scholarly journals The Use of Chinese Yang/Qi-Invigorating Tonic Botanical Drugs/Herbal Formulations in Ameliorating Chronic Kidney Disease by Enhancing Mitochondrial Function

2021 ◽  
Vol 12 ◽  
Author(s):  
Jiayi Tian ◽  
Yuqi Huang ◽  
Tong Wu ◽  
Hsien-Da Huang ◽  
Kam Ming Ko ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mitochondrial Function ◽  
Antioxidant Status ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Mitochondrial Energy Metabolism ◽  
Beneficial Effects ◽  
Mitochondrial Functions ◽  
Herbal Formulations

Background: Chronic kidney disease (CKD) is a leading cause of morbidity and mortality. Mitochondrial dysfunction has been implicated as a key factor in the development of CKD. According to traditional Chinese medicine (TCM) theory, many Chinese Yang/Qi-invigorating botanical drugs/herbal formulations have been shown to produce promising outcomes in the clinical management of CKD. Experimental studies have indicated that the health-promoting action of Yang/Qi invigoration in TCM is related to the up-regulation of mitochondrial energy generation and antioxidant status.Objective: In this review, we aim to test whether Chinese Yang/Qi-invigorating tonic botanical drugs/herbal formulations can provide medical benefits in CKD and its complications. And we also explore the possible involvement of mitochondrial-associated signaling pathway underlying the beneficial effects of Yang/Qi invigoration in TCM.Methods: A systematic search of “PubMed”, “China National Knowledge Infrastructure (CNKI)” and “Google Scholar” was carried out to collect all the available articles in English or Chinese related to Chinese Yang/Qi-invigorating tonic botanical drugs/herbal formulations and their effects on mitochondrial function and chronic kidney disease.Result and Discussion: The relationship between the progression of CKD and mitochondrial function is discussed. The effects of Chinese Yang/Qi-invigorating tonic botanical drugs/herbal formulations and their active ingredients, including phytosterols/triterpenes, flavonoids, and dibenzocyclooctadiene lignans, on CKD and related alterations in mitochondrial signaling pathways are also presented in this review. In the future, exploration of the possible beneficial effects and clinical studies of more Yang- and Qi-invigorating botanical drugs/herbal formulations in the prevention and/or/treatment of CKD and the molecular mechanisms relating to the enhancement of mitochondrial functions warrants further investigation.Conclusion: Given the critical role of mitochondrial function in safeguarding renal functional integrity, the enhancement of mitochondrial energy metabolism and antioxidant status in kidney tissue is likely involved in renal protection. Future studies on the biochemical and chemical basis underlying the effects of Chinese Yang/Qi-invigorating tonic botanical drugs/herbal formulations from a mitochondrial perspective will hopefully provide novel insights into the rational development of new drugs for the prevention and/or treatment of CKD.

scholarly journals The potency of PLGA-Encapsulated Epigallocatechin Gallate (EGCG) as adjuvant therapy for chronic kidney disease

2022 ◽  
Vol 13 (1) ◽  
pp. 273-279
Author(s):  
Deandra Maharani Widiatmaja ◽  
Alyaa Ulaa Dhiya Ul Haq ◽  
Dinda Dwi Purwati ◽  
Arifa Mustika
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Adjuvant Therapy ◽  
Mitochondrial Function ◽  
Kidney Diseases ◽  
Epigallocatechin Gallate ◽  
Pharmacokinetic Profile ◽  
Protective Agent ◽  
Beneficial Effects ◽  
Plga Encapsulation

Chronic kidney disease (CKD) prevalence keeps increasing worldwide and being particular concern due to its morbidity and mortality. However, current CKD therapy are known to be economically costly and not necessarily provide better outcomes. Epigallocatechin gallate (EGCG) is one of the substances that widely studied as perspective therapeutic agents of CKD due to its anti-inflammatory, antioxidant, and enhancing mitochondrial function ability. However, the use of EGCG is limited to low bioavailability and poor pharmacokinetic profile. Encapsulation of EGCG with PLGA is expected to increase the efficacy of EGCG especially for its use as the kidney protective agent and optimize therapy of CKD. Thus, this study aims to analyze the potency of PLGA-encapsulated EGCG as the adjuvant therapy for CKD. This study was a narrative review summarizes studies related to current adjuvant therapy of CKD. EGCG has beneficial effects in reducing pro-inflammatory cytokines among chronic kidney disease. EGCG also can increase scavenging of free radicals to decrease reactive oxygen species. EGCG is known to enhance mitochondrial function and increase mitochondrial protection to prevent apoptosis in various kidney diseases. Combination of PLGA encapsulation with EGCG has a beneficial effect in improving the delivery, bioavailability, stability, and the pharmacokinetic profile of EGCG. PLGA-encapsulated EGCG also provides a better therapeutic effect on preventing and decreasing progression of kidney damage. Finally, this study concluded that combination of PLGA-encapsulated EGCG has a potency as the adjuvant therapy of CKD.

SGLT2 inhibition for cardiovascular diseases, chronic kidney disease and NAFLD

Endocrinology ◽  
2021 ◽  
Author(s):  
Moein Ala
Keyword(s):  
Chronic Kidney Disease ◽  
Clinical Trials ◽  
Cardiovascular Diseases ◽  
Kidney Disease ◽  
Signaling Pathways ◽  
Observational Studies ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Renal Diseases ◽  
Beneficial Effects

Abstract Sodium glucose cotransporter 2 (SGLT-2) inhibitors are the latest class of anti-diabetic medications. They prevent glucose reabsorption in the proximal convoluted tubule to decrease blood sugar. Several animal studies revealed that SGLT-2 is profoundly involved in the inflammatory response, fibrogenesis and regulation of numerous intracellular signaling pathways. Likewise, SGLT-2 inhibitors markedly attenuated inflammation and fibrogenesis and improved the function of damaged organ in animal studies, observational studies and clinical trials. SGLT-2 inhibitors can decrease blood pressure and ameliorate hypertriglyceridemia and obesity. Likewise, they improve the outcome of cardiovascular diseases such as heart failure, arrhythmias and ischemic heart disease. SGLT-2 inhibitors are associated with lower cardiovascular and all-cause mortality, as well. Meanwhile, they protect against non-alcoholic fatty liver disease (NAFLD), chronic kidney disease (CKD), acute kidney injury (AKI), and improve micro- and macroalbuminuria. SGLT-2 inhibitors can reprogram numerous signaling pathways to improve NAFLD, cardiovascular diseases and renal diseases. For instance, they enhance lipolysis, ketogenesis, mitochondrial biogenesis and autophagy while they attenuate renin-angiotensin-aldosterone system (RAAS), lipogenesis, endoplasmic reticulum (ER) stress, oxidative stress, apoptosis and fibrogenesis. This review explains the beneficial effects of SGLT-2 inhibitors on NAFLD, cardiovascular and renal diseases and dissects the underlying molecular mechanisms in detail. This narrative review explains the beneficial effects of SGLT-2 inhibitors on NAFLD, cardiovascular and renal diseases using the results of latest observational studies, clinical trials and meta-analyses. Thereafter, it dissects the underlying molecular mechanisms involved in the clinical effects of SGLT-2 inhibitors on these diseases.

scholarly journals Altered Sphingolipids Metabolism Damaged Mitochondrial Functions: Lessons Learned From Gaucher and Fabry Diseases

2020 ◽  
Vol 9 (4) ◽  
pp. 1116 ◽  
Author(s):  
Margarita Ivanova
Keyword(s):  
Mitochondrial Function ◽  
Critical Role ◽  
Lessons Learned ◽  
Sphingolipid Metabolism ◽  
Lysosomal Storage ◽  
Bioactive Lipids ◽  
Inner Mitochondrial Membrane ◽  
Mitochondrial Energy Metabolism ◽  
Mitochondrial Functions ◽  
The Status

Sphingolipids represent a class of bioactive lipids that modulate the biophysical properties of biological membranes and play a critical role in cell signal transduction. Multiple studies have demonstrated that sphingolipids control crucial cellular functions such as the cell cycle, senescence, autophagy, apoptosis, cell migration, and inflammation. Sphingolipid metabolism is highly compartmentalized within the subcellular locations. However, the majority of steps of sphingolipids metabolism occur in lysosomes. Altered sphingolipid metabolism with an accumulation of undigested substrates in lysosomes due to lysosomal enzyme deficiency is linked to lysosomal storage disorders (LSD). Trapping of sphingolipids and their metabolites in the lysosomes inhibits lipid recycling, which has a direct effect on the lipid composition of cellular membranes, including the inner mitochondrial membrane. Additionally, lysosomes are not only the house of digestive enzymes, but are also responsible for trafficking organelles, sensing nutrients, and repairing mitochondria. However, lysosomal abnormalities lead to alteration of autophagy and disturb the energy balance and mitochondrial function. In this review, an overview of mitochondrial function in cells with altered sphingolipid metabolism will be discussed focusing on the two most common sphingolipid disorders, Gaucher and Fabry diseases. The review highlights the status of mitochondrial energy metabolism and the regulation of mitochondria–autophagy–lysosome crosstalk.

scholarly journals Prohibitins: A Critical Role in Mitochondrial Functions and Implication in Diseases

Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 71 ◽  
Author(s):  
Anna Signorile ◽  
Giuseppe Sgaramella ◽  
Francesco Bellomo ◽  
Domenico De Rasmo
Keyword(s):  
Cell Fate ◽  
Mitochondrial Function ◽  
Cellular Localization ◽  
Molecular Mechanisms ◽  
Kidney Diseases ◽  
Critical Role ◽  
Macromolecular Structure ◽  
Inner Membrane ◽  
Mitochondrial Functions ◽  
Prohibitin 1

Prohibitin 1 (PHB1) and prohibitin 2 (PHB2) are proteins that are ubiquitously expressed, and are present in the nucleus, cytosol, and mitochondria. Depending on the cellular localization, PHB1 and PHB2 have distinctive functions, but more evidence suggests a critical role within mitochondria. In fact, PHB proteins are highly expressed in cells that heavily depend on mitochondrial function. In mitochondria, these two proteins assemble at the inner membrane to form a supra-macromolecular structure, which works as a scaffold for proteins and lipids regulating mitochondrial metabolism, including bioenergetics, biogenesis, and dynamics in order to determine the cell fate, death, or life. PHB alterations have been found in aging and cancer, as well as neurodegenerative, cardiac, and kidney diseases, in which significant mitochondrial impairments have been observed. The molecular mechanisms by which prohibitins regulate mitochondrial function and their role in pathology are reviewed and discussed herein.

Beneficial effects of water-based exercise in patients with chronic kidney disease

2003 ◽  
Vol 26 (2) ◽  
pp. 153-156 ◽  
Author(s):  
??lle Pechter ◽  
Mai Ots ◽  
Siiri Mesikepp ◽  
Kersti Zilmer ◽  
Tiiu Kullissaar ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Beneficial Effects ◽  
Water Based

scholarly journals Cytoprotective Effects of N-Acetylcysteine on Streptozotocin- Induced Oxidative Stress and Apoptosis in RIN-5F Pancreatic β-Cells

2018 ◽  
Vol 51 (1) ◽  
pp. 201-216 ◽  
Author(s):  
Arwa M.T. Al-Nahdi ◽  
Annie John ◽  
Haider  Raza
Keyword(s):  
Oxidative Stress ◽  
Insulin Secretion ◽  
Molecular Mechanisms ◽  
Protective Action ◽  
Mitochondrial Enzymes ◽  
Partial Recovery ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Mitochondrial Energy Metabolism ◽  
Mitochondrial Functions

Background/Aims: Numerous studies have reported overproduction of reactive oxygen species (ROS) and alterations in mitochondrial energy metabolism in the development of diabetes and its complications. The potential protective effects of N-acetylcysteine (NAC) in diabetes have been reported in many therapeutic studies. NAC has been shown to reduce oxidative stress and enhance redox potential in tissues protecting them against oxidative stress associated complications in diabetes. In the current study, we aimed to investigate the molecular mechanisms of the protective action of NAC on STZ-induced toxicity in insulin secreting Rin-5F pancreatic β-cells. Methods: Rin-5F cells were grown to 80% confluence and then treated with 10mM STZ for 24h in the presence or absence of 10mM NAC. After sub-cellular fractionation, oxidative stress, GSH-dependent metabolism and mitochondrial respiratory functions were studied using spectrophotometric, flow cytometric and Western blotting techniques. Results: Our results showed that STZ-induced oxidative stress and apoptosis caused inhibition in insulin secretion while NAC treatment restored the redox homeostasis, enhanced insulin secretion in control cells and prevented apoptosis in STZ-treated cells. Moreover, NAC attenuated the inhibition of mitochondrial functions induced by STZ through partial recovery of the mitochondrial enzymes and restoration of membrane potential. STZ-induced DNA damage and expression of apoptotic proteins were significantly inhibited in NAC-treated cells. Conclusion: Our results suggest that the cytoprotective action of NAC is mediated via suppression of oxidative stress and apoptosis and restoration of GSH homeostasis and mitochondrial bioenergetics. This study may, thus, help in better understanding the cellular defense mechanisms of pancreatic β-cells against STZ-induced cytotoxicity.

Beneficial effects of an intradialytic cycling training program in patients with end-stage kidney disease

2015 ◽  
Vol 40 (6) ◽  
pp. 550-556 ◽  
Author(s):  
Carole Groussard ◽  
Myriam Rouchon-Isnard ◽  
Céline Coutard ◽  
Fanny Romain ◽  
Ludivine Malardé ◽  
...  
Keyword(s):  
Body Composition ◽  
Kidney Disease ◽  
Physical Fitness ◽  
Lipid Profile ◽  
Antioxidant Status ◽  
Density Lipoprotein ◽  
Control Group ◽  
Beneficial Effects ◽  
Cycling Training ◽  
Training Protocol

In chronic kidney disease (CKD), oxidative stress (OS) plays a central role in the development of cardiovascular diseases. This pilot program aimed to determine whether an intradialytic aerobic cycling training protocol, by increasing physical fitness, could reduce OS and improve other CKD-related disorders such as altered body composition and lipid profile. Eighteen hemodialysis patients were randomly assigned to either an intradialytic training (cycling: 30 min, 55%–60% peak power, 3 days/week) group (EX; n = 8) or a control group (CON; n = 10) for 3 months. Body composition (from dual-energy X-ray absorptiometry), physical fitness (peak oxygen uptake and the 6-minute walk test (6MWT)), lipid profile (triglycerides (TG), total cholesterol, high-density lipoprotein, and low-density lipoprotein (LDL)), and pro/antioxidant status (15-F2α-isoprostanes (F2-IsoP) and oxidized LDL in plasma; superoxide dismutase, glutathione peroxidase, and reduced/oxidized glutathione in erythrocytes) were determined at baseline and 3 months later. The intradialytic training protocol did not modify body composition but had significant effects on physical fitness, lipid profile, and pro/antioxidant status. Indeed, at 3 months: (i) performance on the 6MWT was increased in EX (+23.4%, p < 0.001) but did not change in CON, (ii) plasma TG were reduced in EX (–23%, p < 0.03) but were not modified in CON, and (iii) plasma F2-IsoP concentrations were lower in EX than in CON (–35.7%, p = 0.02). In conclusion, our results show that 30 min of intradialytic training, 3 times per week for 3 months, are enough to exert beneficial effects on the most sensitive and reliable marker of lipid peroxidation (IsoP) while improving CKD-associated disorders (lipid profile and physical fitness). Intradialytic aerobic cycling training represents a useful and easy strategy to reduce CKD-associated disorders. These results need to be confirmed with a larger randomized study.

scholarly journals miR-98-5p plays a critical role in depression and antidepressant effect of ketamine

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Chaoli Huang ◽  
Yuanyuan Wang ◽  
Zifeng Wu ◽  
Jiali Xu ◽  
Ling Zhou ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Social Stress ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Rapid Onset ◽  
Therapeutic Strategies ◽  
Antidepressant Effect ◽  
Depression Treatment ◽  
Chronic Social Stress ◽  
Beneficial Effects

AbstractKetamine has been demonstrated to be a rapid-onset and long-lasting antidepressant, but its underlying molecular mechanisms remain unclear. Recent studies have emerged microRNAs as important modulators for depression treatment. In this study, we report that miR-98-5p is downregulated in the prefrontal cortex and hippocampus of mice subjected to chronic social stress, while overexpressing it by its agonist alleviates depression-like behaviors. More importantly, we demonstrate that miR-98-5p is upregulated by ketamine administration, while inhibition of it by its antagonist blocks the antidepressant effect of ketamine. Our data implicate a novel molecular mechanism underlying the antidepressant effect of ketamine, and that therapeutic strategies targeting miR-98-5p could exert beneficial effects for depression treatment.

MO448MICRORNAS IMPLICATED IN CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Laurent Metzinger
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Clinical Outcomes ◽  
Molecular Mechanisms ◽  
Neointimal Hyperplasia ◽  
Uremic Toxins ◽  
University Hospital ◽  
Transcriptional Level ◽  
Uremic Toxin ◽  
Ckd Stage

Abstract Background and Aims The gene program is controlled at the post-transcriptional level by the action of small non-coding RNAs known as microRNAs (miRNAs), short, single-stranded molecules that control mRNA stability or translational repression via base pairing with regions in the 3' untranslated region of their target mRNAs. Recently, considerable progress has been made to elucidate the roles of miRNAs in vascular pathogenesis and develop the use of miRNAs as biomarkers, and innovative drugs. We demonstrated during the last decade that miRNAs miR-126 and miR-223 are implicated in the course of chronic kidney disease (CKD) and cardiovascular damage. miR-223 expression is enhanced in vascular smooth muscle cells (VSMCs) subjected to an uremic toxin and also in aortas of a murine model of CKD. As restenosis is a common complication of angioplasty, in which neointimal hyperplasia results from migration of VSMCs into the vessel lumen we measured the effect of miR-223 modulation on restenosis in a rat model of carotid artery after balloon injury. We over-expressed and inhibited miR-223 expression using adenoviral vectors, coding a pre-miR-223 sequence or a sponge sequence, used to trap endogenous microRNA, respectively. We demonstrated that inhibiting miR-223 function significantly reduced neointimal hyperplasia by almost half in carotids. Thus down-regulating miR-223 could be a potential therapeutic approach to prevent restenosis after angioplasty. We also correlated miR-126 and miR-223 expression with clinical outcomes in a large cohort of CKD patients, in collaboration with the University Hospital of Ghent (Belgium) and Ambroise Paré Hospital, France. We evaluated both miRNA’s link with all-cause mortality and cardiovascular and renal events over a 6-year follow-up period. The serum levels of miR-126 and miR-223 were decreased as CKD stage advanced, and patients with higher levels of miR-126 and miR-223 had a higher survival rate. Similar results were observed for cardiovascular and renal events. In conclusion, CKD is associated with a decrease in circulating miR-126 and miR-223 levels in CKD patients. We will also present links between several uremic toxin concentrations and miRNA concentration in the patients of this cohort. Finally, anemia is a common feature of CKD that is associated with cardiovascular disease and poor clinical outcomes. A mixture of uremic toxins accumulates in the blood of CKD patients during the course of the disease, and there is good evidence that they modulate erythropoiesis, explaining at least partly anemia. The exact molecular mechanisms implicated are however poorly understood, although recent progresses have been made to identify key components in the CKD process. We will present results on the effect of uremic toxins on erythropoiesis, having an impact on cell metabolism during this process. Taken together, our findings could be of interest to both researchers and clinicians working in the field since they might shed new light on the molecular mechanisms involved in the CKD process. MicroRNAs implicated in Chronic Kidney Disease Pr. Laurent Metzinger, UR-UPJV 4666 HEMATIM, CURS, Université de Picardie Jules Verne, CHU Amiens Sud, Avenue René Laënnec, Salouel, F-80054, Amiens, France. Tel: (+33) 22 82 53 56, Email: [email protected]

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