Green tea infusion prevents diabetic nephropathy aggravation in recent-onset type 1 diabetes regardless of glycemic control. (28th June 2021)

• Record Type: Journal Article
• Authors: Ladeira, Luiz Carlos Maia; dos Santos, Eliziária Cardoso; Santos, Talita Amorim; da Silva, Janaina; Lima, Graziela Domingues de Almeida; Machado-Neves, Mariana; da Silva, Renê Chagas; Freitas, Mariella Bontempo; Maldonado, Izabel Regina dos Santos Costa
• Is Part Of: Journal of ethnopharmacology. Volume 274(2021)
• Publication Date: 2021-06-28
• Subjects: Diabetic nephropathy -- Type 1 diabetes -- Recent-onset diabetes -- Diabetic kidney disease -- Green tea; 67LR 67kDa laminin receptor -- ABTS 2, 2'-Azinobis-[3-ethylbenzthiazoline-6-sulfonic acid] -- NOS1 Nitric Oxide Synthase 1 -- AGE/RAGE advanced glycated end-products and its receptor -- AKT protein kinase B -- AMPK 5'-AMP-activated protein kinase -- AO acridine Orange -- APC APC Regulator Of WNT Signaling Pathway -- ATP adenosine triphosphate -- BAX BCL2 Associated X -- BCL2 BCL2 Apoptosis Regulator -- BID BH3 Interacting Domain Death Agonist -- BW body weight -- Ca calcium -- CaCl calcium chloride -- CASP3 Caspase 3 -- CASP8 Caspase 8 -- CASP9 Caspase 9 -- CAT catalase -- CAV1 Caveolin 1 -- CCL2 C-C Motif Chemokine Ligand 2 -- CDK2 Cyclin Dependent Kinase 2 -- CDKN1A Cyclin Dependent Kinase Inhibitor 1 -- CIAPIN1 Cytokine Induced Apoptosis Inhibitor 1 -- c-kit proto-oncogene c-kit -- Cl chlorine -- CPI compound-protein interactions -- CTNNB1 Catenin Beta 1 -- Ctrl control group -- DB02077 L-N(omega)-nitroarginine-(4R)-amino-L-proline amide (NOS3) -- DB08019 DB08018 and NOS3- Nitric Oxide Synthase 3 -- DKG diacylglycerol kinase -- DN Diabetic nephropathy -- EGCG epigallocatechin gallate -- FGF fibroblast growth fator -- FGFR fibroblast growth factor receptor -- FOS Fos Proto-Oncogene -- FRAP ferric reducing antioxidant power -- GSK3β glycogen synthase kinase-3 β -- GST glutathione S-transferase -- GTI Green tea infusion -- H2O2 hydrogen peroxide -- H6PD Hexose-6-Phosphate Dehydrogenase/Glucose 1-Dehydrogenase -- HIF1A Hypoxia Inducible Factor 1 Subunit Alpha -- HMG1 high-mobility group box 1 -- HSP90AA1 Heat Shock Protein 90 Alpha Family Class A Member 1 -- i.p. intraperitoneal -- IL6 Interleukin 6 -- IL8 Interleukin 8 -- JUN Jun Proto-Oncogene -- K potassium -- KCl potassium chloride -- KW kidney weight -- MAP2K1 Mitogen-Activated Protein Kinase Kinase 1 -- MAPK1 Mitogen-Activated Protein Kinase 1 -- MAPK3 Mitogen-Activated Protein Kinase 3 -- MAPK8 Mitogen-Activated Protein Kinase 8 -- MAPKAPK5 MAPK Activated Protein Kinase 5 -- Mg magnesium -- MgCl magnesium chloride -- MLH1 MutL Homolog 1 -- mTOR mammalian target of rapamycin -- MTRR 5-Methyltetrahydrofolate-Homocysteine Methyltransferase Reductase -- Na sodium -- NaCl sodium chloride -- NADPH reduced nicotinamide adenine dinucleotide phosphate -- NDOR1 NADPH-dependent diflavin reductase -- NfκB nuclear factor κ B -- NO2-/NO3- nitric oxide -- NOS2 Nitric Oxide Synthase 2 -- NR1H4 Nuclear Receptor Subfamily 1 Group H Member 4 -- O2 oxygen -- O-2 superoxide -- PARP1 Poly(ADP-Ribose) Polymerase 1 -- PDGF platelet-derived growth fator -- PGD Phosphogluconate Dehydrogenase -- PGLS 6-Phosphogluconolactonase -- PI propidium iodide -- PI3K phosphoinositide 3-kinase -- PIN1 Peptidylprolyl Cis/Trans Isomerase, NIMA-Interacting 1 -- PKC-β protein kinase C beta -- POR Cytochrome P450 Oxidoreductase -- PPI Protein-Protein Interactome -- RPIA Ribose 5-Phosphate Isomerase A -- RSI renal somatic index -- SCF stem cell fator -- SD standard deviation -- SGLT1 sodium-dependent glucose transporter 1 -- SGLT2 sodium-dependent glucose transporter 2 -- SOD superoxide dismutase -- SOES Specific Organ Expression Score -- STAT3 Signal transducer and activator of transcription 3 -- STZ streptozotocin -- TCA Trichloroacetic acid -- TCF7L2 Transcription Factor 7 Like 2 -- TE Trolox equivalente -- TGF-β transforming growth factor-beta -- TLR4 toll-like receptor 4 -- TP53 tumor protein 53 -- TRIF TIR domain-containing adaptor-inducing Interferon- β -- TYW1 TRNA-YW Synthesizing Protein 1 Homolog -- UBC Ubiquitin C; Ethnopharmacology -- Periodicals; Pharmacognosy -- Periodicals; Herbs -- Periodicals; Herbs -- Periodicals; Pharmacognosy -- Periodicals; Pharmacognosie -- Périodiques; Herbes -- Périodiques; 615.1
• DOI: 10.1016/j.jep.2021.114032
• Languages: English
• ISSNs: 0378-8741

Abstract

Abstract: Ethnopharmacological relevance: Green tea, traditionally used as antidiabetic medicine, positively affects the diabetic nephropathy. It was assumed that these beneficial effects were due to the hypoglycemiant capacity of the tea, wich reduces the glycemic overload and, consequently, the advanced glycation end products rate and oxidative damage. However, these results are still controversial, since tea is not always able to exert a hypoglycemic action, as demonstrated by previous studies. Aim: Investigate if green tea infusion can generate positive outcomes for the kidney independently of glycemic control, using a model of severe type 1 diabetes. Material and methods: We treated streptozotocin type 1 diabetic young rats with 100 mg/kg of green tea, daily, for 42 days, and evaluated the serum and tissue markers for stress and function. We also analyzed the ion dynamics in the organ and the morphological alterations promoted by diabetes and green tea treatment. Besides, we analyzed, by an in silico approach, the interactions of the green tea main catechins with the proteins expressed in the kidney. Results: Our findings reveal that the components of green tea can interact with the proteins participating in cell signaling pathways that regulate energy metabolism, including glucose and glycogen synthesis, glucose reabsorption, hypoxia management, and cell death by apoptosis. Such interaction reduces glycogen accumulation in the organ, and protects the DNA. These results also reflect in a preserved glomerulus morphology, with improvement in pathological features, and suggesting a prevention of kidney function impairment. Conclusion: Our results show that such benefits are achieved regardless of the blood glucose status, and are not dependent on the reduction of hyperglycemia. Graphical abstract: Image 1