scholarly journals Solid Lipid Nanoparticles of Myricitrin Have Antioxidant and Antidiabetic Effects on Streptozotocin-Nicotinamide-Induced Diabetic Model and Myotube Cell of Male Mouse

2018 ◽  
Vol 2018 ◽  
pp. 1-18 ◽  
Author(s):  
Akram Ahangarpour ◽  
Ali Akbar Oroojan ◽  
Layasadat Khorsandi ◽  
Maryam Kouchak ◽  
Mohammad Badavi
Keyword(s):  
Oxidative Stress ◽  
C2c12 Cell ◽  
In Vitro Study ◽  
Homogenization Method ◽  
Solid Lipid ◽  
Muscle Tissues ◽  
Diabetic Model ◽  
Cellular Apoptosis

Type 2 diabetes mellitus (T2DM) may occur via oxidative stress. Myricitrin is a plant-derived antioxidant, and its solid lipid nanoparticle (SLN) may be more potent. Hence, the present study was conducted to evaluate the effects of myricitrin SLN on streptozotocin-nicotinamide- (STZ-NA-) induced T2DM of the mouse and hyperglycemic myotube. In this experimental study, cold homogenization method was used to prepare SLN. Then, 120 adult male NMRI mice were divided into 7 groups: control, vehicle, diabetes (received STZ 65 mg/kg 15 min after injected NA 120 mg/kg), diabetes + SLN containing myricitrin 1, 3, and 10 mg/kg, and diabetes + metformin. For in vitro study, myoblast (C2C12) cell line was cultured and divided into 6 groups (n=3): control, hyperglycemia, hyperglycemia + SLN containing myricitrin 1, 3, and, 10 μM, and hyperglycemia + metformin. After the last nanoparticle treatment, plasma samples, pancreas and muscle tissues, and myotubes were taken for experimental assessments. Diabetes increased lipid peroxidation and reduced antioxidant defense along with the hyperglycemia, insulin resistance, and pancreas apoptosis. Hyperglycemia induced oxidative stress, antioxidant impairment, and cellular apoptosis. Myricitrin SLN improved diabetes and hyperglycemia complications in the in vivo and in vitro studies. Therefore, SLN of myricitrin showed antioxidant, antidiabetic, and antiapoptotic effects in the mouse and myotube cells.

scholarly journals Metallothionein-I/II Knockout Mice Aggravate Mitochondrial Superoxide Production and Peroxiredoxin 3 Expression in Thyroid after Excessive Iodide Exposure

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Na Zhang ◽  
Lingyan Wang ◽  
Qi Duan ◽  
Laixiang Lin ◽  
Mohamed Ahmed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Urinary Iodine ◽  
In Vitro Study ◽  
Superoxide Production ◽  
Mitochondrial Oxidative Stress ◽  
Mitochondrial Superoxide ◽  
Iodine Level ◽  
Significant Difference

Purpose. We aim to figure out the effect of metallothioneins on iodide excess induced oxidative stress in the thyroid.Methods. Eight-week-old MT-I/II knockout (MT-I/II KO) mice and background-matched wild-type (WT) mice were used. Mitochondrial superoxide production and peroxiredoxin (Prx) 3 expression were measured.Results. In in vitro study, more significant increases in mitochondrial superoxide production and Prx 3 expression were detected in the MT-I/II KO groups. In in vivo study, significantly higher concentrations of urinary iodine level were detected in MT-I/II KO mice in 100 HI group. Compared to the NI group, there was no significant difference existing in serum thyroid hormones level in either groups (P>0.05), while the mitochondrial superoxide production was significantly increased in 100 HI groups with significantly increased LDH activity and decreased relative cell viability. Compared to WT mice, more significant changes were detected in MT-I/II KO mice in 100 HI groups. No significant differences were detected between the NI group and 10 HI group in both the MT-I/II KO and WT mice groups (P>0.05).Conclusions. Iodide excess in a thyroid without MT I/II protection may result in strong mitochondrial oxidative stress, which further leads to the damage of thyrocytes.

scholarly journals Alpha-1-antitrypsin suppresses oxidative stress in preeclampsia by inhibiting the p38MAPK signaling pathway: An in vivo and in vitro study

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0173711 ◽  
Author(s):  
Ya-Ling Feng ◽  
Yong-Xiang Yin ◽  
Jian Ding ◽  
Hua Yuan ◽  
Lan Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
In Vitro Study ◽  
Vitro Study ◽  
P38mapk Signaling ◽  
Alpha 1 Antitrypsin

scholarly journals Endometriosis Susceptibility to Dapsone-Hydroxylamine-Induced Alterations Can Be Prevented by Licorice Intake: In Vivo and In Vitro Study

2021 ◽  
Vol 22 (16) ◽  
pp. 8476
Author(s):  
Chiara Sabbadin ◽  
Alessandra Andrisani ◽  
Gabriella Donà ◽  
Elena Tibaldi ◽  
Anna Maria Brunati ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
In Vitro Study ◽  
Carbonic Anhydrase Activity ◽  
Control Group ◽  
Beneficial Effects ◽  
Licorice Extract ◽  
Anti Oxidant ◽  
Gynecological Disease

Endometriosis, an estrogen-dependent chronic gynecological disease, is characterized by a systemic inflammation that affects circulating red blood cells (RBC), by reducing anti-oxidant defenses. The aim of this study was to investigate the potential beneficial effects of licorice intake to protect RBCs from dapsone hydroxylamine (DDS-NHOH), a harmful metabolite of dapsone, commonly used in the treatment of many diseases. A control group (CG, n = 12) and a patient group (PG, n = 18) were treated with licorice extract (25 mg/day), for a week. Blood samples before (T0) and after (T1) treatment were analyzed for: i) band 3 tyrosine phosphorylation and high molecular weight aggregates; and ii) glutathionylation and carbonic anhydrase activity, in the presence or absence of adjunctive oxidative stress induced by DDS-NHOH. Results were correlated with plasma glycyrrhetinic acid (GA) concentrations, measured by HPLC–MS. Results showed that licorice intake decreased the level of DDS-NHOH-related oxidative alterations in RBCs, and the reduction was directly correlated with plasma GA concentration. In conclusion, in PG, the inability to counteract oxidative stress is a serious concern in the evaluation of therapeutic approaches. GA, by protecting RBC from oxidative assault, as in dapsone therapy, might be considered as a new potential tool for preventing further switching into severe endometriosis.

scholarly journals Endothelial dysfunction in insulin-resistant rats is associated with oxidative stress and COX pathway dysregulation

2009 ◽  
pp. 499-509
Author(s):  
A Oudot ◽  
D Behr-Roussel ◽  
S Compagnie ◽  
S Caisey ◽  
O Le Coz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Vascular Dysfunction ◽  
Pressor Response ◽  
In Vitro Study ◽  
Cardiovascular Complications ◽  
Insulin Resistant ◽  
Pathway Dysregulation

Because insulin resistance is inevitably associated with cardiovascular complications, there is a need to further investigate the potential involvement of oxidative stress and the cyclo-oxygenase (COX) pathway in the vascular modifications associated to this pathological context. Endothelial function was evaluated in control and fructose-fed rats (FFR) by i) in vitro study of endothelium-dependent and -independent relaxations of aortic rings, and ii) in vivo telemetric evaluation of pressor response to norepinephrine. After 9 weeks of diet, FFR displayed hypertriglyceridemia, hyperinsulinemia and exaggerated response to glucose overload. Aortic rings from control rats and FFR exhibited comparable endothelium-dependent relaxations to Ach. In the presence of indomethacin, relaxations were significantly reduced. FFR showed exaggerated pressor responses to norepinephrine that were abolished with indomethacin. Urinary nitrites/nitrates, 8-isoprostanes and thromboxane B2 excretion levels were markedly enhanced in FFR, whereas the plasma levels of 6-keto prostaglandin F1α were unchanged. In conclusion, fructose overload in rats induced hypertriglyceridemia and insulin resistance associated with an enhanced oxidative stress. This was associated with COX pathway dysregulation which could be one of the contributors to subsequent vascular dysfunction. Consequently, reduction of oxidative stress and regulation of the COX pathway could represent new potential therapeutic strategies to limit vascular dysfunction and subsequent cardiovascular complications associated with insulin resistance.

scholarly journals Inhibitory Effect of Multimodal Nanoassemblies against Glycative and Oxidative Stress in Cancer and Glycation Animal Models

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Hamda Khan ◽  
Mohd Waseem ◽  
Mohammad Faisal ◽  
Abdulrahman A. Alatar ◽  
Ahmed A. Qahtan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Mrna Expression ◽  
Strong Association ◽  
In Vitro Study ◽  
Model Systems ◽  
Fluorescence Studies ◽  
And Oxidative Stress

In recent years, there has been a progress in the study of glycation reaction which is one the possible reason for multiple metabolic disorders. Glycation is a nonenzymatic reaction between nucleic acids, lipids, and proteins resulting into the formation of early glycation products that may further lead to the accumulation of advanced glycation end products (AGEs). The precipitation of AGEs in various cells, tissues, and organs is one of the factors for the initiation and progression of various metabolic derangements including the cancer. The AGE interaction with its receptor “RAGE” activates the inflammatory pathway; yet, the downregulation of RAGE and its role in these pathways are not clear. We explore the effect of anticancer novel nanoassemblies on AGEs to determine its role in the regulation of the expression of RAGE, NFƙB, TNF-α, and IFN-γ. This paper is based on the in vivo and in vitro study in glycation and lung cancer model systems. Upon the treatment of nanoassemblies in both the model systems, we observed a protective effect of nanoassemblies over the inhibition of glycative and oxidative stress via mRNA expression analysis. The mRNA expression results corroborated with the reactive oxygen species (ROS), carboxy-methyl-lysine (CML), and fluorescence studies. In this study, we found that the presence of common factors for glycation and lung cancer is oxidative and glycative stress. This oxidation and glycation might be responsible for the initiation of inflammation which may further lead to uncontrolled growth of cells leading to cancer. This can be a strong association between lung cancer and glycation reaction. The intervention of the anticancer and antiglycation effects of multimodal nanoassemblies throughout the study promises a new pathway for cancer research.

Licochalcone A-loaded solid lipid nanoparticles improve antischistosomal activity in vitro and in vivo

Nanomedicine ◽  
2021 ◽  
Author(s):  
Lívia Mara Silva ◽  
Danielle Gomes Marconato ◽  
Marcos Paulo Nascimento da Silva ◽  
Nádia Rezende Barbosa Raposo ◽  
Gabriela de Faria Silva Facchini ◽  
...  
Keyword(s):  
Solid Lipid Nanoparticles ◽  
Lipid Nanoparticles ◽  
Homogenization Method ◽  
Licochalcone A ◽  
Solid Lipid ◽  
Transmission Electron ◽  
High Shear Homogenization ◽  
Antischistosomal Activity

Aim: To isolate licochalcone A (LicoA) from licorice, prepare LicoA-loaded solid lipid nanoparticles (L-SLNs) and evaluate the L-SLNs in vitro and in vivo against Schistosoma mansoni. Materials & methods: LicoA was obtained by chromatographic fractionation and encapsulated in SLNs by a modified high shear homogenization method. Results: L-SLNs showed high encapsulation efficiency, with satisfactory particle size, polydispersity index and Zeta potential. Transmission electron microscopy revealed that L-SLNs were rounded and homogenously distributed. Toxicity studies revealed that SLNs decreased the hemolytic and cytotoxic properties of LicoA. Treatment with L-SLNs showed in vivo efficacy against S. mansoni. Conclusion: L-SLNs are efficient in reducing worm burden and SLNs may be a promising delivery system for LicoA to treat S. mansoni infections.

scholarly journals Maternal diabetes induces autism-like behavior by hyperglycemia-mediated persistent oxidative stress and suppression of superoxide dismutase 2

2019 ◽  
Vol 116 (47) ◽  
pp. 23743-23752 ◽  
Author(s):  
Xiumin Wang ◽  
Jianping Lu ◽  
Weiguo Xie ◽  
Xiaoyun Lu ◽  
Yujie Liang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
In Vitro Study ◽  
Maternal Diabetes ◽  
Autism Spectrum ◽  
Ros Generation ◽  
Increased Risk ◽  
Superoxide Dismutase 2

Epidemiological studies show that maternal diabetes is associated with an increased risk of autism spectrum disorders (ASDs), although the detailed mechanisms remain unclear. The present study aims to investigate the potential effect of maternal diabetes on autism-like behavior in offspring. The results of in vitro study showed that transient hyperglycemia induces persistent reactive oxygen species (ROS) generation with suppressed superoxide dismutase 2 (SOD2) expression. Additionally, we found that SOD2 suppression is due to oxidative stress-mediated histone methylation and the subsequent dissociation of early growth response 1 (Egr1) on the SOD2 promoter. Furthermore, in vivo rat experiments showed that maternal diabetes induces SOD2 suppression in the amygdala, resulting in autism-like behavior in offspring. SOD2 overexpression restores, while SOD2 knockdown mimics, this effect, indicating that oxidative stress and SOD2 expression play important roles in maternal diabetes-induced autism-like behavior in offspring, while prenatal and postnatal treatment using antioxidants permeable to the blood–brain barrier partly ameliorated this effect. We conclude that maternal diabetes induces autism-like behavior through hyperglycemia-mediated persistent oxidative stress and SOD2 suppression. Here we report a potential mechanism for maternal diabetes-induced ASD.

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