scholarly journals Effect of echinacoside on kidney fibrosis by inhibition of TGF-β1/Smads signaling pathway in the db/db mice model of diabetic nephropathy

2017 ◽  
Vol Volume 11 ◽  
pp. 2813-2826 ◽  
Author(s):  
Fengjuan Tang ◽  
Yarong Hao ◽  
Xue Zhang ◽  
Jian Qin
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
Tgf Beta ◽  
Mice Model ◽  
Kidney Fibrosis

Expression of Ang II/TGF beta 1 signaling pathway in kidney of diabetic nephropathy rats and effects of polydatin on it

2019 ◽  
Vol 6 ◽  
pp. S16
Author(s):  
Fengxian Meng ◽  
Zhengju Zhang ◽  
Ruiyang Xiang ◽  
Jie Wang ◽  
Chengcheng Zhang ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
Ang Ii ◽  
Tgf Beta

scholarly journals WNT1-inducible-signaling pathway protein 1 regulates kidney inflammation through the NF-κB pathway

2021 ◽  
Author(s):  
Bo Wang ◽  
Chenguang Ding ◽  
Xiaoming Ding ◽  
Greg H Tesch ◽  
Jin Zheng ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
Kidney Injury ◽  
Regulatory Function ◽  
Pathological Feature ◽  
Novel Therapy ◽  
Kidney Fibrosis ◽  
Ureter Obstruction ◽  
Function Impairment ◽  
Pharmacological Blockade

Inflammation is a pathological feature of kidney injury and its progression correlates with the development of kidney fibrosis which can lead to kidney function impairment. This project investigated the regulatory function of WNT1-inducible-signaling pathway protein 1 (WISP1) in kidney inflammation. Administration of recombinant WISP1 protein to healthy mice induced kidney inflammation (macrophage accrual and production of TNFα, CCL2 and IL-6), which could be prevented by inhibition of NF-κB. Furthermore, inhibition of WISP1, by gene knockdown or neutralising antibody, could inhibit cultured macrophages producing inflammatory cytokines following stimulation with lipopolysaccharides (LPS) and kidney fibroblasts proliferating in response to TNFα, which both involved NF-κB signalling.  Kidney expression of WISP1 was found to be increased in mouse models of progressive kidney inflammation- unilateral ureter obstruction (UUO) and streptozotocin-induced diabetic nephropathy. Treatment of UUO mice with WISP1 antibody reduced the kidney inflammation in these mice. Therefore, pharmacological blockade of WISP1 exhibits potential as a novel therapy for inhibiting inflammation in kidney disease.

Novel Chalcone BDD-39 Mitigated Diabetic Nephropathy through the Activation of Nrf2/ARE Signaling

2021 ◽  
Vol 14 ◽  
Author(s):  
Temitope Adelusi ◽  
Xizhi Li ◽  
Liu Xu ◽  
Lei Du ◽  
Meng Hao ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Mesangial Cells ◽  
Intraperitoneal Administration ◽  
Mrna Levels ◽  
Glomerular Mesangial Cells ◽  
Kidney Fibrosis

Background: In this study, we investigated the Nrf2/ARE signaling pathway activating capacity of Biphenyl Diester Derivative-39 (BDD-39) in diabetic nephropathy in order to elucidate the mechanism surrounding its antidiabetic potential. Objectives: Protein expressions of Nrf2, HO-1, NQO-1 and biomarkers of kidney fibrosis were executed after which mRNA levels of Nrf2, HO-1 and NQO-1 were estimated after creating the models following BBD-39 treatment. Methods: Type 2 diabetes model was established in mice with high-fat diet feeding combined with streptozocin intraperitoneal administration. The diabetic mice were then treated with BDD-39 (15, 45mg· kg-1· d-1, ig) or a positive control drug resveratrol (45mg· kg-1·d-1, ig) for 8 weeks. Staining techniques were used to investigate collagen deposition in the glomerulus of the renal cortex and also to investigate the expression and localization of Nrf2 and extracellular matrix (ECM) proteins (collagen IV and laminin) in vitro and in vivo. Furthermore, we studied the mechanism of action of BDD-39 using RNA-mediated Nrf2 silencing technique in mouse SV40 glomerular mesangial cells (SV40 GM cells). Results : We found that BDD-39 activates Nrf2/ARE signaling pathway, promotes Nrf2 nuclear translocation (Nrf2nuc/Nrf2cyt) and modulate prominent biomarkers of kidney fibrosis at the protein level. However, BDD-39 could not activate Nrf2/ARE signaling in RNA-mediated Nrf2-silenced HG-cultured SV40 GM cells. Conclusion: Taken together, this study demonstrates for the first time that BDD-39 ameliorates experimental DN through attenuation of renal fibrosis progression and modulation of Nrf2/ARE signaling pathway.

Sitagliptin relieves diabetic nephropathy fibrosis via the MAPK/ERK signaling pathway

2020 ◽  
Vol 45 (3) ◽  
Author(s):  
Shufeng Cheng ◽  
Liang Li ◽  
Chunquan Song ◽  
Huijing Jin ◽  
Shouguo Ma ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
Erk Signaling

scholarly journals Bv8-Like Toxin from the Frog Venom of Amolops jingdongensis Promotes Wound Healing via the Interleukin-1 Signaling Pathway

Toxins ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 15 ◽  
Author(s):  
Jiajia Chang ◽  
Xiaoqin He ◽  
Jingmei Hu ◽  
Peter Muiruri Kamau ◽  
Ren Lai ◽  
...  
Keyword(s):  
Wound Healing ◽  
Signaling Pathway ◽  
Wide Spectrum ◽  
Interleukin 1 ◽  
Full Thickness ◽  
Mice Model ◽  
Small Peptides ◽  
Newborn Mice ◽  
Proliferative Effect ◽  
Inflammatory Phase

Prokineticins are highly conserved small peptides family expressed in all vertebrates, which contain a wide spectrum of functions. In this study, a prokineticin homolog (Bv8-AJ) isolated from the venom of frog Amolops jingdongensis was fully characterized. Bv8-AJ accelerated full-thickness wounds healing of mice model by promoting the initiation and the termination of inflammatory phase. Moreover, Bv8-AJ exerted strong proliferative effect on fibroblasts and keratinocytes isolated from newborn mice by activating interleukin (IL)-1 production. Our findings indicate that Bv8 is a potent wound healing regulator and may reveal the mechanism of rapid wound-healing in amphibian skins.

LncRNA TUG1 ameliorates diabetic nephropathy via inhibition of PU.1/RTN1 signaling pathway

2021 ◽  
Author(s):  
Dongdong Meng ◽  
Lina Wu ◽  
Zhifu Li ◽  
Xiaojun Ma ◽  
Shuiying Zhao ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
Lncrna Tug1

scholarly journals DNA demethylase Tet2 suppresses cisplatin-induced acute kidney injury

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yinwu Bao ◽  
Mengqiu Bai ◽  
Huanhuan Zhu ◽  
Yuan Yuan ◽  
Ying Wang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Signaling Pathway ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Kidney Injury ◽  
Renal Tissue ◽  
Clinical Samples ◽  
Mice Model ◽  
Expression Levels ◽  
Ppar Signaling

AbstractDemethylase Tet2 plays a vital role in the immune response. Acute kidney injury (AKI) initiation and maintenance phases are marked by inflammatory responses and leukocyte recruitment in endothelial and tubular cell injury processes. However, the role of Tet2 in AKI is poorly defined. Our study determined the degree of renal tissue damage associated with Tet2 gene expression levels in a cisplatin-induced AKI mice model. Tet2-knockout (KO) mice with cisplatin treatment experienced severe tubular necrosis and dilatation, inflammation, and AKI markers’ expression levels than the wild-type mice. In addition, the administration of Tet2 plasmid protected Tet2-KO mice from cisplatin-induced nephrotoxicity, but not Tet2-catalytic-dead mutant. Tet2 KO was associated with a change in metabolic pathways like retinol, arachidonic acid, linolenic acid metabolism, and PPAR signaling pathway in the cisplatin-induced mice model. Tet2 expression is also downregulated in other AKI mice models and clinical samples. Thus, our results indicate that Tet2 has a renal protective effect during AKI by regulating metabolic and inflammatory responses through the PPAR signaling pathway.

scholarly journals Chaperonin-Containing t-Complex Protein-1 Subunitβas a Possible Biomarker for the Phase of Glomerular Hyperfiltration of Diabetic Nephropathy

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Chung-Ze Wu ◽  
Li-Chien Chang ◽  
Yuh-Feng Lin ◽  
Yi-Jen Hung ◽  
Dee Pei ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Cell Model ◽  
Clinical Investigation ◽  
Mechanistic Study ◽  
Renal Tubules ◽  
Mice Model ◽  
Type 2 Diabetic Mellitus ◽  
T Complex ◽  
Type 2 Dm

In cell model, we discovered the association between chaperonin-containing t-complex polypeptide 1 subunitβ(TCP-1β) and early diabetic nephropathy (DN). In this study, we further explored the relationships between TCP-1βand type 2 diabetic mellitus (DM). To mimic the clinical hyperfiltration state, a type 2 DM mice model was established by feeding a high-fat diet in combination with treatment of streptozotocin and nicotinamide. Blood and urine were collected to determine creatinine clearance (Ccr), and kidney tissues were harvested for evaluation of TCP-1βexpression by immunohistochemistry and Western blot. Meanwhile, clinical subjects of healthy controls and type 2 DM were recruited to strengthen the evidence with urine TCP-1β. Results showed thatCcrand the expression of TCP-1βin kidney were significantly higher one week after hyperglycemia development, suggesting that the hyperfiltration state was successfully established in the mice model. TCP-1βwas expressed predominantly on renal tubules. By using the estimated glomerular filtration rate to index progression in clinical investigation, urine TCP-1βlevel was associated with the hyperfiltration phase in type 2 DM patients. Conclusively, we confirmed that TCP-1βis a possible biomarker for early nephropathy of type 2 DM, but further mechanistic study to elucidate its cause and pathway is needed.

Sign in / Sign up

Export Citation Format

Share Document