Animal models of nephrotic syndrome

Simić, Ivana; Tabatabaeifar, Mansoureh; Schaefer, Franz

doi:10.1007/s00467-012-2376-5

Cited by 26 publications

(21 citation statements)

References 71 publications

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“…The mechanism by which ADR induces podocyte injury has been widely investigated, including both non-immune and immune factors [16,21]. The level of several serum cytokines was assessed in the mice AN model, including TGF-β, IL-6, IL-23, IL-17, IL-10 and IL-4.…”

Section: Resultsmentioning

confidence: 99%

Induction of C-Mip by IL-17 Plays an Important Role in Adriamycin-Induced Podocyte Damage

Yan-Bo

Lin

et al. 2015

Cell Physiol Biochem

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Background/Aims: Although the disturbance of T lymphocyte and glomerular podocyte exerts a crucial function in the pathogenesis of proteinuria, the potential link is still unclear. Methods: The balance of Treg and Th17 cells, and the expression of IL-17/IL-17R and c-mip were investigated in adrimycin-induced nephropathy (AN) mice. The effect and mechanism of IL-17 on podocyte were explored in cultured podocytes. Results: The proportion of Th17 cells in peripheral blood mononuclear cells, the amount of IL-17 in serum and kidney cortical homogenates, and the expression of IL-17R and c-mip in glomerular podocyte were increased obviously in AN mice. In cultured podocytes, recombinant IL-17 led to an induction of apoptosis and cytoskeletal disorganization, an overproduction of c-mip while down-regulation of phosphor-nephrin, and an increased binding of c-mip to NF-κB/RelA. Silence of c-mip prevented podocyte apoptosis and reduction of phosphor-nephrin by prompting nuclear translocation of NF-κB/RelA in IL-17 treated cells. Persistent activation of NF-κB up-regulated pro-survival protein Bcl-2 and decreased podocyte apoptosis, but had no effect on phosphor-nephrin level. Conclusion: These findings demonstrated that induction of IL-17 released by Th17 cells plays a key role in podocytopathy most likely through down-regulation of phosphor-nephrin and Bcl-2 level via overproduction of c-mip.

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Section: Resultsmentioning

confidence: 99%

Induction of C-Mip by IL-17 Plays an Important Role in Adriamycin-Induced Podocyte Damage

Yan-Bo

Lin

et al. 2015

Cell Physiol Biochem

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“…Moreover, it has not been proven that platelet alterations play a role in the pathogenesis of the prothrombotic state in NS. Therefore, future research should focus on the pathogenesis of platelet alterations in NS, using an NS animal model, such as puromycin aminonucleoside-treated rats [88]. Furthermore, prospective epidemiologic studies are needed to investigate the relationship between platelet alterations and the incidence of thrombotic complications.…”

Section: Conclusion and Direction Of Future Researchmentioning

confidence: 97%

Platelet abnormalities in nephrotic syndrome

et al. 2015

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Nephrotic syndrome (NS) is a common kidney disease associated with a significantly increased risk of thrombotic events. Alterations in plasma levels of pro- and anti-coagulant factors are involved in the pathophysiology of venous thrombosis in NS. However, the fact that the risk of both venous and arterial thrombosis is elevated in NS points to an additional role for blood platelets. Increased platelet counts and platelet hyperactivity have been observed in nephrotic children. Platelet hyperaggregability, increased release of active substances, and elevated surface expression of activation-dependent platelet markers have been documented. The mechanisms underlying those platelet alterations are multifactorial and are probably due to changes in plasma levels of platelet-interfering proteins and lipid changes, as a consequence of nephrosis. The causal relationship between platelet alterations seen in NS and the occurrence of thromboembolic phenomena remains unclear. Moreover, the efficiency of prophylactic treatment using antiplatelet agents for the prevention of thrombotic complications in nephrotic patients is also unknown. Thus, antiplatelet medication is currently not generally recommended for routine prophylactic therapy.

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“…In the kidney, ROS are important causes of acute and subacute renal failure in most cases. Also, in certain animal models of NS, superoxide anions and hydroxyl radicals are the main causes of nephrotoxicity [11]. It has also been reported that renal failure that results from increased ROS and decreased antioxidant enzyme can be prevented by antioxidant therapy [12, 13].…”

Section: Introductionmentioning

confidence: 99%

Protection Effect of Zhen‐Wu‐Tang on Adriamycin‐Induced Nephrotic Syndrome via Inhibiting Oxidative Lesions and Inflammation Damage

Liang

Lai

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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Zhen-wu-tang (ZWT), a well-known formula in China, is widely used to treat chronic kidney diseases. However, very little information on ZWT's mechanism of action is currently available. In this study, we investigated the possible protective role and underlying mechanism of ZWT on nephrotic syndrome (NS) induced by Adriamycin (intravenous injection, 6.0 mg/kg) in rats using biochemical and histopathological approaches. ZWT decreased urine protein excretion and the serum levels of total cholesterol, triglycerides, blood urea nitrogen, and creatinine significantly in diseased rats. A decrease in plasma levels of total protein and albumin was also recorded in nephropathic rats. Pathological results show an improved pathological state and recovering glomerular structure in ZWT treatment groups. ZWT decreased renal IL-8 level but increased renal IL-4 level. In addition, rats subjected to ZWT exhibited less IgG deposition in glomerulus compared with model group. RT-PCR results showed that ZWT decreased the mRNA expression of NF-κB p65 and increased the mRNA expression of IκB. Furthermore, ZWT reduced the level of MDA and increased SOD activity. These results demonstrated that ZWT ameliorated Adriamycin-induced NS in rats possibly by inhibiting Adriamycin-induced inflammation damage, enhancing body's antioxidant capacity, thereby protecting glomerulus from injury.

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Animal models of nephrotic syndrome

Cited by 26 publications

References 71 publications

Induction of C-Mip by IL-17 Plays an Important Role in Adriamycin-Induced Podocyte Damage

Induction of C-Mip by IL-17 Plays an Important Role in Adriamycin-Induced Podocyte Damage

Platelet abnormalities in nephrotic syndrome

Protection Effect of Zhen‐Wu‐Tang on Adriamycin‐Induced Nephrotic Syndrome via Inhibiting Oxidative Lesions and Inflammation Damage

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