Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease-Volume II.

The kidney performs fundamental functions by eliminating metabolic waste and reabsorbing essential nutrients and electrolytes such as glucose, proteins, ions, and anions [...

Roles of Dihydrolipoamide Dehydrogenase in Health and Disease.

Dihydrolipoamide dehydrogenase (DLDH) is a flavin-dependent disulfide oxidoreductase. The active form of DLDH is a stable homodimer, and its deficiencies have been linked to numerous metabolic disorders. A better understanding of redox and nonredox features of DLDH may reveal druggable targets for disease interventions or preventions.

Renal-Protective Roles of Lipoic Acid in Kidney Disease.

The kidney is a crucial organ that eliminates metabolic waste and reabsorbs nutritious elements. It also participates in the regulation of blood pressure, maintenance of electrolyte balance and blood pH homeostasis, as well as erythropoiesis and vitamin D maturation. Due to such a heavy workload, the kidney is an energy-demanding organ and is constantly exposed to endogenous and exogenous insults, leading to the development of either acute kidney injury (AKI) or chronic kidney disease (CKD).

Long-term intermittent fasting improves neurological function by promoting angiogenesis after cerebral ischemia via growth differentiation factor 11 signaling activation.

Intermittent fasting (IF), an alternative to caloric restriction, is a form of time restricted eating. IF conditioning has been suggested to have neuroprotective effects and potential long-term brain health benefits. But the mechanism underlying remains unclear.

The Nicotinamide/Streptozotocin Rodent Model of Type 2 Diabetes: Renal Pathophysiology and Redox Imbalance Features.

Diabetic nephropathy (DN) is a common complication of diabetes mellitus. While there has been a great advance in our understanding of the pathogenesis of DN, no effective managements of this chronic kidney disease are currently available. Therefore, continuing to elucidate the underlying biochemical and molecular mechanisms of DN remains a constant need.

Cisplatin-Induced Kidney Toxicity: Potential Roles of Major NAD-Dependent Enzymes and Plant-Derived Natural Products.

Cisplatin is an FDA approved anti-cancer drug that is widely used for the treatment of a variety of solid tumors. However, the severe adverse effects of cisplatin, particularly kidney toxicity, restrict its clinical and medication applications. The major mechanisms of cisplatin-induced renal toxicity involve oxidative stress, inflammation, and renal fibrosis, which are covered in this short review.

Redox Imbalance and Mitochondrial Abnormalities in Kidney Disease.

The kidneys carry out fundamental life-sustaining functions by removing waste substances, controlling salt and water balance, retaining substances vital to the body such as glucose and proteins, and maintaining blood pH balance [...

Folic acid-induced animal model of kidney disease.

The kidneys are a vital organ that is vulnerable to both acute kidney injury (AKI) and chronic kidney disease (CKD) which can be caused by numerous risk factors such as ischemia, sepsis, drug toxicity and drug overdose, exposure to heavy metals, and diabetes. In spite of the advances in our understanding of the pathogenesis of AKI and CKD as well AKI transition to CKD, there is still no available therapeutics that can be used to combat kidney disease effectively, highlighting an urgent need to further study the pathological mechanisms underlying AKI, CKD, and AKI progression to CKD. In this regard, animal models of kidney disease are indispensable.

Cadmium-Induced Kidney Injury: Oxidative Damage as a Unifying Mechanism.

Cadmium is a nonessential metal that has heavily polluted the environment due to human activities. It can be absorbed into the human body via the gastrointestinal tract, respiratory tract, and the skin, and can cause chronic damage to the kidneys. The main site where cadmium accumulates and causes damage within the nephrons is the proximal tubule.

Activation of peripheral group III metabotropic glutamate receptors suppressed formalin-induced nociception.

Intraplantar injection of formalin produces persistent spontaneous nociception and hyperalgesia. The underlying mechanism, however, remains unclear. The present study was, therefore, designed to determine the roles of peripheral group III metabotropic glutamate receptors (mGluRs) in formalin-evoked spontaneous nociception.

Comment on Kobroob et al. Effectiveness of N-Acetylcysteine in the Treatment of Renal Deterioration Caused by Long-Term Exposure to Bisphenol A. 2021, , 655.

Bisphenol A (BPA: 2,2-bis-(4-hydroxyphenyl)-propane) is an industrial chemical that is widely used in the production of epoxy resins and polycarbonate for food containers and plastic bottles [...

NADH/NAD Redox Imbalance and Diabetic Kidney Disease.

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.

Potential Biochemical Mechanisms of Brain Injury in Diabetes Mellitus.

The goal of this review was to summarize current biochemical mechanisms of and risk factors for diabetic brain injury. We mainly summarized mechanisms published in the past three years and focused on diabetes induced cognitive impairment, diabetes-linked Alzheimer's disease, and diabetic stroke. We think there is a need to conduct further studies with increased sample sizes and prolonged period of follow-ups to clarify the effect of DM on brain dysfunction.

Antioxidative and Hypoglycemic Effect of Ta-ermi Extracts on Streptozotocin-Induced Diabetes.

Introduction: The purpose of the present study was to reveal the potential positive effect of the Ta-ermi extracts on oxidative stress and streptozotocin (STZ)-diabetic mice and rats treated with Ta-ermi water- and alcohol-extracts.

Methods: The study was carried out using three experimental model: 1) in vitro experiments whereby Ta-ermi extracts were incubated with free radical generators such as 2,2-diphenyl-1-picryl-hydrazyl-hydrate (DPPH) and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS) to evaluate Ta-ermi's antioxidant effects; 2) testing the hypoglycemic effects of Ta-ermi extracts in streptozotocin (STZ)-induced diabetic mice; and 3) testing the beneficial effects of Ta-ermi extracts on mitochondrial complex I function using STZ-diabetic rats.

Results: In vitro antioxidant experiments showed that both of the extracts could scavenge free radicals and exhibited inhibitory effects on glucosidase and aldose reductase with differential effects between water extract and alcohol extract.

Reductive Stress-Induced Mitochondrial Dysfunction and Cardiomyopathy.

The goal of this review was to summarize reported studies focusing on cellular reductive stress-induced mitochondrial dysfunction, cardiomyopathy, dithiothreitol- (DTT-) induced reductive stress, and reductive stress-related free radical reactions published in the past five years. Reductive stress is considered to be a double-edged sword in terms of antioxidation and disease induction. As many underlying mechanisms are still unclear, further investigations are obviously warranted.

5-Methoxyindole-2-Carboylic Acid (MICA) Fails to Retard Development and Progression of Type II Diabetes in ZSF1 Diabetic Rats.

5-Methoxyindole-2-carboxylic acid (MICA) is a well-established reversible inhibitor of mitochondrial dihydrolipoamide dehydrogenase (DLDH). This chemical, as an indole derivative, has been shown to be neuroprotective against ischemic stroke injury when administered either before or after ischemic stroke in animal models. MICA has also been studied as a potential antidiabetic agent by numerous investigators, though the underlying mechanisms remain sketchy.

Urine Sample-Derived Cerebral Organoids Suitable for Studying Neurodevelopment and Pharmacological Responses.

Cerebral organoids (COs) developed from human induced pluripotent stem cells (hiPSCs) have been noticed for their potential in research and clinical applications. While skin fibroblast-derived hiPSCs are proficient at forming COs, the cellular and molecular features of COs developed using hiPSCs generated from other somatic cells have not been systematically examined. Urinary epithelial cells (UECs) isolated from human urine samples are somatic cells that can be non-invasively collected from most individuals.

Regulation of the SIRT1 signaling pathway in NMDA-induced Excitotoxicity.

Silent Information Regulator 1 (SIRT1), an NAD-dependent deacetylase, contributes to the neuroprotective effect. However, intracellular signaling pathways that affect SIRT1 function remain unknown. It is well known that N-methyl-D-aspartate (NMDA) receptor activation induces calcium influx which then activates PKC, and SIRT1 is a mRNA target for HuR protein.

Role of Catalase in Oxidative Stress- and Age-Associated Degenerative Diseases.

Reactive species produced in the cell during normal cellular metabolism can chemically react with cellular biomolecules such as nucleic acids, proteins, and lipids, thereby causing their oxidative modifications leading to alterations in their compositions and potential damage to their cellular activities. Fortunately, cells have evolved several antioxidant defense mechanisms (as metabolites, vitamins, and enzymes) to neutralize or mitigate the harmful effect of reactive species and/or their byproducts. Any perturbation in the balance in the level of antioxidants and the reactive species results in a physiological condition called "oxidative stress.

Effects of mesencephalic astrocyte-derived neurotrophic factor on cerebral angiogenesis in a rat model of cerebral ischemia.

Mesencephalic astrocyte-derived neurotrophic factor (MANF) is an endoplasmic reticulum stress-related protein that exhibits neuroprotective effects. Recent studies have shown that MANF promotes poststroke functional recovery in rats. However, the underlying mechanisms have not yet been fully understood.

Effects of dietary 5-methoxyindole-2-carboxylic acid on brain functional recovery after ischemic stroke.

Stroke leads to devastating outcomes including impairments of sensorimotor and cognitive function that may be long lasting. New intervention strategies are needed to overcome the long-lasting effects of ischemic injury. Previous studies determined that treatment with 5-methoxyindole-2-carboxylic acid (MICA) conferred chemical preconditioning and neuroprotection against stroke.

Neuroprotection of L. orientin against cerebral ischemia/reperfusion induced brain injury.

Orientin is a flavonoid monomer. In recent years, its importance as a source of pharmacological active substance is growing rapidly due to its properties such as anti-myocardial ischemia, anti-apoptosis, anti-radiation, anti-tumor, and anti-aging. However, the neuroprotective effects of Orientin on stroke injury have not been comprehensively evaluated.