Tiliacora triandra extract and its major constituent attenuates diabetic kidney and testicular impairment by modulating redox imbalance and pro‐inflammatory responses in rats

2020 ◽  
Author(s):  
Peng Song ◽  
Chen Sun ◽  
Jinbo Li ◽  
Tong Long ◽  
Yixin Yan ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Major Constituent ◽  
Diabetic Kidney ◽  
Redox Imbalance ◽  
Testicular Impairment

scholarly journals Qing-Re-Xiao-Zheng Formula Modulates Gut Microbiota and Inhibits Inflammation in Mice With Diabetic Kidney Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Yabin Gao ◽  
Ruibing Yang ◽  
Lan Guo ◽  
Yaoxian Wang ◽  
Wei Jing Liu ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Gut Microbiota ◽  
Diabetic Kidney Disease ◽  
Inflammatory Responses ◽  
Protective Effects ◽  
Mice Model ◽  
Diabetic Kidney ◽  
Metabolic Inflammation ◽  
Gut Microbiota Dysbiosis

Evidence indicates that the metabolic inflammation induced by gut microbiota dysbiosis contributes to diabetic kidney disease. Prebiotic supplementations to prevent gut microbiota dysbiosis, inhibit inflammatory responses, and protect the renal function in DKD. Qing-Re-Xiao-Zheng formula (QRXZF) is a Traditional Chinese Medicine (TCM) formula that has been used for DKD treatment in China. Recently, there are growing studies show that regulation of gut microbiota is a potential therapeutic strategy for DKD as it is able to reduce metabolic inflammation associated with DKD. However, it is unknown whether QRXZF is effective for DKD by regulating of gut microbiota. In this study, we investigated the reno-protective effect of QRXZF by exploring its potential mechanism between gut microbiota and downstream inflammatory pathways mediated by gut-derived lipopolysaccharide (LPS) in the kidney. High-fat diet (HFD) and streptozotocin injection-induced DKD mice model was established to assess the QRXZF effect in vivo. Mice treated with QRXZF for 8 weeks had significantly lower levels of urinary albumin, serum cholesterol and triglycerides. The renal injuries observed through histological analysis were attenuated as well. Also, mice in the QRXZF group had higher levels of Zonula occludens protein-1 (ZO-1) expression, lower levels of serum fluorescein-isothiocyanate (FITC)-dextran and less-damaged colonic mucosa as compared to the DKD group, implying the benefit role for the gut barrier integrity. QRXZF treatment also reversed gut dysbiosis and reduced levels of gut-derived LPS. Notably, the expression of toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB), which are important inflammation pathways in DKD, were suppressed in the QRXZF groups. In conclusion, our results indicated that the reno-protective effects of QRXZF was probably associated with modulating gut microbiota and inhibiting inflammatory responses in the kidney.

scholarly journals Targeting Redox Imbalance as an Approach for Diabetic Kidney Disease

Biomedicines ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 40 ◽  
Author(s):  
Keiichiro Matoba ◽  
Yusuke Takeda ◽  
Yosuke Nagai ◽  
Tamotsu Yokota ◽  
Kazunori Utsunomiya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Public Health Problem ◽  
Cardiovascular Complications ◽  
Current Status ◽  
Diabetic Kidney ◽  
Redox Imbalance ◽  
Stage Renal Disease ◽  
End Stage

Diabetic kidney disease (DKD) is a worldwide public health problem. It is the leading cause of end-stage renal disease and is associated with increased mortality from cardiovascular complications. The tight interactions between redox imbalance and the development of DKD are becoming increasingly evident. Numerous cascades, including the polyol and hexosamine pathways have been implicated in the oxidative stress of diabetes patients. However, the precise molecular mechanism by which oxidative stress affects the progression of DKD remains to be elucidated. Given the limited therapeutic options for DKD, it is essential to understand how oxidants and antioxidants are controlled in diabetes and how oxidative stress impacts the progression of renal damage. This review aims to provide an overview of the current status of knowledge regarding the pathological roles of oxidative stress in DKD. Finally, we summarize recent therapeutic approaches to preventing DKD with a focus on the anti-oxidative effects of newly developed anti-hyperglycemic agents.

scholarly journals Use of Anti-Diabetic Agents in Non-Diabetic Kidney Disease: From Bench to Bedside

Life ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 389
Author(s):  
Sungjin Chung ◽  
Gheun-Ho Kim
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Inflammatory Responses ◽  
New Drugs ◽  
Tubuloglomerular Feedback ◽  
Systemic Hypertension ◽  
Diabetic Kidney ◽  
Glucose Transporter 2 ◽  
Kidney Morphology

New drugs were recently developed to treat hyperglycemia in patients with type 2 diabetes mellitus (T2D). However, metformin remains the first-line anti-diabetic agent because of its cost-effectiveness. It has pleiotropic action that produces cardiovascular benefits, and it can be useful in diabetic nephropathy, although metformin-associated lactic acidosis is a hindrance to its use in patients with kidney failure. New anti-diabetic agents, including glucagon-like peptide-1 receptor (GLP-1R) agonists, dipeptidyl peptidase-4 (DPP-4) inhibitors, and sodium-glucose transporter-2 (SGLT-2) inhibitors, also produce cardiovascular or renal benefits in T2D patients. Their glucose-independent beneficial actions can lead to cardiorenal protection via hemodynamic stabilization and inflammatory modulation. Systemic hypertension is relieved by natriuresis and improved vascular dysfunction. Enhanced tubuloglomerular feedback can be restored by SGLT-2 inhibition, reducing glomerular hypertension. Patients with non-diabetic kidney disease might also benefit from those drugs because hypertension, proteinuria, oxidative stress, and inflammation are common factors in the progression of kidney disease, irrespective of the presence of diabetes. In various animal models of non-diabetic kidney disease, metformin, GLP-1R agonists, DPP-4 inhibitors, and SGLT-2 inhibitors were favorable to kidney morphology and function. They strikingly attenuated biomarkers of oxidative stress and inflammatory responses in diseased kidneys. However, whether those animal results translate to patients with non-diabetic kidney disease has yet to be evaluated. Considering the paucity of new agents to treat kidney disease and the minimal adverse effects of metformin, GLP-1R agonists, DPP-4 inhibitors, and SGLT-2 inhibitors, these anti-diabetic agents could be used in patients with non-diabetic kidney disease. This paper provides a rationale for clinical trials that apply metformin, GLP-1R agonists, DPP-4 inhibitors, and SGLT-2 inhibitors to non-diabetic kidney disease.

scholarly journals NADH/NAD+ Redox Imbalance and Diabetic Kidney Disease

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 730
Author(s):  
Liang-Jun Yan
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Redox Balance ◽  
Pathophysiological Mechanism ◽  
Diabetic Kidney ◽  
Nad Metabolism ◽  
Redox Imbalance ◽  
Nadh Generation ◽  
Stage Renal Disease ◽  
End Stage

Diabetic kidney disease (DKD) is a common and severe complication of diabetes mellitus. If left untreated, DKD can advance to end stage renal disease that requires either dialysis or kidney replacement. While numerous mechanisms underlie the pathogenesis of DKD, oxidative stress driven by NADH/NAD+ redox imbalance and mitochondrial dysfunction have been thought to be the major pathophysiological mechanism of DKD. In this review, the pathways that increase NADH generation and those that decrease NAD+ levels are overviewed. This is followed by discussion of the consequences of NADH/NAD+ redox imbalance including disruption of mitochondrial homeostasis and function. Approaches that can be applied to counteract DKD are then discussed, which include mitochondria-targeted antioxidants and mimetics of superoxide dismutase, caloric restriction, plant/herbal extracts or their isolated compounds. Finally, the review ends by pointing out that future studies are needed to dissect the role of each pathway involved in NADH-NAD+ metabolism so that novel strategies to restore NADH/NAD+ redox balance in the diabetic kidney could be designed to combat DKD.

scholarly journals KEAP1, a cysteine-based sensor and a drug target for the prevention and treatment of chronic disease

Open Biology ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 200105 ◽  
Author(s):  
Sharadha Dayalan Naidu ◽  
Albena T. Dinkova-Kostova
Keyword(s):  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Inflammatory Responses ◽  
Redox Homeostasis ◽  
Redox Balance ◽  
Related Factor ◽  
Redox Imbalance ◽  
Persistent Inflammation ◽  
Activation Of Transcription

Redox imbalance and persistent inflammation are the underlying causes of most chronic diseases. Mammalian cells have evolved elaborate mechanisms for restoring redox homeostasis and resolving acute inflammatory responses. One prominent mechanism is that of inducing the expression of antioxidant, anti-inflammatory and other cytoprotective proteins, while also suppressing the production of pro-inflammatory mediators, through the activation of transcription factor nuclear factor-erythroid 2 p45-related factor 2 (NRF2). At homeostatic conditions, NRF2 is a short-lived protein, which avidly binds to Kelch-like ECH-associated protein 1 (KEAP1). KEAP1 functions as (i) a substrate adaptor for a Cullin 3 (CUL3)-based E3 ubiquitin ligase that targets NRF2 for ubiquitination and proteasomal degradation, and (ii) a cysteine-based sensor for a myriad of physiological and pharmacological NRF2 activators. Here, we review the intricate molecular mechanisms by which KEAP1 senses electrophiles and oxidants. Chemical modification of specific cysteine sensors of KEAP1 results in loss of NRF2-repressor function and alterations in the expression of NRF2-target genes that encode large networks of diverse proteins, which collectively restore redox balance and resolve inflammation, thus ensuring a comprehensive cytoprotection. We focus on the cyclic cyanoenones, the most potent NRF2 activators, some of which are currently in clinical trials for various pathologies characterized by redox imbalance and inflammation.

scholarly journals Anti-Inflammatory Effects of Fermented Lotus Root and Linoleic Acid in Lipopolysaccharide-Induced RAW 264.7 Cells

Life ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 293
Author(s):  
Sung Min Kim ◽  
Eun-Jung Park ◽  
Jong-Yeon Kim ◽  
Jihee Choi ◽  
Hae-Jeung Lee
Keyword(s):  
Linoleic Acid ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Innate Immune ◽  
Gastric Ulcers ◽  
Raw 264.7 Cells ◽  
Major Constituent ◽  
Raw 264.7 ◽  
Lotus Root ◽  
Anti Inflammatory

Inflammation is a protective response of the innate immune system. However, aberrant inflammatory responses lead to various diseases. Lotus root, the edible rhizome of Nelumbo nucifera, is a popular traditional herbal medicine in East Asia. In a previous study, we reported that fermented lotus root (FLR) alleviated ethanol/HCl-induced gastric ulcers in rats by modulating inflammation-related genes. However, the mechanisms underlying the anti-inflammatory effects of FLR and its major constituent, linoleic acid (LA), are still largely unknown. In this study, we investigated the anti-inflammatory effects of FLR and LA on lipopolysaccharide (LPS)-induced inflammation in RAW 264.7 murine macrophages. We found that FLR inhibited LPS-induced expression of inflammatory mediators through down-regulation of NF-κB activity. Similarly, LA also attenuated LPS-induced inflammatory responses and reduced LPS-induced phosphorylation of proteins associated with NF-κB signaling, such as ERK, JNK, and p38. Overall, our results suggested that FLR and LA may effectively ameliorate inflammatory diseases.

scholarly journals An Indole-2-Carboxamide Derivative, LG4, Alleviates Diabetic Kidney Disease Through Inhibiting MAPK-Mediated Inflammatory Responses

2021 ◽  
Vol Volume 14 ◽  
pp. 1633-1645
Author(s):  
Jianchang Qian ◽  
Sihui Yin ◽  
Lin Ye ◽  
Zhe Wang ◽  
Sheng Shu ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Inflammatory Responses ◽  
Diabetic Kidney

scholarly journals Epidermal Endocannabinoid System (EES) and its Cosmetic Application

Cosmetics ◽  
2019 ◽  
Vol 6 (2) ◽  
pp. 33
Author(s):  
Sekyoo Jeong ◽  
Min Kim ◽  
Sin Lee ◽  
Byeong Park
Keyword(s):  
Cannabinoid Receptors ◽  
Cannabinoid Receptor ◽  
Inflammatory Responses ◽  
Endocannabinoid System ◽  
Major Constituent ◽  
Health Improvement ◽  
Hemp Seed ◽  
Therapeutic Benefits

Recently, cannabis, or its major constituent cannabidiol (CBD), has emerged as an attractive cosmetic ingredient. Initiated as a basic investigation of the physiological roles of cannabinoid receptors and their endogenous ligands, endocannabinoids’ diverse potential benefits have been proposed for using cannabinoid receptor modulating compounds in skin health. Improvement in skin barrier functions, alleviating inflammatory responses, and the relief of itching sensations are some commonly expected therapeutic benefits, which have been supported by many in vitro, in vivo, and clinical studies. While hemp seed oils or hemp extracts might be used for the cosmetic formulation, the potential for contamination with a psychoactive cannabinoid, such as 9-THC, should be carefully checked. Instead of using hemp-derived ingredients, the use of cannabinomimetics, synthetic ligands on cannabinoid receptors, or entourage compounds (which modulate intracellular synthesis and the degradation of endocannabinoids), have been tried. In this review, a brief introduction of the epidermal endocannabinoid system (EES) and its physiological roles will be followed by a review of the cosmetic and dermatologic application of cannabinomimetics and entourage compounds. The practical application of newly developed endocannabinomimetics will be discussed as well.

scholarly journals Redox Imbalance Differentially Inhibits Lipopolysaccharide-Induced Macrophage Activation in the Mouse Liver

1999 ◽  
Vol 67 (10) ◽  
pp. 5409-5416 ◽  
Author(s):  
Fuan Wang ◽  
Luke Y. Wang ◽  
Douglas Wright ◽  
Michael J. Parmely
Keyword(s):  
Kupffer Cells ◽  
Inflammatory Responses ◽  
Buthionine Sulfoximine ◽  
Redox Balance ◽  
Glutathione Depletion ◽  
Redox Stress ◽  
Redox Imbalance ◽  
Tnf Α

ABSTRACT Endotoxemia is accompanied by significant changes in the reductive-oxidative (redox) balance of critical target organs. Redox stress has been shown to regulate the expression of proinflammatory genes that are induced by endotoxic lipopolysaccharide (LPS) in vitro; however, much less is known about the effects of redox imbalance on LPS-induced gene expression in vivo. To assess the effects of redox stress on inflammatory responses in endotoxemia, mice were treated with either diethyl maleate (DEM), a glutathione-depleting agent, or buthionine sulfoximine (BSO), an inhibitor of glutathione synthesis, and challenged with LPS. While serum tumor necrosis alpha (TNF-α) responses and the appearance of TNF-α-positive Kupffer cells in the liver were virtually eliminated by DEM or BSO treatment, the expression of both CD14 and inducible NO synthase (iNOS) by Kupffer cells was unaffected by glutathione depletion. By contrast, LPS-induced hepatocyte and hepatic sinusoidal endothelial cell iNOS expression was significantly inhibited in DEM-treated mice. Hepatocyte iNOS induced by recombinant mouse TNF-α was also inhibited by DEM treatment. These results indicate that the effects of oxidative stress in this organ are cell type specific and suggest that both the production and the action of TNF-α are substantially influenced by the redox state of the liver during endotoxemia.

Effect of light intensity on the ultrastructure of the filamentous cyanobacterium, Anabaena variabilis

1988 ◽  
Vol 46 ◽  
pp. 300-301
Author(s):  
C. S. Bricker ◽  
S. R. Barnum ◽  
B. Huang ◽  
J. G. Jaworskl
Keyword(s):  
Fatty Acid ◽  
Light Intensity ◽  
Acid Content ◽  
Fatty Acid Content ◽  
Anabaena Variabilis ◽  
Chloroplast Envelope ◽  
Major Constituent ◽  
Filamentous Cyanobacterium ◽  
Photosynthetic Membrane ◽  
Effect Of Light

Cyanobacteria are Gram negative prokaryotes that are capable of oxygenic photosynthesis. Although there are many similarities between eukaryotes and cyanobacteria in electron transfer and phosphorylation during photosynthesis, there are two features of the photosynthetic apparatus in cyanobacteria which distinguishes them from plants. Cyanobacteria contain phycobiliproteins organized in phycobilisomes on the surface of photosynthetic membrane. Another difference is in the organization of the photosynthetic membranes. Instead of stacked thylakolds within a chloroplast envelope membrane, as seen In eukaryotes, IntracytopIasmlc membranes generally are arranged in three to six concentric layers. Environmental factors such as temperature, nutrition and light fluency can significantly affect the physiology and morphology of cells. The effect of light Intensity shifts on the ultrastructure of Internal membrane in Anabaena variabilis grown under controlled environmental conditions was examined. Since a major constituent of cyanobacterial thylakolds are lipids, the fatty acid content also was measured and correlated with uItrastructural changes. The regulation of fatty acid synthesis in cyanobacteria ultimately can be studied if the fatty acid content can be manipulated.

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