scholarly journals Effect ofCentella asiaticaon Oxidative Stress and Lipid Metabolism in Hyperlipidemic Animal Models

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Yun Zhao ◽  
Ping Shu ◽  
Youzhi Zhang ◽  
Limin Lin ◽  
Haihong Zhou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Metabolic Diseases ◽  
Centella Asiatica ◽  
Ethanol Extract ◽  
Hypolipidemic Effect ◽  
Mice Model ◽  
Hamster Model

Hyperlipidemia and many other metabolic diseases are related to oxidative stress.Centella asiaticais a traditional Chinese medicine whose antioxidant effect in vitro has been reported. We are interested in whether it possesses this effect in vivo and hence modulates lipid metabolism. Therefore, experiments were carried out on mice and golden hamsters regarding its antioxidant and hypolipidemic effect. We observed that a fraction (CAF3) of the ethanol extract (CAE) ofCentella asiaticahad a cholesterol decrease of 79% and a triglyceride decrease of 95% in acute mice model, so CAF3 was further investigated in high-fat-fed hamster model. It was shown that CAF3 increased SOD and GSH-Px activities and decreased MDA level, and it also improved TC, TG, LDL-C, HDL-C, AST, and ALT levels. L-CAT and SR-BI gene expression in hamsters were increased. Taken together, our data suggest that the CAF3 fraction ofCentella asiaticahas antioxidant and hypolipidemic properties.

scholarly journals Proanthocyanidins against Oxidative Stress: From Molecular Mechanisms to Clinical Applications

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Lingyu Yang ◽  
Dehai Xian ◽  
Xia Xiong ◽  
Rui Lai ◽  
Jing Song ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Low Cost ◽  
Natural Agents ◽  
Molecular Damage ◽  
And Control

Proanthocyanidins (PCs) are naturally occurring polyphenolic compounds abundant in many vegetables, plant skins (rind/bark), seeds, flowers, fruits, and nuts. Numerousin vitroandin vivostudies have demonstrated myriad effects potentially beneficial to human health, such as antioxidation, anti-inflammation, immunomodulation, DNA repair, and antitumor activity. Accumulation of prooxidants such as reactive oxygen species (ROS) exceeding cellular antioxidant capacity results in oxidative stress (OS), which can damage macromolecules (DNA, lipids, and proteins), organelles (membranes and mitochondria), and whole tissues. OS is implicated in the pathogenesis and exacerbation of many cardiovascular, neurodegenerative, dermatological, and metabolic diseases, both through direct molecular damage and secondary activation of stress-associated signaling pathways. PCs are promising natural agents to safely prevent acute damage and control chronic diseases at relatively low cost. In this review, we summarize the molecules and signaling pathways involved in OS and the corresponding therapeutic mechanisms of PCs.

scholarly journals Astaxanthin Ameliorates Lipopolysaccharide-Induced Neuroinflammation, Oxidative Stress and Memory Dysfunction through Inactivation of the Signal Transducer and Activator of Transcription 3 Pathway

Marine Drugs ◽  
2019 ◽  
Vol 17 (2) ◽  
pp. 123 ◽  
Author(s):  
Ji Han ◽  
Yong Lee ◽  
Jun Im ◽  
Young Ham ◽  
Hee Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Binding ◽  
Inflammatory Responses ◽  
Memory Loss ◽  
Signal Transducer ◽  
Mice Model ◽  
Neuroinflammatory Response ◽  
Transcription 3

Astaxanthin (AXT), a xanthophyll carotenoid compound, has potent antioxidant, anti-inflammatory and neuroprotective properties. Neuroinflammation and oxidative stress are significant in the pathogenesis and development of Alzheimer’s disease (AD). Here, we studied whether AXT could alleviate neuroinflammation, oxidative stress and memory loss in lipopolysaccharide (LPS) administered mice model. Additionally, we investigated the anti-oxidant activity and the anti-neuroinflammatory response of AXT in LPS-treated BV-2 microglial cells. The AXT administration ameliorated LPS-induced memory loss. This effect was associated with the reduction of LPS-induced expression of inflammatory proteins, as well as the production of reactive oxygen species (ROS), nitric oxide (NO), cytokines and chemokines both in vivo and in vitro. AXT also reduced LPS-induced β-secretase and Aβ1–42 generation through the down-regulation of amyloidogenic proteins both in vivo and in vitro. Furthermore, AXT suppressed the DNA binding activities of the signal transducer and activator of transcription 3 (STAT3). We found that AXT directly bound to the DNA- binding domain (DBD) and linker domain (LD) domains of STAT3 using docking studies. The oxidative stress and inflammatory responses were not downregulated in BV-2 cells transfected with DBD-null STAT3 and LD-null STAT3. These results indicated AXT inhibits LPS-induced oxidant activity, neuroinflammatory response and amyloidogenesis via the blocking of STAT3 activity through direct binding.

scholarly journals Inhibitory Effects of Raw-Extract Centella asiatica (RECA) on Acetylcholinesterase, Inflammations, and Oxidative Stress Activities via In Vitro and In Vivo

Molecules ◽  
2020 ◽  
Vol 25 (4) ◽  
pp. 892 ◽  
Author(s):  
Zetty Zulikha Hafiz ◽  
Muhammad ‘Afif Mohd Amin ◽  
Richard Muhammad Johari James ◽  
Lay Kek Teh ◽  
Mohd Zaki Salleh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Centella Asiatica ◽  
Raw 264.7 Cells ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Concentration Dependent Manner ◽  
Sprague Dawley Rats ◽  
And Oxidative Stress

Centella asiatica (C. asiatica) is one of the medicinal plants that has been reported to exert comprehensive neuroprotection in vitro and in vivo. In view of this, the present study was performed to investigate the effect of ethanolic extract of C. asiatica, designated as raw-extract of C. asiatica (RECA) in reducing the acetylcholinesterase (AChE), inflammations, and oxidative stress activities via both in vitro (SH-SY5Y and RAW 264.7 cells) and in vivo (Sprague Dawley rats). Quantitative high-performance liquid chromatography analysis reveals that RECA contains a significantly high proportion of glycosides than the aglycones with madecassoside as the highest component, followed by asiaticoside. Treatment of SH-SY5Y cells with RECA significantly reduced the AChE activity in a concentration-dependent manner with an IC50 value of 31.09 ± 10.07 µg/mL. Furthermore, the anti-inflammatory and antioxidant effects of RECA were evaluated by lipopolysaccharides (LPS)-stimulated RAW 264.7 cells. Our results elucidated that treatment with RECA significantly suppressed the level of pro-inflammatory cytokine/mediators and oxidative stress released in a concentration-dependent manner. Interestingly, these patterns of inhibition were consistent as observed in the LPS-induced neuroinflammation Sprague Dawley rats’ model. The highest concentration used in the two models presented the most significant results. Herein, our findings strongly suggest that RECA may offer therapeutic potential for the treatment of Alzheimer’s disease through inhibiting the AChE, inflammation, and oxidative stress activities.

scholarly journals Camphene Attenuates Skeletal Muscle Atrophy by Regulating Oxidative Stress and Lipid Metabolism in Rats

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3731
Author(s):  
Suji Baek ◽  
Jisu Kim ◽  
Byung Seok Moon ◽  
Sun Mi Park ◽  
Da Eun Jung ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Lipid Metabolism ◽  
Muscle Atrophy ◽  
Gas Analysis ◽  
Skeletal Muscle Atrophy ◽  
Ros Scavenging ◽  
In Vivo Models

Sarcopenia- or cachexia-related muscle atrophy is due to imbalanced energy metabolism and oxidative stress-induced muscle dysfunction. Monoterpenes play biological and pharmacological reactive oxygen species (ROS) scavenging roles. Hence, we explored the effects of camphene, a bicyclic monoterpene, on skeletal muscle atrophy in vitro and in vivo. We treated L6 myoblast cells with camphene and then examined the ROS-related oxidative stress using Mito TrackerTM Red FM and anti-8-oxoguanine antibody staining. To investigate lipid metabolism, we performed real-time polymerase chain reactions, holotomographic microscopy, and respiratory gas analysis. Rat muscle atrophy in in vivo models was observed using 18F-fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography and immunocytochemistry. Camphene reversed the aberrant cell size and muscle morphology of L6 myoblasts under starvation and in in vivo models. Camphene also attenuated E3 ubiquitin ligase muscle RING-finger protein-1, mitochondrial fission, and 8-oxoguanine nuclear expression in starved myotubes and hydrogen peroxide (H2O2)-treated cells. Moreover, camphene significantly regulated lipid metabolism in H2O2-treated cells and in vivo models. These findings suggest that camphene may potentially affect skeletal muscle atrophy by regulating oxidative stress and lipid metabolism.

scholarly journals The Role of Ophiopogonin D in Atherosclerosis: Impact on Lipid Metabolism and Gut Microbiota

2021 ◽  
pp. 1-19
Author(s):  
Ya-Xin Zhang ◽  
Shan-Shan Qu ◽  
Li-Hua Zhang ◽  
Yu-Yan Gu ◽  
Yi-Hao Chen ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Gut Microbiota ◽  
Structural Changes ◽  
Metabolic Diseases ◽  
Cholesterol Metabolism ◽  
Control Group ◽  
Oral Glucose ◽  
Model Group

Gut microbiota has been proven to play an important role in many metabolic diseases and cardiovascular disease, particularly atherosclerosis. Ophiopogonin D (OPD), one of the effective compounds in Ophiopogon japonicus, is considered beneficial to metabolic syndrome and cardiovascular diseases. In this study, we have illuminated the effect of OPD in ApoE knockout (ApoE[Formula: see text] mice on the development of atherosclerosis and gut microbiota. To investigate the potential ability of OPD to alleviate atherosclerosis, 24 eight-week-old male ApoE[Formula: see text] mice (C57BL/6 background) were fed a high-fat diet (HFD) for 12 weeks, and 8 male C57BL/6 mice were fed a normal diet, serving as the control group. ApoE[Formula: see text] mice were randomly divided into the model group, OPD group, and simvastatin group ([Formula: see text]= 8). After treatment for 12 consecutive weeks, the results showed that OPD treatment significantly decreased the plaque formation and levels of serum lipid compared with those in the model group. In addition, OPD improved oral glucose tolerance and insulin resistance as well as reducing hepatocyte steatosis. Further analysis revealed that OPD might attenuate atherosclerosis through inhibiting mTOR phosphorylation and the consequent lipid metabolism signaling pathways mediated by SREBP1 and SCD1 in vivo and in vitro. Furthermore, OPD treatment led to significant structural changes in gut microbiota and fecal metabolites in HFD-fed mice and reduced the relative abundance of Erysipelotrichaceae genera associated with cholesterol metabolism. Collectively, these findings illustrate that OPD could significantly protect against atherosclerosis, which might be associated with the moderation of lipid metabolism and alterations in gut microbiota composition and fecal metabolites.

scholarly journals Exploration of Antidiabetic Activity of Stephania japonica Leaf Extract in Alloxan-Induced Swiss Albino Diabetic Mice

2019 ◽  
pp. 1-12
Author(s):  
Md. Dobirul Islam ◽  
Syeda Farida Akter ◽  
Md. Amirul Islam ◽  
Md. Salim Uddin
Keyword(s):  
Gallic Acid ◽  
Ethanol Extract ◽  
Antidiabetic Activity ◽  
Diabetic Mice ◽  
Mice Model ◽  
Leaf Extracts ◽  
Alternative Source ◽  
Dry Extract

Aims: Presently the medicinal world is rapidly turning more on the therapeutic health benefits of natural product and medicinal plants in the management of major crucial disease and their complications. Medicinal plant, Stephania japonica has been studied for exploring antidiabetic potentiality as an alternative source of medicine against the global threat of Diabetes mellitus (DM). Methods: The extraction of S. japonica leaf was carried out by acetone and ethanol. Phytochemical screening and quantitative analysis of S. japonica leaf extracts were evaluated through chemically forming characterized color formation and calibration method respectively, by using standard reference substances (ascorbic acid, gallic acid, and quercetin) to assess the probable compounds present in the extract. Anti-diabetic potentiality of highest phytochemicals containing two extracts were investigated in in vitro as a ⍺-amylase inhibitors and in vivo through alloxan-induced Swiss albino diabetes mice model. Results: Alkaloids, carbohydrates, steroids, flavonoids, resins, saponins, tannins and coumarins were present in the leaf extracts. The estimated amount of total phenolics, flavonoids, flavonols and proanthrocyanidins contents of acetone and ethanol extract were 92.12±0.64 and 56.54±1.05 mg of gallic acid equivalent (GAE)/gm of dry extract, 66.02±1.42 and 46.17±0.54 mg of catechin equivalent (CAE)/gm of dry extract, 7.05±0.108 and 5.26±0.083 mg of quercetin equivalent (QUE)/gm of dry extract, 35.19±0.67 and 9.55±1.11 mg CAE/gm of dry extract, respectively. In 3, 5-dinitrosalicylic acid method, acetone and ethanol extract showed α-amylase inhibition of 51.02% and 46.62%, respectively at the concentration of 1000 µg/mL whereas in starch iodine color assay, acetone and ethanol extract showed inhibition of 57.32% and 52.12%, respectively at the concentration of 800 µg/mL. In contrast, both of the leaf extracts significantly (p<0.05 to p<0.001) improved the lipid profile parameters, blood glucose level and serum hepatic marker proteins in alloxan-induced diabetic mice. Conclusion: The present study strongly concluded that S. japonica leaf extracts process potent antidiabetic potentiality that might be significance for the management of diabetes and its complications.

Anti-fatigue Effects of Ginseng Antler Yam Tang Modulation of Oxidative Stress Signaling in a Mice Model

2020 ◽  
Author(s):  
Lei Miao ◽  
Rongrong Zhang ◽  
Shuai Shao ◽  
Hongyin Zhang ◽  
Fengqin Xiao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase ◽  
High Performance ◽  
Antioxidant Activities ◽  
Chemical Components ◽  
Stress Signaling ◽  
Mice Model ◽  
Biochemical Index

Abstract Background: Ginseng Antler Yam Tang (GAYT), believe to invigorate “Qi” (vital energy), nourish “Blood” (body circulation) and engender “liquid” (body fluid), is a traditional Chinese medicine formula derived from the traditional prescription and Chinese traditional medicine partner theory. Methods: In this study, we aimed to evaluate the anti-fatigue effects of GAYT and its mechanisms are related to oxidative stress signaling using GAYT composition, in vitro and in vivo antioxidant, and biochemical index detection. Chemical components analysis of GAYT was performed by high performance liquid chromatography (HPLC) and ultraviolet spectrophotometry (UV). Results: The results show that the GAYT is rich in protein, total flavonoids, total polysaccharide and saponin. The mice model was treatment by GAYT (0.9, 1.8 and 3.6g/kg) for 4 weeks. GAYT treatment enhanced antioxidant activities. GAYT significantly enhances the exercise performance in weight-loaded swimming, rotating rod, and forced running test. Biochemical index levels showed that these effects were closely correlated with inhibiting the depletion of glycogen, blood lactic acid (LD) and adenosine triphosphate (ATP) stores, regulating oxidative stress-related parameters (superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and malonaldehyde (MDA)) in serum and liver of mice. Moreover, the results show that the effects of GAYT may be related with its regulation on the activations of AMP-activated protein kinase and protein kinase B in liver of mice.Conclusions: GAYT can induce recovery from fatigue in mice via the activation of the AMPK and AKT/mTOR pathways. Provide a theoretical basis for the study of GAYT's anti-fatigue effect

In Vitro and In Vivo Neuroprotective Effects of Etifoxine in β-Amyloidinduced Toxicity Models

2020 ◽  
Vol 19 (3) ◽  
pp. 227-240 ◽  
Author(s):  
Veronique Riban ◽  
Johann Meunier ◽  
Dorothee Buttigieg ◽  
Vanessa Villard ◽  
Marc Verleye
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Memory Test ◽  
Neuronal Cultures ◽  
Tau Hyperphosphorylation ◽  
Mice Model ◽  
Neuroprotective Effects ◽  
Synaptic Loss

Aim: The aim of this study is to examine the effect of etifoxine on β-amyloid-induced toxicity models. Background: Etifoxine is an anxiolytic compound with a dual mechanism of action; it is a positive allosteric modulator of GABAergic receptors as well as a ligand for the 18 kDa mitochondrial Translocator Protein (TSPO). TSPO has recently raised interest in Alzheimer’s Disease (AD), and experimental studies have shown that some TSPO ligands could induce neuroprotective effects in animal models. Objective: In this study, we examined the potential protective effect of etifoxine in an in vitro and an in vivo model of amyloid beta (Aβ)-induced toxicity in its oligomeric form, which is a crucial factor in AD pathologic mechanisms. Method: Neuronal cultures were intoxicated with Aβ1-42, and the effects of etifoxine on oxidative stress, Tau-hyperphosphorylation and synaptic loss were quantified. In a mice model, behavioral deficits induced by intracerebroventricular administration of Aβ25-35 were measured in a spatial memory test, the spontaneous alternation and in a contextual memory test, the passive avoidance test. Results: In neuronal cultures intoxicated with Aβ1-42, etifoxine dose-dependently decreased oxidative stress (methionine sulfoxide positive neurons), tau-hyperphosphorylation and synaptic loss (ratio PSD95/synaptophysin). In a mice model, memory impairments were fully alleviated by etifoxine administered at anxiolytic doses (12.5-50mg/kg). In addition, markers of oxidative stress and apoptosis were decreased in the hippocampus of these animals. Conclusion: Our results have shown that in these two models, etifoxine could fully prevent neurotoxicity and pathological changes induced by Aβ. These results confirm that TSPO ligands could offer an interesting therapeutic approach to Alzheimer’s disease.

scholarly journals Novel Anticancer Platinum(IV) Complexes with Adamantylamine: Their Efficiency and Innovative Chemotherapy Strategies Modifying Lipid Metabolism

2008 ◽  
Vol 2008 ◽  
pp. 1-15 ◽  
Author(s):  
Alois Kozubík ◽  
Alena Vaculová ◽  
Karel Souček ◽  
Jan Vondráček ◽  
Jaroslav Turánek ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Platinum Complexes ◽  
The Other ◽  
Stress Signaling ◽  
Cell Death Pathway ◽  
Cellular Lipids ◽  
In Vivo Effects

The impressive impact of cisplatin on cancer on one side and severe side effects, as well as the development of drug resistance during treatment on the other side, were the factors motivating scientists to design and synthesize new more potent analogues lacking disadvantages of cisplatin. Platinum(IV) complexes represent one of the perspective groups of platinum-based drugs. In this review, we summarize recent findings on both in vitro and in vivo effects of platinum(IV) complexes with adamantylamine. Based on a literary overview of the mechanisms of activity of platinum-based cytostatics, we discuss opportunities for modulating the effects of novel platinum complexes through interactions with apoptotic signaling pathways and with cellular lipids, including modulations of the mitochondrial cell death pathway, oxidative stress, signaling of death ligands, lipid metabolism/signaling, or intercellular communication. These approaches might significantly enhance the efficacy of both novel and established platinum-based cytostatics.

scholarly journals Aldosterone Excess Induced Mitochondria Decrease and Dysfunction via Mineralocorticoid Receptor and Oxidative Stress In Vitro and In Vivo

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 946
Author(s):  
Cheng-Hsuan Tsai ◽  
Chien-Ting Pan ◽  
Yi-Yao Chang ◽  
Shih-Yuan Peng ◽  
Po-Chin Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dna ◽  
Mitochondrial Dysfunction ◽  
Mineralocorticoid Receptor ◽  
Cardiac Mitochondria ◽  
Mice Model ◽  
Atp Production ◽  
And Oxidative Stress

Aldosterone excess plays a major role in the progression of cardiac dysfunction and remodeling in clinical diseases such as primary aldosteronism and heart failure. However, the effect of aldosterone excess on cardiac mitochondria is unclear. In this study, we investigated the effect of aldosterone excess on cardiac mitochondrial dysfunction and its mechanisms in vitro and in vivo. We used H9c2 cardiomyocytes to investigate the effect and mechanism of aldosterone excess on cardiac mitochondria, and further investigated them in an aldosterone-infused ICR mice model. The results of the cell study showed that aldosterone excess decreased mitochondrial DNA, COX IV and SOD2 protein expressions, and mitochondria ATP production. These effects were abolished or attenuated by treatment with a mineralocorticoid receptor (MR) antagonist and antioxidant. With regard to the signal transduction pathway, aldosterone suppressed cardiac mitochondria through an MR/MAPK/p38/reactive oxygen species pathway. In the mouse model, aldosterone infusion decreased the amount of cardiac mitochondrial DNA and COX IV protein, and the effects were also attenuated by treatment with an MR antagonist and antioxidant. In conclusion, aldosterone excess induced a decrease in mitochondria and mitochondrial dysfunction via MRs and oxidative stress in vitro and in vivo.

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