Wuling San protects kidney dysfunction by inhibiting renal TLR4/MyD88 signaling and NLRP3 inflammasome activation in high fructose-induced hyperuricemic mice

Yang, Ying; Zhang, Dongmei; Liu, Jiahui; Hu, Lin-Shui; Xue, Qiaochu; Ding, Xiaoqin; Kong, Ling-Dong

doi:10.1016/j.jep.2015.04.011

Cited by 67 publications

(43 citation statements)

References 45 publications

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“…Literature shows that increased expressions of GLUT9 and URAT1 were observed in the kidney of fructose‐fed rats . In this study, the levels of renal GLUT9 and URAT1 were markedly increased in 10% fructose group compared with the normal group ( Figure B, p < 0.01).…”

Section: Resultssupporting

confidence: 54%

“…The level of uric acid in serum is partly regulated by urate transport‐related proteins. The expression of glucose transporter 9 (GLUT9) and renal transporter 1 (URAT1) are significantly increased in fructose‐induced hyperuricemic mice, which is associated with inflammatory responses . In the inflammation system, toll‐like receptor 4 (TLR4) plays an important role in regulating a cascade of events in the body .…”

Section: Introductionmentioning

confidence: 99%

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Conjugated Linoleic Acid Ameliorates High Fructose‐Induced Hyperuricemia and Renal Inflammation in Rats via NLRP3 Inflammasome and TLR4 Signaling Pathway

Tan

Wan

Chen

et al. 2019

Molecular Nutrition Food Res

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Scope: Conjugated linoleic acid (CLA), a bioactive substance predominantly found in ruminant products, improves insulin resistance and exhibits anti-inflammatory activity. The chief objective of the study is to investigate the effects and potential mechanisms of CLA on high fructose-induced hyperuricemia and renal inflammation. Methods and results: Hyperuricemia and renal inflammation are induced in rats by 10% fructose. Hyperuricemia, insulin resistance, and renal inflammation are evaluated. CLA potently ameliorates fructose-induced hyperuricemia with insulin resistance and significantly reduces the levels of inflammation factors in serum and kidney. It reverses fructose-induced upregulation of glucose transporter 9 (GLUT9) and urate transporter 1 (URAT1) in the kidney. Moreover, CLA dramatically inhibits the activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome. Additionally, CLA suppresses toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) signaling activation to inhibit nuclear factor-kB (NF-kB) signaling in the kidney of fructose-fed rats. Conclusion: CLA ameliorates hyperuricemia along with insulin resistance and renal inflammatory, which may be associated with the suppression of renal GLUT9 and URAT1 in fructose-fed rats. Its molecular mechanism may be related to the inhibition of NLRP3 inflammasome and TLR4/MyD88 signaling pathway. Therefore, CLA may be a promising candidate for preventing fructose-induced hyperuricemia and renal inflammation.

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Section: Resultssupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Conjugated Linoleic Acid Ameliorates High Fructose‐Induced Hyperuricemia and Renal Inflammation in Rats via NLRP3 Inflammasome and TLR4 Signaling Pathway

Tan

Wan

Chen

et al. 2019

Molecular Nutrition Food Res

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“…Nearly 10% of the TCM preparations, recorded in the Chinese Pharmacopoeia (2015 edition), contain P. cocos . One of these preparation, Wulinsan, was shown to confer a significant renoprotective effect (Yang et al, ; Yoon et al, ) and is widely used in the treatment of patients with CKD. A number of studies have demonstrated the renoprotective effect of P. cocos (Lee et al, ; Yoon et al, ; Lee et al, ).…”

Section: Discussionmentioning

confidence: 99%

Novel inhibitors of the cellular renin‐angiotensin system components, poricoic acids, target Smad3 phosphorylation and Wnt/β‐catenin pathway against renal fibrosis

Wang

Chen

Lin

et al. 2018

British J Pharmacology

146

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“…Furthermore, ROS generation under fructose-induced hyperuricemia is the crucial factor for podocyte injury by activating p38 MAPK/thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome pathway [97]. While upregulation of TLR4/myeloid differentiation primary response gene 88 (MyD88) signaling promotes NF-κB signaling in kidney of hyperuricemic mice with high fructose diet [105]. High serum UA also causes inflammation in hypothalamic, vascular endothelium, primary gouty arthritis via acting NF-κB signaling.…”

Section: Direct Dangerous Factors Under High Fructose Consumptionmentioning

confidence: 99%

High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions

2017

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High dietary fructose is a major contributor to insulin resistance and metabolic syndrome, disturbing tissue and organ functions. Fructose is mainly absorbed into systemic circulation by glucose transporter 2 (GLUT2) and GLUT5, and metabolized in liver to produce glucose, lactate, triglyceride (TG), free fatty acid (FFA), uric acid (UA) and methylglyoxal (MG). Its extrahepatic absorption and metabolism also take place. High levels of these metabolites are the direct dangerous factors. During fructose metabolism, ATP depletion occurs and induces oxidative stress and inflammatory response, disturbing functions of local tissues and organs to overproduce inflammatory cytokine, adiponectin, leptin and endotoxin, which act as indirect dangerous factors. Fructose and its metabolites directly and/or indirectly cause oxidative stress, chronic inflammation, endothelial dysfunction, autophagy and increased intestinal permeability, and then further aggravate the metabolic syndrome with tissue and organ dysfunctions. Therefore, this review addresses fructose-induced metabolic syndrome, and the disturbance effects of direct and/or indirect dangerous factors on the functions of liver, adipose, pancreas islet, skeletal muscle, kidney, heart, brain and small intestine. It is important to find the potential correlations between direct and/or indirect risk factors and healthy problems under excess dietary fructose consumption.

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Wuling San protects kidney dysfunction by inhibiting renal TLR4/MyD88 signaling and NLRP3 inflammasome activation in high fructose-induced hyperuricemic mice

Cited by 67 publications

References 45 publications

Conjugated Linoleic Acid Ameliorates High Fructose‐Induced Hyperuricemia and Renal Inflammation in Rats via NLRP3 Inflammasome and TLR4 Signaling Pathway

Conjugated Linoleic Acid Ameliorates High Fructose‐Induced Hyperuricemia and Renal Inflammation in Rats via NLRP3 Inflammasome and TLR4 Signaling Pathway

Novel inhibitors of the cellular renin‐angiotensin system components, poricoic acids, target Smad3 phosphorylation and Wnt/β‐catenin pathway against renal fibrosis

High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions

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