Combined treatment of epigallocatechin gallate and Coenzyme Q10 attenuates cisplatin-induced nephrotoxicity via suppression of oxidative/nitrosative stress, inflammation and cellular damage

2016 ◽  
Vol 94 ◽  
pp. 213-220 ◽  
Author(s):  
Sabiha Fatima ◽  
Noura Al-Mohaimeed ◽  
Yazeed Al-Shaikh ◽  
Poonam Tyagi ◽  
Naheed Banu ◽  
...  
Keyword(s):  
Coenzyme Q10 ◽  
Nitrosative Stress ◽  
Combined Treatment ◽  
Epigallocatechin Gallate ◽  
Cellular Damage

Effects of Quercetin and Coenzyme Q10 on Biochemical, Molecular, and Morphological Parameters of Skeletal Muscle in Trained Diabetic Rats

2021 ◽  
Vol 14 ◽  
Author(s):  
Amal M. Youssef ◽  
Dalia A. Mohamed ◽  
Samia Hussein ◽  
Doaa M. Abdullah ◽  
Shaimaa A. Abdelrahman
Keyword(s):  
Skeletal Muscle ◽  
Coenzyme Q10 ◽  
Combined Treatment ◽  
Diabetic Rats ◽  
Molecular Structures ◽  
Treadmill Training ◽  
Albino Rats ◽  
Musculoskeletal Function ◽  
Sugar Levels ◽  
Fibronectin Type Iii Domain

Background: Diabetes mellitus (DM) affects the musculoskeletal system through its metabolic perturbations. Exercise modulates blood sugar levels and increases the body’s sensitivity to insulin in patients with DM. Objective: This study aimed to investigate the potential effects of combined quercetin and coenzyme Q10 (CoQ10) supplements with or without exercise on the histological, biochemical and molecular structures of diabetic rat’s skeletal muscle. Method: A total of 64 adult male albino rats were divided into six groups: control, trained nondiabetic, non-trained diabetic, diabetic rats treated with combined CoQ10 and quercetin, diabetic rats with treadmill training, and diabetic rats treated with treadmill training and CoQ10 and quercetin. Blood and skeletal muscle samples were obtained from all groups for routine histological examination and biochemical determination of cytokine levels and protein activities. Quantitative real-time polymerase chain reaction (qRT-PCR) and morphometric analysis of PAS and Bax expressions were also performed. Results: Biochemical analysis revealed improvement in all studied parameters with combined CoQ10 and quercetin than exercise training alone. Combined treatment and exercise showed significant improvement in all parameters especially interleukin 6 and malondialdehyde. Fibronectin type III domain-containing protein 5 (FNDC5) expression and irisin levels increased in all trained groups but combined treatment with exercise significantly increased their levels than exercise alone. Histological analysis revealed improvement after exercise or combined treatment; however, when exercise was combined with CoQ10 and quercetin, marked improvement was observed. Conclusion: the combination of CoQ10 and quercetin could be promising in preserving musculoskeletal function in patients with DM concomitantly with physical exercise.

Effect of Pre- and Post-Combined Multidoses of Epigallocatechin Gallate and Coenzyme Q10 on Cisplatin-Induced Oxidative Stress in Rat Kidney

2014 ◽  
Vol 29 (2) ◽  
pp. 91-97 ◽  
Author(s):  
Sabiha Fatima ◽  
Noura Al-Mohaimeed ◽  
Sadia Arjumand ◽  
Naheed Banu ◽  
Noura Al-Jameil ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coenzyme Q10 ◽  
Rat Kidney ◽  
Epigallocatechin Gallate

scholarly journals Protective effect of coenzyme Q10 against hypoxic cellular damage.

1985 ◽  
Vol 33 (7) ◽  
pp. 2896-2903 ◽  
Author(s):  
NOBORU SUZUKI ◽  
TETSUYA NAKAMURA ◽  
HIDEYUKI ISHIDA ◽  
KIYOSHI HOSONO
Keyword(s):  
Protective Effect ◽  
Coenzyme Q10 ◽  
Cellular Damage

scholarly journals Combination of green tea catechins, polysaccharides, and flavonols against urban fine dust particle-induced bronchial damage mediated by modulation of inflammation factors and airway cilia

2020 ◽  
Author(s):  
Juewon Kim ◽  
Hyunjung Choi ◽  
Dong-Hwa Choi ◽  
Kyuhee Park ◽  
Hyung-June Kim ◽  
...  
Keyword(s):  
Air Pollution ◽  
Cell Survival ◽  
Green Tea ◽  
Combined Treatment ◽  
Cellular Damage ◽  
Dust Particles ◽  
Public Health Issue ◽  
Epithelial Cell Line ◽  
Protective Effects ◽  
Fine Dust

Abstract Background Many studies have reported that environmental pollution has become a serious public health issue. Airborne fine dust particles (FDPs) have been identified as major toxins in air pollution that threaten human respiratory health. Developing strategies for defense against FDPs is one of the primary goals of air pollution research. Results While searching for an anti-FDP reagent, we found that green tea extract (GTE) and green tea fractions rich in flavonol glycosides (FLGs) and crude green tea polysaccharides (CTPs) had protective effects against FDP-stimulated cellular damage in the BEAS-2B airway epithelial cell line. The results demonstrated that GTE, FLGs, and CTPs significantly increased viability and lowered oxidative stress levels in FDP-treated cells. Major catechin and flavonol compounds increased cell survival, and (-)-epigallocatechin gallate (EGCG) and myricetin exerted synergistic effects on cell survival under FDP stimulation. Combined treatment with GTE, FLGs, and CTPs also exerted synergistic protective effects on cells, and the green tea components attenuated FDP-induced elevations in inflammatory gene expression. Moreover, the green tea components increased the proportion of ciliated cells and upregulated ciliogenesis in the airway in FDP-stimulated BEAS-2B cells. Conclusions Our findings provide insights into how natural phytochemicals protect the airway and suggest that green tea could be used to reduce FDP-induced airway damage as an individual therapeutic agent or as an ingredient in pharmaceutical and cosmeceutical products.

scholarly journals Disinhibited-Like Behavior Correlates With Frontal Cortex Damage in Alcohol-Induced Wernicke-Korsakoff Syndrome

2021 ◽  
Author(s):  
Marta Moya ◽  
Leticia López-Valencia ◽  
Borja García-Bueno ◽  
Laura Orio
Keyword(s):  
Frontal Cortex ◽  
Nitrosative Stress ◽  
Inflammatory Responses ◽  
Cell Damage ◽  
Combined Treatment ◽  
Memory Deficits ◽  
Combined Treatments ◽  
Therapeutic Approaches ◽  
Korsakoff Syndrome ◽  
Disease Specific

Wernicke-Korsakoff syndrome (WKS) is induced by thiamine deficiency (TD) and mainly related to alcohol consumption. Frontal cortex dysfunction has been associated to impulsivity and disinhibition in WKS patients. The pathophysiology involves oxidative stress, excitotoxicity and inflammatory responses leading to neuronal death, but the relative contributions of each factor (alcohol and TD, isolate or in interaction) to these phenomena are still poorly understood. A rat model was used by forced consumption of 20% (w/v) alcohol for 9 months (CA), TD hit (TD diet + pyrithiamine 0.25 mg/kg, i.p. daily injections the last 12 days of experimentation; TDD), and both combined treatments (CA+TDD). Motor and cognitive performance and cortical damage were examined. CA caused hyperlocomotion as a possible sensitization of ethanol-induced excitatory effects and recognition memory deficits. In addition, CA+TDD animals showed a disinhibited-like behavior, which appears to be dependent on TDD. Also, combined treatment led to more pronounced alterations in nitrosative stress, lipid peroxidation, apoptosis and cell damage markers. Correlations between injury signals and disinhibition suggest that CA+TDD disrupts behaviors dependent on the frontal cortex. Our study sheds light on the potential disease-specific mechanisms, reinforcing the need for neuroprotective therapeutic approaches along with preventive treatments for the nutritional deficiency in WKS.

scholarly journals Nitric oxide – mediated signalization and nitrosative stress in neuropathology / Azot oksid – posredovana signalizacija i nitrozativni stres u neuropatologiji

2012 ◽  
Vol 31 (4) ◽  
pp. 295-300 ◽  
Author(s):  
Ivana Stojanović ◽  
Srđan Ljubisavljević ◽  
Ivana Stevanović ◽  
Radmila Pavlović ◽  
Tatjana Cvetković ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Nitrosative Stress ◽  
Cellular Damage ◽  
Glutamate Excitotoxicity ◽  
Cns Inflammation ◽  
Physiological Processes ◽  
Signalling Molecule ◽  
Protein Functions ◽  
The Central Nervous System

Summary Nitric oxide (NO) is an important signalling molecule in a variety of physiological processes. NO, a gas, is produced from L-arginine by different isoforms of the nitric oxide synthase and serves as mediator in important physiological functions, such as promoting vasodilation of blood vessels and mediating communication between nervous system cells. Contradictory to its physiologic actions, free radical activity of NO can cause cellular damage by the induction of nitrosative stress with significant implications on nervous system diseases. Although the mechanism of NOmediated neurodegeneration still remains unclear, numerous studies suggest its crucial role in modification of protein functions by nitrosylation and nitro-tyrosination. NO contributes to glutamate excitotoxicity, participates in organelle fragmentation, inhibits mitochondrial respiratory complexes and mobilizes zinc from the internal stores. Recently, NO has been emerged as a mediator of epigenetic gene expression and chromatin changes. Besides, NO is a key mediator in the regulation of inflammatory and immune response of the central nervous system. It is involved in down regulation of several aspects of CNS inflammation, but also has a dual role in that it is required for inflammation in some situations.

Combined treatment of menadione and calcitriol increases the antiproliferative effect by promoting oxidative/nitrosative stress, mitochondrial dysfunction, and autophagy in breast cancer MCF-7 cells

2020 ◽  
Vol 98 (8) ◽  
pp. 548-556
Author(s):  
Solange Guizzardi ◽  
Gabriela Picotto ◽  
Valeria Rodriguez ◽  
JoEllen Welsh ◽  
Carmen Narvaez ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Molecular Mechanisms ◽  
Nitrosative Stress ◽  
Combined Therapy ◽  
Combined Treatment ◽  
Single Agent ◽  
Coupling Efficiency ◽  
Antiproliferative Action ◽  
Oncogenic Pathways ◽  
Mcf 7

The aim of this study was to determine new insights into the molecular mechanisms involved in the antiproliferative action of menadione + calcitriol (MEN+D) on MCF-7 cells. After 24 h, MEN+D inhibited the cell growth but was not observed with each single treatment. The combined drugs reduced the mitochondrial respiration at that time, as judged by an increase in the proton leak and a decrease in the ATP generation and coupling efficiency. At longer times, 48 or 96 h, either D or MEN reduced the proliferation, but the effect was higher when both drugs were used together. The combined treatment increased the superoxide anion ([Formula: see text]) and nitric oxide (NO•) contents as well as acidic vesicular organelles (AVOs) formation. The percentage of cells showing the lower mitochondrial membrane potential (ΔΨm) was highly increased by the combined therapy. LC3-II protein expression was enhanced by any treatment. In conclusion, the antiproliferative action of MEN+D involves oxidative/nitrosative stress, mitochondrial alteration, and autophagy. This combined therapy could be useful to treat breast cancer cells because it inhibits multiple oncogenic pathways more effectively than each single agent.

scholarly journals Effects of agmatine on chlorpromazine-induced neuronal injury in rat

2018 ◽  
Vol 87 (2) ◽  
pp. 145-153 ◽  
Author(s):  
Bratislav Dejanovic ◽  
Vesna Vukovic-Dejanovic ◽  
Milica Ninkovic ◽  
Irena Lavrnja ◽  
Ivana Stojanovic ◽  
...  
Keyword(s):  
Nitrosative Stress ◽  
Combined Treatment ◽  
Brain Regions ◽  
Antioxidant Defence ◽  
Superoxide Anion Production ◽  
Beneficial Effects ◽  
Antioxidant Defence System ◽  
Oxide Concentration ◽  
Nitric Oxide Concentration ◽  
The Brain

This study was aimed to study the potentially beneficial effects of agmatine on oxidative/nitrosative stress development in the brain of Wistar rats during subacute chlorpromazine treatment. The animals were divided into control (0.9% saline), chlorpromazine (38.7 mg/kg b.w.), chlorpromazine+agmatine (agmatine 75 mg/kg b.w. immediately after chlorpromazine, 38.7 mg/kg b.w. i.p.) and agmatine (75 mg/kg b.w.) groups. All the tested substances were administered intraperitoneally for 15 consecutive days and the rats were sacrificed by decapitation on day 15. Subacute administration of chlorpromazine resulted in increased lipid peroxidation, nitric oxide concentration and superoxide anion production, while completely damaging the antioxidant defence system in the cerebral cortex, striatum, and hippocampus. However, the combined treatment with chlorpromazine and agmatine significantly attenuated the oxidative/nitrosative stress indices and restored the antioxidant capacity to the control values in all of the examined brain regions. Western blot analysis supported biochemical findings in all groups, but the most notable changes were found in the hippocampus. Our results suggest potentially beneficial effects of agmatine, which may be useful in the modified antioxidant approach in chlorpromazine-therapy.

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