Protective effect of tea polyphenols on renal ischemia/reperfusion injury via suppressing the activation of TLR4/NF-κB p65 signal pathway

Li, Yanwei; Zhang, Yan; Zhang, Ling; Xu, Lixin; Yu, Jianbo; Zhang, Hongtao; Tan, B. K. H.; Jiang, Lianhao; Wang, Yaxin; Yu, Liang; Zhang, Xiushan; Wang, Wensheng; Liu, Hai-Gen

doi:10.1016/j.gene.2014.03.021

Cited by 80 publications

(51 citation statements)

References 43 publications

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“…Previously, NF-κB was demonstrated to regulate the genes, such as TNF-α, IL-1 and IL-6, responsible for mediating inflammation. In addition, the inhibition of NF-κB could protect against ischemic brain damage and the acute stage of ischemia [19,38]. Furthermore, it was shown that the functional inhibition of pro-inflammatory cytokines (including TNF-α and IL-6) could prevent the progression of renal I/R injury, while TLR4-deficient mice were less vulnerable to ischemic renal injury [39].…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, NF-κB, a transcription factor, activates the transcription of cytokines and the cascade of proinflammatory chemokines [18]. A previous study by Li et al suggested that the pre-treatment with tea polyphenol could inhibit the TLR4/NF-κB signaling pathway, and consequently protect renal tubular epithelial cells against I/R-induced apoptosis [19]. Importantly, a recent report demonstrated that I/R-induced AKI could be suppressed when cell apoptosis is inhibited [20].…”

Section: Introductionmentioning

confidence: 99%

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Lentivirus-Mediated Silencing of Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase 2 Inhibits Release of Inflammatory Cytokines and Apoptosis in Renal Tubular Epithelial Cells Via Inhibition of the TLR4/NF-kB Pathway in Renal Ischemia-Reperfusion Injury

Teng

Wang

Jia

et al. 2018

Kidney Blood Press Res

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Background/Aims: Renal reperfusion injury occurs after the blood flow to the ischemic kidney is re-established under various clinical conditions, such as organ transplantation, renal artery stenosis, embolic disease, and the repair of descending aortic. The current study aims to explore the effects of src homology 2 domain-containing protein tyrosine phosphatase 2 (SHP-2) on the release of inflammatory cytokines and the apoptosis of renal tubular epithelial cells by regulating the TLR4/NF-κB signaling pathway in rats with renal ischemia-reperfusion (I/R) injury. Methods: A total of 60 normal clean Sprague Dawley (SD) (WT) rats were used in this study. The levels of creatinine (Cr) and blood urea nitrogen (BUN) were determined using an automatic biochemical analyzer. The apoptosis in renal tissue was detected by TUNEL assay. The renal tubular epithelial cells of rats were cultured, infected and treated with different lentivirus vectors. The serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), IL-1β and SHP27 were measured. Reverse transcription quantitative polymerases chain reaction and Western blot analysis were performed to measure the expression of relevant genes and proteins. Furthermore, the effect of SHP-2 on the proliferation, cell cycle and apoptosis of renal tubular epithelial cells was also investigated. Results: In the serum of rats with renal I/R injury and prolonged reperfusion time, the contents of Cr and BUN were increased, the positive expression of SHP-2 was higher, the level of apoptosis was promoted, IL-6, TNF-α, IL-1β and SHP27 expression in the serum was increased, the expression of SHP2, TLR4, NF-κB, IL-6, TNF-α and Bax was up-regulated, and the expression of Bcl-2 was down-regulated. Lentivirus-mediated silencing of SHP-2 promoted the proliferation of renal tubular epithelial cells, inhibited their apoptosis, and reduced the expression of inflammatory factors in these cells by functionally suppressing the TLR4/NF-κB signaling pathway. Conclusion: The results indicated that lentivirus-mediated silencing of SHP-2 inhibited the release of inflammatory cytokines and the apoptosis of renal tubular epithelial cells, and promoted the proliferation of these cells by inhibiting the TLR4/NF-κB signaling pathway in rats with renal I/R injury.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Lentivirus-Mediated Silencing of Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase 2 Inhibits Release of Inflammatory Cytokines and Apoptosis in Renal Tubular Epithelial Cells Via Inhibition of the TLR4/NF-kB Pathway in Renal Ischemia-Reperfusion Injury

Teng

Wang

Jia

et al. 2018

Kidney Blood Press Res

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“…TNF-α is a very important proinflammatory factor, which stimulates renal tubular epithelial cells to produce chemokines and recruitment of inflammatory cells [25, 26]. IL-1β and IL-6 are the vital cytokines secreted by inflammatory cells in the process of renal interstitial fibrosis, and is closely related to the development of renal fibrosis [27]. We detected the expression of IL-1β, IL-6, and TNF-α mRNA by R-T PCR, and the results showed that the expression of IL-1β and TNF-α mRNA was increased in a dose- and time-dependent manner except IL-6.…”

Section: Discussionmentioning

confidence: 99%

High Uric Acid-Induced Epithelial-Mesenchymal Transition of Renal Tubular Epithelial Cells via the TLR4/NF-kB Signaling Pathway

Liu

Xiong

et al. 2017

Am J Nephrol

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Background: Hyperuricemia is an independent risk factor for causing chronic kidney disease and contributes to kidney fibrosis. After urate crystals get deposited in the kidney, they can cause hyperuricemia nephropathy, leading to glomerular hypertrophy and renal tubular interstitial fibrosis. Recent data showed that uric acid (UA) could induce epithelial mesenchymal transition (EMT) of renal tubular cells, in which NRLP3 inflammatory pathway was involved. However, whether TLR4/NF-κB signaling pathway is also involved in EMT of renal tubular cells induced by UA is not clear. Methods: Human renal tubular epithelial cells (HK-2) were directly treated with UA and the phenotypic transition was detected by morphological changes and the molecular markers of EMT. The activation of the TLR4/NF-κB signaling pathway induced by UA was measured by Western blot and its involvement was further confirmed by the inhibition of NF-κB activation or knockdown of toll like receptor 4 (TLR4) expression. Results: UA induced obvious morphological changes of HK-2 cell, accompanied with altered molecular markers of EMT including fibronectin, α-SMA and E-cadherin. In addition, UA significantly upregulated the gene expression of interleukin-1β and tumor necrosis factor-α in a time- and dose-dependent manner. Furthermore, UA significantly activated the TLR4/NF-κB signaling pathway in HK-2 cells, while the inhibition of the TLR4 expression by siRNA and NF-κB activation by PDTC significantly attenuated EMT induced by UA in HK-2 cells. Conclusions: UA can induce EMT in renal tubular epithelial cells by the activation of the TLR4/NF-κB signaling pathway, and the targeted intervention of the TLR4/NF-κB signaling pathway might effectively inhibit UA-induced renal interstitial fibrosis mediated by EMT.

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“…The activation of NF-κB results in the expression of related inflammatory factors such as TNF-α and IL-1β and inhibition of NF-κB, which may result in the downregulation of Bcl-2-family proteins (31). Previous studies have shown that the activation of NF-κB may mediate apoptosis in RGCs (32), which are closely related to RIR injury. In the present study, the expression of the phosphorylated p65-NF-κB subunit was attenuated by IL-33.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-33 Prevents Retinal Ischemia Reperfusion Injury in Rats by Preventing Apoptosis

Xing

Yang

et al. 2016

Iran Red Crescent Med J

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Background: Retinal ischemia reperfusion (RIR) injury is a common pathological process that can result in visual impairment in many ophthalmic diseases. Inflammation and apoptosis play an important role in RIR injury. Objectives: This experimental study was designed to explore the ability of a new cytokine, IL-33, to attenuate RIR injury via an apoptosis-inhibitory mechanism. Methods: From June, 2015 to October, 2015, 40 Sprague-Dawley (SD) rats from Wuhan university in China were divided into the following four groups: normal control group (NCG), RIR injury model group (MG), IL-33 pretreatment group (IL-33), and PBS group

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Protective effect of tea polyphenols on renal ischemia/reperfusion injury via suppressing the activation of TLR4/NF-κB p65 signal pathway

Cited by 80 publications

References 43 publications

Lentivirus-Mediated Silencing of Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase 2 Inhibits Release of Inflammatory Cytokines and Apoptosis in Renal Tubular Epithelial Cells Via Inhibition of the TLR4/NF-kB Pathway in Renal Ischemia-Reperfusion Injury

Lentivirus-Mediated Silencing of Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase 2 Inhibits Release of Inflammatory Cytokines and Apoptosis in Renal Tubular Epithelial Cells Via Inhibition of the TLR4/NF-kB Pathway in Renal Ischemia-Reperfusion Injury

High Uric Acid-Induced Epithelial-Mesenchymal Transition of Renal Tubular Epithelial Cells via the TLR4/NF-kB Signaling Pathway

Interleukin-33 Prevents Retinal Ischemia Reperfusion Injury in Rats by Preventing Apoptosis

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