Effect of Intervention in Mast Cell Function Before Reperfusion on Renal Ischemia-Reperfusion Injury in Rats

Tong, Fei; Luo, Lei; Liu, Daojun

doi:10.1159/000443437

Cited by 23 publications

(18 citation statements)

References 33 publications

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“…Of note in this context, Baba et al (55) recently showed in a rat model of chronic renal failure unchanged fibrosis progression after tranilast treatment, a potent MC stabilizer. Thus, our data strongly support that the degree of initial injury by MCs represents the major factor of pathologic development, calling for early MC-targeting therapeutic interventions as suggested recently (41).…”

Section: Discussionsupporting

confidence: 82%

“…Indeed, recent data showed that treatment before reperfusion with cromolyn sodium or ketotifen, which are known MC stabilizers, markedly alleviated IRI-mediated kidney injury in rats, whereas exacerbated MC degranulation by compound 48/80 further aggravated kidney injury (41). Likewise, in another model of acute nephrotoxicity based on administration of the anticancer drug cisplatin, MCs were shown to significantly contribute to the initial renal injury by promoting neutrophil infiltration via the production of TNF (44).…”

Section: Discussionmentioning

confidence: 99%

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Early Phase Mast Cell Activation Determines the Chronic Outcome of Renal Ischemia–Reperfusion Injury

Danelli

Madjène

Madera-Salcedo

et al. 2017

The Journal of Immunology

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Ischemia–reperfusion injury (IRI) is an important cause of acute kidney injury that can lead to end-stage renal failure. Although the ensuing inflammatory response can restore homeostasis, a consecutive maladaptive repair and persistent inflammation represent important risk factors for postischemic chronic kidney disease development. In this study, we investigated the role of mast cells in both the early and late phases of the inflammatory response in experimental models of acute and chronic renal IRI using our recently developed mouse model that allows conditional ablation of mast cells. Depletion of mast cells prior to IRI resulted in improved renal function due to diminished local inflammatory cytokine/chemokine levels and neutrophil recruitment to the kidneys after the acute injury phase (48 h post-IRI). Furthermore, although not completely protected, mast cell–depleted mice displayed less organ atrophy and fibrosis than did wild-type mice during the chronic phases (2 and 6 wk post-IRI) of disease development. Conversely, mast cell ablation after the acute phase of IRI had no impact on organ atrophy, tubular necrosis, or fibrosis. Thus, our results suggest a deleterious role of mast cells during the acute inflammatory phase of IRI promoting subsequent fibrosis development, but not during the chronic phase of the disease.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Early Phase Mast Cell Activation Determines the Chronic Outcome of Renal Ischemia–Reperfusion Injury

Danelli

Madjène

Madera-Salcedo

et al. 2017

The Journal of Immunology

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“…It has been shown that TNF-α levels are associated with the development of nephropathy [13], with diverse actions potentially involved in the development of complications [14]. In type 2 diabetic patients, serum and urine TNF-α level increased significantly with the degree of albuminuria [15].…”

Section: Introductionmentioning

confidence: 99%

TNF-α Deficiency Prevents Renal Inflammation and Oxidative Stress in Obese Mice

Wang¹,

Gai

et al. 2017

Kidney Blood Press Res

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Background/Aims: Obese patients and experimental animals exhibit high levels of inflammatory cytokines, such as tumor necrosis factor (TNF)-α. However, the role of TNF-α in the pathophysiologic process in obesity induced kidney damage is still unknown. Methods: We used TNF-α deficient mice and wild-type (WT) C57/BJ6 mice controls to study the effect of TNF-α on inflammation and oxidative stress in kidney by the model of high-fat diet (HFD) and primary isolated mouse renal proximal tubule cells treated with a mixture of free fatty acids (FFA). Results: Compared with the chow diet group, HFD-fed WT mice had higher urinary albumin and increased levels of renal fibrosis, glomerulosclerosis, inflammation, oxidative stress and apoptosis in the kidney. These changes were co-related with increased expression of TNF-α in the kidney and were attenuated by TNF-α deficiency. In vitro, accumulation of intracellular lipids induced TNF-α expression and oxidative stress in FFA treated primary proximal tubule cells. However, TNF-α inhibition with siRNA or TNF-α deficiency decreased the lipid induced oxidative stress in these cells. Conclusion: These findings suggest that TNF-α plays an important role in the HFD induced kidney damage, and targeting TNF-α and/or its receptors could be a promising therapeutic regimen for progressive nephropathy.

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“…assessment of sOD activity and MDa level of renal tissues in DN Both SOD activity and MDA level were examined with the xanthine oxidase and thiobarbituric acid method. 25,26 SOD activity was measured after eight weeks ( Figure 10A). SOD activity in the DN group was less than in the sham group (P0.01; SOD activity: sham 76.32±2.39 U, DN group 31.25±1.45 U).…”

Section: Blood Glucose Levelsmentioning

confidence: 99%

Preparation of exenatide-loaded linear poly(ethylene glycol)-brush poly(L-lysine) block copolymer: potential implications on diabetic nephropathy

Tong¹

2017

IJN

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The poly(ethylene glycol)- b -brush poly( l -lysine) polymer (PEG- b -(PELG 50 - g -PLL 3 )) was synthesized and evaluated as a nanocarrier for prolonging delivery of exenatide through the abdominal subcutaneous injection route. The isoelectric point of exenatide was 4.86, and exenatide could combine with PEG- b -(PELG 50 - g -PLL 3 ) polymers via electrostatic interactions at pH 7.4. This polymer was a good candidate for achieving prolonged drug delivery for exenatide, considering its high molecular weight. Besides the physicochemical characterization of the polymer, in vitro and in vivo applications were researched as a sustained exenatide delivery system. In the in vitro release research, 20.16%–76.88% of total exenatide was released from the PEG- b -(PELG 50 - g -PLL 3 ) polymer within 7 days. The synthesized block-brush polymers and exenatide–block-brush polymers were analyzed by nuclear magnetic resonance spectroscopy, gel permeation chromatography, transmission electron microscopy, nanoparticle size instrument, and scanning electron microscopy. The best formulation was selected for in vivo experimentation to achieve blood glucose control in diabetic rat models using free exenatide as the control. The hypoglycemic action of the formulation following subcutaneous injection in diabetic rats lasted 7 days, and the results indicated that exenatide–block-brush polymers demonstrate enhanced long-acting hypoglycemic action. Besides the hypoglycemic action, exenatide–block-brush polymers significantly alleviated diabetic nephropathy via improving renal function, decreasing oxidative stress injury, decreasing urinary albumin excretion rate, mitigating albumin/creatinine ratio, reducing blood lipids, abating kidney index, weakening apoptosis, and downregulating expression of connective tissue growth factor. All of the results suggested that PEG- b -(PELG 50 - g -PLL 3 ) polymers could be used as potential exenatide nanocarriers, with efficient encapsulation and sustained release.

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Effect of Intervention in Mast Cell Function Before Reperfusion on Renal Ischemia-Reperfusion Injury in Rats

Cited by 23 publications

References 33 publications

Early Phase Mast Cell Activation Determines the Chronic Outcome of Renal Ischemia–Reperfusion Injury

Early Phase Mast Cell Activation Determines the Chronic Outcome of Renal Ischemia–Reperfusion Injury

TNF-α Deficiency Prevents Renal Inflammation and Oxidative Stress in Obese Mice

Preparation of exenatide-loaded linear poly(ethylene glycol)-brush poly(L-lysine) block copolymer: potential implications on diabetic nephropathy

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