Effects of SA13353, a Transient Receptor Potential Vanilloid 1 Agonist, on Leukocyte Infiltration in Lipopolysaccharide-Induced Acute Lung Injury and Ovalbumin-Induced Allergic Airway Inflammation

Tsuji, Fumio; Murai, Masaaki; Oki, Kenji; Inoue, Hiroyuki; Sasano, Minoru; Tanaka, Hiroyuki; Inagaki, Nobuya; Aono, Hiroyuki

doi:10.1254/jphs.09295sc

Cited by 23 publications

(11 citation statements)

References 15 publications

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“…On the other hand, the anti-inflammatory cytokine IL-10 has been shown recently to inhibit ischemic and cisplatin-induced AKI [7]. In addition, we have demonstrated recently that SA13353 attenuated neutrophil infiltration and the increase of TNF-α and CINC-1 level in lung inflammation [32]. Therefore, we investigated the effects of SA13353 on TNF-α, CINC-1, and IL-10 mRNA expression in the postischemic kidneys.…”

Section: Discussionmentioning

confidence: 95%

Preventive Effect of SA13353, a Novel Transient Receptor Potential Vanilloid 1 Agonist, on Ischemia/Reperfusion-Induced Renal Injury in Rats

Ueda¹,

Tsuji²,

Hirata³

et al. 2015

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Tumor necrosis factor (TNF)-α plays a crucial role in the pathogenesis of ischemia/reperfusion-induced renal injury. We demonstrated recently that the preischemic treatment with resiniferatoxin, a transient receptor potential vanilloid 1 (TRPV1) agonist, attenuates renal TNF-α mRNA expression, and improves ischemia/reperfusion-induced renal injury in rats. In the present study, we investigated effects of treatment with SA13353, a novel orally active TRPV1 agonist, on ischemia/reperfusion-induced renal injury in rats. Ischemic acute kidney injury (AKI) was induced by occlusion of the left renal artery and vein for 45 min followed by reperfusion, 2 weeks after contralateral nephrectomy. Renal function in vehicle-treated AKI rats markedly decreased at 24 h after reperfusion. Treatment with SA13353 (3, 10, and 30 mg/kg, p.o.) 30 min before ischemia dose-dependently attenuated the ischemia/reperfusion-induced renal dysfunction. Histopathological examination of the kidney of AKI rats revealed severe renal damage, which were significantly suppressed by the SA13353 treatment. In renal tissues exposed to ischemia/reperfusion, TNF-α and cytokine-induced neutrophil chemoattractant-1 mRNA expressions were augmented, but these alterations were attenuated by the treatment with SA13353. On the other hand, ischemia/reperfusion-enhanced renal interleukin-10 mRNA expression and its plasma concentration were further augmented by SA13353 treatment. These results demonstrate that the orally active TRPV1 agonist SA13353 prevents the ischemia/reperfusion-induced AKI. This renoprotective effects seem to be closely related to the inhibition of inflammatory response via TRPV1 activation.

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Section: Discussionmentioning

confidence: 95%

Preventive Effect of SA13353, a Novel Transient Receptor Potential Vanilloid 1 Agonist, on Ischemia/Reperfusion-Induced Renal Injury in Rats

Ueda¹,

Tsuji²,

Hirata³

et al. 2015

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“…Bone marrowderived macrophages (BMDM) were generated and stimulated with LPS, a well characterized bacterial stimulus of macrophage responses and a major cause of death in septic shock (36). After being stimulated with LPS for 18 h (37) or 24 h, macrophages from IL-19 −/− mice produced significantly more TNF-α and IL-12 than did wild-type (WT) cells.…”

Section: Il-19mentioning

confidence: 99%

Interleukin-19 Is a Negative Regulator of Innate Immunity and Critical for Colonic Protection

et al. 2011

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Abstract. The cytokine, interleukin (IL)-19, is a member of the IL-10 family that includes . Recent studies have shown that IL-19 is produced by keratinocytes, epithelial cells, macrophages, and B-cells. Little is known about the exact biological role of IL-19 in immunological regulation, although there is an increasing body of data demonstrating that IL-19 is associated with the development of Th2 responses and the pathogenesis of psoriasis. In this review, I shall attempt to discuss current knowledge about the role of IL-19 on macrophages and the potential role in inflammatory bowel disease.

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“…Later, similar beneficial effects were also shown in a different rat model of sepsis, where capsaicin significantly attenuated systemic inflammation and multiple organ damage caused by sepsis, and protected against mortality 177. Other TRPV1 agonists and antagonists have also been evaluated in different models of sepsis, all showing a consistent decrease in the development of sepsis or a reduction in some of the pathological symptoms when TRPV1 is activated 178–180…”

Section: Is Trpv1 Involved In Sepsis?mentioning

confidence: 74%

Role of the transient receptor potential vanilloid 1 in inflammation and sepsis

Devesa¹,

Planells-Cases²,

Fernández‐Ballester³

et al. 2011

JIR

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The transient receptor potential vanilloid 1 (TRPV1) is a thermoreceptor that responds to noxious temperatures, as well as to chemical agonists, such as vanilloids and protons. In addition, its channel activity is notably potentiated by proinflammatory mediators released upon tissue damage. The TRPV1 contribution to sensory neuron sensitization by proalgesic agents has signaled this receptor as a prime target for analgesic and anti-inflammatory drug intervention. However, TRPV1 antagonists have notably failed in clinical and preclinical studies because of their unwanted side effects. Recent reports have unveiled previously unrecognized anti-inflammatory and protective functions of TRPV1 in several diseases. For instance, this channel has been suggested to play an anti-inflammatory role in sepsis. Therefore, the use of potent TRPV1 antagonists as a general strategy to treat inflammation must be cautiously considered, given the deleterious effects that may arise from inhibiting the population of channels that have a protective function. The use of TRPV1 antagonists may be limited to treating those pathologies where enhanced receptor activity contributes to the inflamed state. Alternatively, therapeutic paradigms, such as reduction of inflammatory-mediated increase of receptor expression in the cell surface, may be a better strategy to prevent abrogation of the TRPV1 subpopulation involved in anti-inflammatory and protective processes.

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Effects of SA13353, a Transient Receptor Potential Vanilloid 1 Agonist, on Leukocyte Infiltration in Lipopolysaccharide-Induced Acute Lung Injury and Ovalbumin-Induced Allergic Airway Inflammation

Cited by 23 publications

References 15 publications

Preventive Effect of SA13353, a Novel Transient Receptor Potential Vanilloid 1 Agonist, on Ischemia/Reperfusion-Induced Renal Injury in Rats

Preventive Effect of SA13353, a Novel Transient Receptor Potential Vanilloid 1 Agonist, on Ischemia/Reperfusion-Induced Renal Injury in Rats

Interleukin-19 Is a Negative Regulator of Innate Immunity and Critical for Colonic Protection

Role of the transient receptor potential vanilloid 1 in inflammation and sepsis

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