Vicenin-2 Treatment Attenuated the Diethylnitrosamine-Induced Liver Carcinoma and Oxidative Stress through Increased Apoptotic Protein Expression in Experimental Rats

The efficacy of stem cells for the treatment of renal failure is widely recognized; however, an excessive volume of stem cells can block the capillaries; thus, the potential risks should not be ignored. Stem cell exosomes are secretory extracellular vesicles with a size of 30–150 nm, which have similar functions to stem cells but are much smaller in size. This study aims to investigate the role of human umbilical cord mesenchymal stem cells (UCMSCs)-derived exosomes in the treatment of renal failure caused by ischemia-reperfusion. Fifty 8-week-old female C57 mice underwent bilateral renal ischemia-reperfusion surgery for 30 minutes. After 4 weeks, the treated group received UCMSCs-derived exosomes treatment, and the control group was solely injected with the same amount of PBS. At the age of 16 weeks, the kidney function, kidney damage, inflammatory responses and oxidative stress were measured. Moreover, the effect of UCMSCs-derived exosomes on the phenotype of M1 macrophages was also tested. The results showed that UCMSCsderived exosomes significantly reduced the levels of blood urea nitrogen (BUN), serum creatinine (SCR), and urinary albumin and creatinine (ACR) and 8-isoprostane. UCMSCs-derived exosomes also improved the atrophy of the kidney and glomerulus, decreased kidney pro-inflammatory factors expression (mRNA of II-1β, II-6, Tnf-α, and Mcp-1) and oxidative stress (malondialdehyde), and increased glutathione level. However, F4/80 immunohistochemistry did not show significant differences between the two groups. In systemic inflammation measurement, UCMSCs-derived exosomes decreased proinflammatory factors TNF-α, IL-6, and IL-1β levels, and increased anti-inflammatory factor IL-10 level. In vitro experiments showed that UCMSCs-derived exosomes decreased the protein expression level of TNF-α and increased the protein expression level of IL-10 in M1 macrophages. UCMSCs-derived exosomes reduce kidney inflammation and oxidative stress by improving systemic inflammation, and thus reduce kidney damage and improve kidney function. This study shows the potential application value of exosomes in the treatment of renal failure.

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Effects of Dietary Taurine Supplementation to Gilts during Late Gestation and Lactation on Offspring Growth and Oxidative Stress

Animals ◽

10.3390/ani9050220 ◽

2019 ◽

Vol 9 (5) ◽

pp. 220 ◽

Cited By ~ 2

Author(s):

Mengmeng Xu ◽

Long Che ◽

Kaiguo Gao ◽

Li Wang ◽

Xuefen Yang ◽

...

Keyword(s):

Oxidative Stress ◽

Protein Expression ◽

Growth Performance ◽

Barrier Function ◽

Average Daily Gain ◽

Basal Diet ◽

Intestinal Morphology ◽

Late Gestation ◽

Villus Height ◽

And Oxidative Stress

Birth is one of the most important events of animal production agriculture, as newborns are abruptly forced to adapt to environmental and nutritional disruptions that can lead to oxidative damage and delay in growth. Taurine (Tau) is an important regulator of oxidative stress and possesses growth-enhancing properties. In the present study, we investigated the effects of dietary Tau supplementation in gilts during late gestation and lactation on the growth performance of piglets by assessing intestinal morphology and barrier function, and oxidative stress status. Sixteen gilts were randomly allocated to the Con (basal diet) and Tau (basal diet with 1% Tau) groups from 75 d of gestation to weaning. Maternal dietary Tau supplementation significantly increased weaning weight and average daily gain weight in piglets. Piglets in the Tau group had higher villus height and villus height-to-crypt depth ratio (VCR), ZO-1 protein expression, and secretory immunoglobulin A (sIgA) content in the jejunum. Meanwhile, Tau bebeficial affected the milk quality of gilts, as indicated by decreased malondialdehyde (MDA) concentration and increased total superoxide dismutase (T-SOD), total antioxidative capability (T-AOC), glutathione peroxidase (GPx), and catalase (CAT) activity. Furthermore, Tau supplementation increased T-SOD activity in plasma and SOD2 protein expression in the jejunum in the piglets. In conclusion, this study provides evidence that dietary Tau supplementation to gilts improves growth performance in piglets, owing to improved intestinal morphology and barrier function, as well as inhibition of oxidative stress.

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Effects of SLIRP on Sperm Motility and Oxidative Stress

BioMed Research International ◽

10.1155/2020/9060356 ◽

2020 ◽

Vol 2020 ◽

pp. 1-5

Author(s):

Dan Shan ◽

Samuel Kofi Arhin ◽

Junzhao Zhao ◽

Haitao Xi ◽

Fan Zhang ◽

...

Keyword(s):

Oxidative Stress ◽

Protein Expression ◽

Manganese Superoxide Dismutase ◽

Mrna Level ◽

Atp Content ◽

Human Male ◽

Manganese Superoxide ◽

Polymerase Chain ◽

And Oxidative Stress ◽

Relative Mrna Expression

Background. Deficient spermatozoon motility is one of the main causes of male infertility. However, there are still no accurate and effective treatments in a clinical setting for male asthenospermia. Exploring the genes and mechanism of asthenospermia has become one of the hot topics in reproductive medicine. Our aim is to study the effect of SLRIP on human spermatozoon motility and oxidative stress. Methods. Sperm samples were collected including a normospermia group (60 cases) and an asthenospermia group (50 cases). SLIRP protein expression in spermatozoa was examined by western blotting, and relative mRNA expression of SLIRP in spermatozoa was quantified by reverse transcription polymerase chain reaction. Levels of reactive oxygen species (ROS), adenosine triphosphate (ATP) content, and the activity of manganese superoxide dismutase (MnSOD) in spermatozoa were also measured. Results. The mRNA level and protein expression of SLIRP in the asthenospermia group were significantly reduced compared with those in the normospermia group. The ROS active oxygen level in the asthenospermia group significantly increased; however, the ATP content decreased significantly as well as the activity of MnSOD. Conclusion. SLIRP regulates human male fertility, and SLIRP and sperm progressive motility are positively correlated. The expression of SLIRP is declined, oxidative damage is increased, and energy metabolism is decreased in spermatozoa of asthenospermia patients compared to normospermia participants.

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Anti-adipogenesis and antioxidative defense status of a crude extract of ‘Kalasin 2’ peanut sprouts in 3T3-L1 mouse adipocytes

Biochemistry and Cell Biology ◽

10.1139/bcb-2018-0391 ◽

2019 ◽

Vol 97 (6) ◽

pp. 740-749

Author(s):

Tantip Boonsong ◽

Siriporn Pakwan ◽

Wanida Chawnawa

Keyword(s):

Oxidative Stress ◽

Protein Expression ◽

Oxidative Status ◽

Peroxisome Proliferator ◽

Antioxidative Defense ◽

Peroxisome Proliferator Activated Receptor ◽

Defense Systems ◽

Treatment Of Obesity ◽

Mouse Adipocytes ◽

And Oxidative Stress

The aim of this study was to investigate the effects of extracts from germinated (GPE) and non-germinated peanuts (NGPE) on adipogenesis and oxidative status in normal and oxidative-stress-induced 3T3-L1 mouse adipocytes. The treated cells were analysed for cell growth, lipid accumulation, levels of intracellular reactive oxygen species (ROS), and the expression levels of mRNAs and proteins related to adipogenesis and antioxidative defense systems. The results indicated that an extract from peanuts made 9 days after germination (9GPE) reduced lipid contents and mRNA expression of adipogenesis-related genes to a greater extent than an extract from peanuts made 1-day after germination (1GPE) or from NGPE, respectively. In oxidative-stress-induced adipocytes, 9GPE decreased ROS levels, lipid content, and the protein expression of peroxisome-proliferator-activated receptor gamma, and also increased the protein expression of antioxidants. These results illustrate the anti-adipogenic capacity and oxidative status improvement achievable with GPE, and that it could be used as a putative therapeutic agent in the prevention of and (or) treatment of obesity and diseases associated with oxidative stress.

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Tributyltin Exposure Is Associated With Recognition Memory Impairments, Alterations in Estrogen Receptor α Protein Levels, and Oxidative Stress in the Brain of Female Mice

Frontiers in Toxicology ◽

10.3389/ftox.2021.654077 ◽

2021 ◽

Vol 3 ◽

Author(s):

Igor Ferraz da Silva ◽

Eduardo Merlo ◽

Charles S. Costa ◽

Jones B. Graceli ◽

Lívia C. M. Rodrigues

Keyword(s):

Oxidative Stress ◽

Estrogen Receptor ◽

Recognition Memory ◽

Protein Expression ◽

Estrogen Receptor Α ◽

Behavioral Alterations ◽

Brain Areas ◽

Female Mice ◽

Toxicological Effects ◽

And Oxidative Stress

Tributyltin (TBT) is a persistent organometallic pollutant widely used in several agricultural and industrial processes. TBT exposure is associated with various metabolic, reproductive, immune, and cardiovascular abnormalities. However, few studies have evaluated the effects of TBT on behavior. In the present study, we aimed to investigate whether TBT exposure results in oxidative, neuroendocrine, and behavioral alterations. TBT was administered to adult female mice (250, 500, or 750 ng/kg/day or veh for 14 days), and their recognition memory was assessed. We have also evaluated estrogen receptor (ER)α protein expression and oxidative stress (OS) in brain areas related to memory, as well as the correlation between them. A reduction in short- and long-term recognition memory (STM and LTM) performance, as well as in total exploration time was observed in TBT mice. Reduced ERα protein expression was observed in the prefrontal cortex (PFC) and hippocampus of TBT mice, while an increase in TBARS concentration was observed in the PFC of treated animals. Collectively, these data suggest that TBT exposure impairs recognition memory in female mice as a result of, at least in part, its toxicological effects on ERα expression and OS in specific brain areas related to memory.

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Alleviation of Inflammation and Oxidative Stress in Pressure Overload-Induced Cardiac Remodeling and Heart Failure via IL-6/STAT3 Inhibition by Raloxifene

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/6699054 ◽

2021 ◽

Vol 2021 ◽

pp. 1-15

Author(s):

Shengqi Huo ◽

Wei Shi ◽

Haiyan Ma ◽

Dan Yan ◽

Pengcheng Luo ◽

...

Keyword(s):

Oxidative Stress ◽

Heart Failure ◽

Protein Expression ◽

Cardiac Remodeling ◽

Pressure Overload ◽

Left Ventricular ◽

Stat3 Signaling ◽

H9c2 Myoblasts ◽

And Oxidative Stress ◽

Stat3 Inhibition

Background. Inflammation and oxidative stress are involved in the initiation and progress of heart failure (HF). However, the role of the IL6/STAT3 pathway in the pressure overload-induced HF remains controversial. Methods and Results. Transverse aortic constriction (TAC) was used to induce pressure overload-HF in C57BL/6J mice. 18 mice were randomized into three groups (Sham, TAC, and TAC+raloxifene, n = 6 , respectively). Echocardiographic and histological results showed that cardiac hypertrophy, fibrosis, and left ventricular dysfunction were manifested in mice after TAC treatment of eight weeks, with aggravation of macrophage infiltration and interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) expression in the myocardium. TAC (four and eight weeks) elevated the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) and prohibitin2 (PHB2) protein expression. Importantly, IL-6/gp130/STAT3 inhibition by raloxifene alleviated TAC-induced myocardial inflammation, cardiac remodeling, and dysfunction. In vitro, we demonstrated cellular hypertrophy with STAT3 activation and oxidative stress exacerbation could be elicited by IL-6 (25 ng/mL, 48 h) in H9c2 myoblasts. Sustained IL-6 stimulation increased intracellular reactive oxygen species, repressed mitochondrial membrane potential (MMP), decreased intracellular content of ATP, and led to decreased SOD activity, an increase in iNOS protein expression, and increased protein expression of Pink1, Parkin, and Bnip3 involving in mitophagy, all of which were reversed by raloxifene. Conclusion. Inflammation and IL-6/STAT3 signaling were activated in TAC-induced HF in mice, while sustained IL-6 incubation elicited oxidative stress and mitophagy-related protein increase in H9c2 myoblasts, all of which were inhibited by raloxifene. These indicated IL-6/STAT3 signaling might be involved in the pathogenesis of myocardial hypertrophy and HF.

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Lactobacillus casei Strain Shirota Enhances the Ability of Geniposide to Activate SIRT1 and Decrease Inflammation and Oxidative Stress in Septic Mice

Frontiers in Physiology ◽

10.3389/fphys.2021.678838 ◽

2021 ◽

Vol 12 ◽

Author(s):

Chao Mai ◽

Li Qiu ◽

Yong Zeng ◽

Xingqin Tan

Keyword(s):

Oxidative Stress ◽

Protein Expression ◽

Lactobacillus Casei ◽

P53 Protein ◽

Cecal Ligation ◽

Morris Water Maze Test ◽

Gardenia Jasminoides ◽

Tnf Α ◽

Anti Oxidant ◽

And Oxidative Stress

Gardenia jasminoides Ellis is rich in geniposide, which can be transformed into the anti-oxidant and anti-inflammatory agent genipin. Genipin exhibits greater efficacy than geniposide, but it is unstable and difficult to preserve. In this study, a mouse model for sepsis was established by cecal ligation and puncture, and then we explored the effects and mechanism of Lactobacillus casei strain Shirota (LcS) on the enhancement of the ability of geniposide to reduce sepsis and decrease inflammatory and oxidative levels in mice by the regulation of sirtuin type 1 (SIRT1). The mice were evaluated and analyzed by the open field test, Morris water maze test, flow cytometry, kit assay, qPCR, and western blot. The LcS + geniposide increased the survival rate in mice with sepsis, and increased the total travel distance, number of times the mice stood up, amount of time the mice spent grooming their fur, duration in the target quadrant, and crossing area number. The testing of mouse nerve cells showed that LcS + geniposide reduced the rate of nerve cell apoptosis caused by sepsis. LcS + geniposide also decreased the amount of inflammatory-related indicators of TNF-α, IL-6, and IL-1β, and the oxidation-related levels of malondialdehyde (MDA) in the hippocampi of septic mice, and it increased the oxidase activities of superoxide dismutase (SOD) and catalase (CAT). Additionally, LcS + geniposide increased the SOD1, SOD2, and CAT mRNA expression in the hippocampi of mice with sepsis and decreased the expression of TNF-α, IL-1β, NF-κB, and p53 mRNA. LcS+geniposide also increased the SIRT1 protein expression and decreased the Ac-FOXO1, Ac-NF-κB, and Ac-p53 protein expression in the hippocampi of mice with sepsis. We also observed that LcS + geniposide decreased the inflammatory and oxidative damage in the mice with sepsis. The effect of LcS + geniposide was similar to that of the drug dexamethasone and stronger than the effect of geniposide utilized alone. LcS also enhanced the ability of geniposide to activate SIRT1 and decrease the inflammation and oxidative stress in the septic mice, and it achieved an effect same with that obtained by the use of the drug dexamethasone.

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17β-Estradiol alters oxidative damage and oxidative stress response protein expression in the mouse mammary gland

Molecular and Cellular Endocrinology ◽

10.1016/j.mce.2016.02.007 ◽

2016 ◽

Vol 426 ◽

pp. 11-21 ◽

Cited By ~ 4

Author(s):

Lisi Yuan ◽

Alicia K. Dietrich ◽

Yvonne S. Ziegler ◽

Ann M. Nardulli

Keyword(s):

Oxidative Stress ◽

Mammary Gland ◽

Stress Response ◽

Oxidative Damage ◽

Protein Expression ◽

Mouse Mammary Gland ◽

Oxidative Stress Response ◽

17Β Estradiol ◽

And Oxidative Stress

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Biological role, protein expression, subcellular localization, and oxidative stress response of paraoxonase 2 in the intestine of humans and rats

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00369.2007 ◽

2007 ◽

Vol 293 (6) ◽

pp. G1252-G1261 ◽

Cited By ~ 40

Author(s):

Emile Levy ◽

Karine Trudel ◽

Moise Bendayan ◽

Ernest Seidman ◽

Edgard Delvin ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Stress Response ◽

Subcellular Localization ◽

Protein Expression ◽

Oxidative Stress Response ◽

Butylated Hydroxytoluene ◽

Cell Fractionation ◽

Rat Intestine ◽

And Oxidative Stress

Oxidative stress is a cardinal manifestation of various intestinal disorders. However, very little knowledge is available on the intestine's inherent defense mechanisms against free radicals. This study was designed to determine the protein expression, subcellular localization and oxidative stress response of paraoxonase 2 (PON2), a member of a powerful antioxidant family in human and rat intestine. Biochemical and ultrastructural experiments all showed a substantial expression of PON2 in human and rat intestine. Western blot analysis disclosed higher levels of PON2 in the jejunum than in the duodenum, ileum, and colon. Cell fractionation revealed a predominant PON2 association with microsomes and lysosomes in the human jejunum, which differed from that in rats. PON2 was detected in the intestine as early as week 15 of gestation and was significantly increased by week 20. Iron ascorbate-mediated lipid peroxidation induced a marked decrease in PON2 expression in intestinal specimens coincidental to an abundant rise in malondialdehyde (MDA). On the other hand, preincubation with potent antioxidants, such as butylated hydroxytoluene, Trolox, and N-acetylcysteine, prevented iron-ascorbate-generating PON2 reduction in parallel with MDA suppression. Finally, the preincubation of permeabilized Caco-2 cells with purified PON2 led to a protection against iron-ascorbate-induced lipid peroxidation. These observations demonstrate that the human intestine is preferentially endowed with a marked PON2 expression compared with the rat intestine and this expression shows a developmental and intracellular pattern of distribution. Furthermore, our observations suggest PON2 protective effects against prooxidant stimuli in the small intestine.

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