Resveratrol Ameliorates Diabetes-induced Renal Damage through Regulating the Expression of TGF-B1, Collagen IV and Th17/Treg Related Cytokines in Rats

Zhou, Wuyi; Gao, Guoquan

doi:10.7727/wimj.2014.008

Cited by 9 publications

(5 citation statements)

References 8 publications

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“…In recent years, several researches have proposed that IL-35 exhibits potent anti-inflammatory properties in the etiology and pathogenesis of inflammatory and autoimmune diseases. For instance, Zhou et al [26] recently revealed that IL-35 was downregulated in serum and kidney tissues of STZ-induced diabetic rats. Additionally, Bettini et al [27] reported that ectopic expression of IL-35 by pancreatic β-cells provided long-term protection against autoimmune diabetes via decreasing islet infiltration with substantial reductions in the number of CD4 + and CD8 + T cells.…”

Section: Discussionmentioning

confidence: 99%

IL-35 alleviates inflammation progression in a rat model of diabetic neuropathic pain via inhibition of JNK signaling

Jiang

Wang

et al. 2019

J Inflamm

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Background Emerging evidence has demonstrated that inflammation is involved in the occurrence and development of diabetic neuropathic pain (DNP). The anti-inflammatory property of interleukin (IL)-35 makes it a promising candidate to block the pain perception. The present study was undertaken to investigate whether IL-35 could attenuate DNP in streptozotocin (STZ)-induced rat model and its potential mechanism. Methods The rat model of DNP was established by a single STZ injection followed by measurements of fasting blood glucose and insulin. Fourteen days after STZ injection, DNP rats were intrathecally injected with IL-35, c-Jun N-terminal kinase (JNK) inhibitor or activator or dimethylsulfoxide (DMSO) as vehicle control, respectively. The mechanical allodynia was assayed to evaluate the therapeutic effect of IL-35. In mechanism study, the serum and protein levels of inflammatory cytokines using ELISA and western blotting and the activation of JNK signaling were further evaluated by quantitative reverse transcription PCR (qRT-PCR). Histopathologic changes were evaluated by Nissl staining. Apoptosis was examined using TUNEL staining. Results DNP rats exhibited increased fasting blood glucose and insulin levels and reduced insulin sensitivity index (ISI). Intrathecal injection of IL-35 reduced accumulation of pro-inflammatory cytokines in the spinal cord of DNP rats. Furthermore, IL-35 displayed anti-inflammatory and anti-apoptotic effects via inhibition of JNK pathway. Conclusion IL-35 treatment mitigated DNP via downregulating JNK signaling pathway.

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Section: Discussionmentioning

confidence: 99%

IL-35 alleviates inflammation progression in a rat model of diabetic neuropathic pain via inhibition of JNK signaling

Jiang

Wang

et al. 2019

J Inflamm

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“…In an experimental model of hypertension and angiotensin II-induced fibrosis, the IL-17A or IL-17RA blockade with specific antibodies significantly reduced the fibrosis marker TGF-β1 (152). On the other hand, the antifibrotic effect of many agents in the kidney has been associated with reducing IL-17 (153)(154)(155)(156).…”

Section: Il-17 Renal Tubular Epithelial Cells and Fibrosismentioning

confidence: 99%

The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis

Paquissi

Abensur

2021

Front. Med.

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Systemic lupus erythematosus (SLE) is a disease characterized by dysregulation and hyperreactivity of the immune response at various levels, including hyperactivation of effector cell subtypes, autoantibodies production, immune complex formation, and deposition in tissues. The consequences of hyperreactivity to the self are systemic and local inflammation and tissue damage in multiple organs. Lupus nephritis (LN) is one of the most worrying manifestations of SLE, and most patients have this involvement at some point in the course of the disease. Among the effector cells involved, the Th17, a subtype of T helper cells (CD4+), has shown significant hyperactivation and participates in kidney damage and many other organs. Th17 cells have IL-17A and IL-17F as main cytokines with receptors expressed in most renal cells, being involved in the activation of many proinflammatory and profibrotic pathways. The Th17/IL-17 axis promotes and maintains repetitive tissue damage and maladaptive repair; leading to fibrosis, loss of organ architecture and function. In the podocytes, the Th17/IL-17 axis effects include changes of the cytoskeleton with increased motility, decreased expression of health proteins, increased oxidative stress, and activation of the inflammasome and caspases resulting in podocytes apoptosis. In renal tubular epithelial cells, the Th17/IL-17 axis promotes the activation of profibrotic pathways such as increased TGF-β expression and epithelial-mesenchymal transition (EMT) with consequent increase of extracellular matrix proteins. In addition, the IL-17 promotes a proinflammatory environment by stimulating the synthesis of inflammatory cytokines by intrinsic renal cells and immune cells, and the synthesis of growth factors and chemokines, which together result in granulopoiesis/myelopoiesis, and further recruitment of immune cells to the kidney. The purpose of this work is to present the prognostic and immunopathologic role of the Th17/IL-17 axis in Kidney diseases, with a special focus on LN, including its exploration as a potential immunotherapeutic target in this complication.

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“…The reason is unclear, but previous studies showed contradictory results in regard to the effect of Resv on Tregs. [35–37]. Another possible reason may be that Resv did not overcome the suppressive effect of Tac on Tregs, but further studies are required to clarify this issue.…”

Section: Discussionmentioning

confidence: 99%

Effects of resveratrol on Th17 cell-related immune responses under tacrolimus-based immunosuppression

Doh

Kim

et al. 2019

BMC Complement Altern Med

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Background We previously reported that tacrolimus (Tac) does not decrease T helper 17 cells (Th17) response in kidney transplantation. In this study, we evaluated whether Resveratrol (Resv) has immunosuppressive effects by decreasing Th17 responses in Tac-based immunosuppression. Methods We investigated the effects of Resv under Tac-treatment conditions, on CD4 + T cell differentiation to Th17 cells in peripheral blood mononuclear cells (PBMCs), and proliferation of CD4 + T cells co-cultured with human renal proximal tubular epithelial cells (HRPTEpiCs). The effects of Resv on Th17 cells were tested in the murine skin transplant model. Results In PBMCs, Tac did not but combination of Tac and Resv further suppressed Th17 immune response. In the co-culture study, combination of Resv to Tac significantly decreased HRPTEpiC-induced T cell proliferation compared to Tac alone. Resv treatment in the Jurkat cell induced the expression of AMP-activated protein kinase and suppressed the expression of mammalian target of rapamycin (mTOR), suggesting blocking Th17 pathway by Resv. In the murine skin transplant model, combination of Resv to Tac significantly prolonged skin graft survival accompanied by the suppression of Th17 cells, compared to either the Tac-alone or control groups. Conclusion The results of our study suggest that Resv provides additional immunosuppressive effects to Tac by suppressing effector CD4 + T cells, especially Th17 cells, in the transplantation setting .

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Resveratrol Ameliorates Diabetes-induced Renal Damage through Regulating the Expression of TGF-B1, Collagen IV and Th17/Treg Related Cytokines in Rats

Cited by 9 publications

References 8 publications

IL-35 alleviates inflammation progression in a rat model of diabetic neuropathic pain via inhibition of JNK signaling

IL-35 alleviates inflammation progression in a rat model of diabetic neuropathic pain via inhibition of JNK signaling

The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis

Effects of resveratrol on Th17 cell-related immune responses under tacrolimus-based immunosuppression

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