Animal models for the assessment of acute renal dysfunction and injury

Endre, Z. H.; Edelstein, Charles L.

doi:10.1007/978-0-387-84843-3_9

Cited by 4 publications

(3 citation statements)

References 308 publications

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“…Experimental studies in AKI have utilized ischemia-reperfusion, sepsis-endotoxemia, and nephrotoxic models [ 20 ]. These models of AKI are associated with a strong inflammatory reaction.…”

Section: Introductionmentioning

confidence: 99%

Mediators of Inflammation in Acute Kidney Injury

Akçay

Nguyen

Edelstein

2009

Mediators of Inflammation

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435

368

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Acute kidney injury (AKI) remains to be an independent risk factor for mortality and morbidity. Inflammation is now believed to play a major role in the pathopathophysiology of AKI. It is hypothesized that in ischemia, sepsis and nephrotoxic models that the initial insult results in morphological and/or functional changes in vascular endothelial cells and/or in tubular epithelium. Then, leukocytes including neutrophils, macrophages, natural killer cells, and lymphocytes infiltrate into the injured kidneys. The injury induces the generation of inflammatory mediators like cytokines and chemokines by tubular and endothelial cells which contribute to the recruiting of leukocytes into the kidneys. Thus, inflammation has an important role in the initiation and extension phases of AKI. This review will focus on the mediators of inflammation contributing to the pathogenesis of AKI.

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“…Experimental studies in AKI have utilized ischemia-reperfusion, sepsis-endotoxemia, and nephrotoxic models [ 20 ]. These models of AKI are associated with a strong inflammatory reaction.…”

Section: Introductionmentioning

confidence: 99%

Mediators of Inflammation in Acute Kidney Injury

Akçay

Nguyen

Edelstein

2009

Mediators of Inflammation

Self Cite

435

368

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“…An inflammatory cascade reaction is one of the main causes of renal injury caused by cisplatin [24]. Experimental studies of AKI often use models such as ischemia and reperfusion injury-, drug nephrotoxicity, and sepsis endotoxemia [25], all of which involve inflammation [11,26,27]. Apoptosis, or programmed necrosis, of renal tubular epithelial cells is a common pathological feature in AKI models [13,14].…”

Section: Discussionmentioning

confidence: 99%

Eleutheroside B Protects against Acute Kidney Injury by Activating IGF Pathway

Zang

Yang

2019

Molecules

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Acute kidney injury (AKI) is a common, complex, and severe clinical syndrome characterized by rapid decline in renal function, combined with tissue damage. Currently, the prevention and treatment of AKI are focused on symptomatic treatment, rather than treating the underlying causes. Therefore, there is no specific treatment to prevent renal injury except for renal dialysis. In this study, we used cisplatin-induced AKI mouse and human kidney-2 (HK-2) cell models to evaluate the renal protective effect of eleutheroside B, an active compound in traditional Chinese medicines. MTT assay was used to detect the effect of eleutheroside B on proliferation of human HK-2 cells in presence and in absence of cisplatin. Western blot and immunostaining were used to detect the protein level of kidney injury molecule-1 (KIM-1), cleaved caspase-3, receptor-interacting protein kinase (RIPK)-1, and RIPK-3. Real-time PCR was used to detect the mRNA levels of chemokines (like monocyte chemotactic protein 1, MCP-1) and pro-inflammatory cytokines including interleukin-6 (IL-6) and tumor necrosis factor (TNF-α). Flow cytometry assay was used to detect apoptosis of HK-2 cells. In vivo results showed that eleutheroside B reduced the increase in serum creatinine and blood urea nitrogen (BUN) levels in the AKI model. Periodic acid-Schiff staining and Western blot analysis of KIM-1 showed that eleutheroside B alleviated tubular cell injury. Further, eleutheroside B reduced macrophage infiltration and production of inflammatory cytokines, inhibited the activation of nuclear factor (NF)-κB, and inhibited apoptosis and programmed necrosis. The mechanism may be that eleutheroside B can activate the insulin-like growth factor (IGF) pathway and its downstream pathway by downregulating the expression of IGFBP-7, thus promoting cell proliferation. Therefore, our results suggest that eleutheroside B is a potential drug for AKI treatment.

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“…20,21 Experimental studies in AKI have utilized I/R, sepsiseendotoxemia, and nephrotoxic models. 22 These models of AKI are associated with an increase in infiltrating neutrophils in the kidneyand induced inflammatory reactions which can be attenuated by antiintercellular adhesion molecule-1 (ICAM-1) and/or anti-CD44 therapy. 23e29 Other leukocytes such as natural killer cells also play an important role in renal tubular cell apoptosis during ischemia/ reperfusion (I/R) injury.…”

Section: Acute Kidney Injury and Inflammationmentioning

confidence: 99%