaluated by measuring serum levels of blood urea nitrogen (BUN) and creatinine as previously described (16). Blood samples were taken from the abdominal aorta 24 h after reperfusion.…”

Section: Measurement Of Serum Levels Of Blood Urea Nitrogen and Creatmentioning

confidence: 99%

“…Accumulation of neutrophis in the kidney was evaluated by measuring renal myeloperoxidase (MPO) activity at 6 h after reperfusion as described previously (16). In brief, the kidney was removed, weighed, and homogenized in 10% (w/v) 0.05 M phosphate buffer (pH 6.0) containing 0.5% hexadecyltrimethylammonium bromide and sonicated for 20 s. After centrifugation (4500g for 20 min at 4˚C), 0.1 ml of the supernatant was added to 0.55 ml 0.1 M phosphate buffer (pH 6.0) containing 1.25 mg/ml o-dianisidine and 0.05% hydrogen peroxide.…”

Section: Determination Of Renal Myeloperoxidase Activitymentioning

confidence: 99%

“…Activated neutrophils play a critical role in the development of various types of tissue injury induced by endotoxin (14), shock (15), and ischemia/reperfusion (I/R) (16,17) by releasing a wide variety of inflammatory mediators.…”

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confidence: 99%

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Stimulation of FcγRI on Primary Sensory Neurons Increases Insulin-Like Growth Factor-I Production, Thereby Reducing Reperfusion-Induced Renal Injury in Mice

Harada¹,

Zhao²,

Kurihara

et al. 2010

The Journal of Immunology

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Biological role(s) of FcγRI on mouse primary sensory neurons are not fully understood. Sensory neuron stimulation increases insulin-like growth factor-I (IGF-I) production, thereby reducing ischemia/reperfusion (I/R)-induced tissue injury in mice. In this study, we examined whether the Fc fragment of IgG (IgGFc) increases IGF-I production through sensory neuron stimulation, thereby reducing I/R-induced renal injury in mice. IgGFc increased the calcitonin-gene–related peptide (CGRP) release and cellular cAMP levels in dorsal root ganglion neurons isolated from wild-type (WT) mice, whereas, native IgG did not. Pretreatment with anti-FcγRI Ab, a protein kinase A inhibitor KT5710, and a phospholipase A2 inhibitor 4-bromophenylacyl bromide inhibited these effects induced by IgGFc. Administration of IgGFc enhanced increases of renal tissue levels of CGRP and IGF-I and reduced I/R-induced renal injury in WT mice. Increases of renal tissue level of caspase-3, renal accumulation of neutorphils, and renal tubular apoptosis were inhibited by administration of IgGFc in WT mice subjected to renal I/R. Pretreatment with anti–IGF-I Ab completely reversed these effects induced by IgGFc in WT mice. Administration of native IgG did not show any effects in WT mice subjected to renal I/R. None of the effects observed in WT mice was seen after IgGFc administration in CGRP-knockout mice and denervated WT mice. These observations suggest that activation of FcγRI by IgGFc may stimulate sensory neurons, thereby promoting IGF-I production, contributing to reduction of the reperfusion-induced renal injury via attenuation of inflammatory responses in mice.

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Section: Measurement Of Serum Levels Of Blood Urea Nitrogen and Creatmentioning

confidence: 99%

Section: Determination Of Renal Myeloperoxidase Activitymentioning

confidence: 99%

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Stimulation of FcγRI on Primary Sensory Neurons Increases Insulin-Like Growth Factor-I Production, Thereby Reducing Reperfusion-Induced Renal Injury in Mice

Harada¹,

Zhao²,

Kurihara

et al. 2010

The Journal of Immunology

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“…A large number of cytokines generated by I/RIRI, including TNF-α, may promote the expression of ICAM-1 and induce adhesion, aggregation of neutrophile granulocytes on microvascular endothelial cells (9). It is an indicator of I/RIRI inflammatory reactions in vascular endothelial cells (10). In the present study, tanshinone IIA significantly mitigated the TNF-α and IL-6 activities in I/RIRI rats.…”

Section: Discussionmentioning

confidence: 51%

“…The occurrence of I/RIRI may trigger acute rejection and induce early allograft function failure, or it may lead to delayed recovery of allograft function, accelerate loss of allograft function and shorten lifespan (9). The pathogenetic mechanism underlying I/RIRI is complicated, involved in free radical, calcium overloading, energy metabolism dysfunction, inflammatory medium and adhesion molecule, upregulation of cytokines, endothelial dysfunction, abnormal blood rheology and increased apoptosis (10,11).…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA pretreatment attenuates ischemia/reperfusion-induced renal injury

Ding

Huang

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Tanshinone IIA is a chemical compound extracted from the root of traditional Chinese herb Salvia miltiorrhiza Bunge. Tanshinone IIA has been suggested to possess anti-inflammatory activity and antioxidizing capability. Recently, accumulating results have indicated the antitumor activity of tanshinone IIA; thus, it has attracted increasing attention. In addition, tanshinone IIA has been indicated to attenuate ischemia/reperfusion induced renal injury (I/RIRI); however, little is known regarding the underlying mechanisms involved in this process. In the present study an I/RIRI rat model was used to analyze the effects of tanshinone IIA on myeloperoxidase (MPO), TNF-α and IL-6 activities using ELISA kits. Furthermore, macrophage migration inhibitory factor (MIF), cleaved caspase-3, B-cell lymphoma 2 (Bcl-2) and p38 mitogen-activated protein kinase (MAPK) protein expression levels were evaluated using western blot analysis. The results indicated that tanshinone IIA protected renal function in I/RIRI rats. ELISA demonstrated that tanshinone IIA significantly reduced MIF, TNF-α and IL-6 activities in I/RIRI rats. Western blot analysis showed that tanshinone IIA significantly suppressed MIF, cleaved caspase-3 and p38 MAPK protein expression levels in I/RIRI rats. The present results suggest that tanshinone IIA pretreatment attenuates I/RIRI via the downregulation of MPO expression, inflammation, MIF, cleaved caspase-3 and p38 MAPK.

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Inflammation and Coagulation

Levi

2017

Inflammation - From Molecular and Cellular Mechanisms to the Clinic

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Antithrombin reduces ischemia/reperfusion-induced renal injury in rats by inhibiting leukocyte activation through promotion of prostacyclin production

Cited by 120 publications

References 39 publications

Stimulation of FcγRI on Primary Sensory Neurons Increases Insulin-Like Growth Factor-I Production, Thereby Reducing Reperfusion-Induced Renal Injury in Mice

Stimulation of FcγRI on Primary Sensory Neurons Increases Insulin-Like Growth Factor-I Production, Thereby Reducing Reperfusion-Induced Renal Injury in Mice

Tanshinone IIA pretreatment attenuates ischemia/reperfusion-induced renal injury

Inflammation and Coagulation

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