scholarly journals Vitamin E Can Ameliorate Oxidative Damage of Ovine Hepatocytes In Vitro by Regulating Genes Expression Associated with Apoptosis and Pyroptosis, but Not Ferroptosis

Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4520
Author(s):  
Luyang Jian ◽  
Ying Xue ◽  
Yuefeng Gao ◽  
Bo Wang ◽  
Yanghua Qu ◽  
...  

(1) Background: the current research was conducted to investigate the potential non-antioxidant roles of vitamin E in the protection of hepatocysts from oxidative damage. (2) Methods: primary sheep hepatocytes were cultured and exposed to 200, 400, 600, or 800 μmol/L hydrogen peroxide, while their viability was assessed using a CCK-8 kit. Then, cells were treated with 400 μmol/L hydrogen peroxide following a pretreatment with 50, 100, 200, 400, and 800 μmol/L vitamin E and their intracellular ROS levels were determined by means of the DCF-DA assay. RNA-seq, verified by qRT-PCR, was conducted thereafter: non-treated control (C1); cells treated with 400 μmol/L hydrogen peroxide (C2); and C2 plus a pretreatment with 100 μmol/L vitamin E (T1). (3) Results: the 200–800 μmol/L hydrogen peroxide caused significant cell death, while 50, 100, and 200 μmol/L vitamin E pretreatment significantly improved the survival rate of hepatocytes. ROS content in the cells pretreated with vitamin E was significantly lower than that in the control group and hydrogen-peroxide-treated group, especially in those pretreated with 100 μmol/L vitamin E. The differentially expressed genes (DEGs) concerning cell death involved in apoptosis (RIPK1, TLR7, CASP8, and CASP8AP2), pyroptosis (NLRP3, IL-1β, and IRAK2), and ferroptosis (TFRC and PTGS2). The abundances of IL-1β, IRAK2, NLRP3, CASP8, CASP8AP2, RIPK1, and TLR7 were significantly increased in the C1 group and decreased in T1 group, while TFRC and PTGS2 were increased in T1 group. (4) Conclusions: oxidative stress induced by hydrogen peroxide caused cellular damage and death in sheep hepatocytes. Pretreatment with vitamin E effectively reduced intracellular ROS levels and protected the hepatocytes from cell death by regulating gene expression associated with apoptosis (RIPK1, TLR7, CASP8, and CASP8AP2) and pyroptosis (NLRP3, IL-1β, and IRAK2), but not ferroptosis (TFRC and PTGS2).

2021 ◽  
Author(s):  
Rahat Naseer ◽  
Affan Tariq ◽  
Munazza Raza Mirza ◽  
Muhammad Rashid ◽  
Syed Qasim Raza ◽  
...  

Abstract Background; Dinotefuran is a new class of neonicotinoids claimed to be harmless to mammals and humans. This claim was daunted by the documented effect of dinotefuran on honeybees and further studies were required. Aim: The study was designed to assess the capaciousness of damage caused by prolonged exposure of dinotefuran in mammals and probable strategy to neutralize its effect. Methodology: Ninety-day trial using Wistar rats (n=45) was conducted while dividing them into three groups: untreated control group, insecticide (dinotefuran) treated group, and dinotefuran treated and vitamin E supplemented group. Dinotefuran was administrated orally (LD25). Vitamin E (alpha-tocopherol) supplementation was given in water ad libitum. Blood sampling was done twice a month, and hematological and biochemical data were recorded. After expiry of trial period, the experimental rats were anesthetized and sacrificed. Organs (kidneys, liver, and heart) were isolated from each groups, weighed, and stored at approximately -20°C till further processing, analysis and histopathology were performed. Results: All the hematological parameters were affected significantly. Histopathology of tissues showed clear necrosis in all the tissues except kidneys. All the biomarkers of oxidative stress and comet assay demonstrated significant cell damage. All the parameters showed improvement after vitamin E supplementation but non-significantly. Significance: These findings were suggestive that even low dose persistent exposure can lead to mutagenicity and carcinogenicity in mammals and other non-target species hence revised policy guidelines and more intelligent use of these chemicals is required.


2017 ◽  
Vol 41 (S1) ◽  
pp. S707-S707 ◽  
Author(s):  
Y. Zhang ◽  
F. Liu ◽  
Z. Dai ◽  
Q. Wu

ObjectiveTo investigate the effect of saikosaponin B2 on the damage of cultured SH-SY5Y cells.Methods10% calf serum including volume fraction 0.05, 0.10, 0.20 saikosaponin B2 (10−4mol·L−1) were added respectively into the SH-SY5Y cells, which were then treated with 140 μmol· L−1 hydrogen peroxide(H2O2). 10% calf serum group and blank serum without H2O2-treated group were as the model group and the control group. The effect of saikosaponin B2 was observed by morphological identification, colorimetric MTT assay.ResultsBoth saikosaponin B2 of 10−6mol·L−1 and 2 × 10−6mol·L−1 can relieve the damage of SH-SY5Y cells and increase the survival of the cells.Conclusionsaikosaponin B2 can protect the cultured SH-SY5Y cells from damage induced by H2O2.Disclosure of interestThe authors have not supplied their declaration of competing interest.


Author(s):  
J. A. Fernandez-Pol ◽  
M. T. Hays

The acute ultrastructural effects of Thyroid Stimulating Hormone (TSH) in vivo or in vitro are well documented. However, little is known about chronic effects of TSH administration. The purpose of the present study was to define the ultrastructural changes induced by chronic TSH administration.Ten Mongrel dogs weighing between 18-20 kg were used in these studies. They were divided in two groups:Control group: (4 dogs) These dogs were administered saline solution, (0.09% NaCl) intramuscular for 10 days.TSH treated group: (6 dogs) These dogs received a daily intramuscular injection of TSH, 15 IU for 10 days.All dogs received 300 mg of Thyroid extract per day for 3 days prior to the operation. Then, they were thyroidectomized on the 11th day. Immediately after removal of the thyroid gland, tissues were fixed in glutaraldehyde 37, in phosphate buffer at pH 7.4 for 2 hrs.


2018 ◽  
Vol 69 (8) ◽  
pp. 2081-2088 ◽  
Author(s):  
Alin Alexandru Odor ◽  
Edwin Sever Bechir ◽  
Deborah Violant ◽  
Victoria Badea

Moderate and severe periodontitis represents a challenge in the non-surgical periodontal therapy. Due to the lack of evidence regarding the antimicrobial effectiveness of 940 nm diode laser in periodontal treatment, this study aimed to evaluate the antimicrobial effect of hydrogen peroxide (H2O2) photolysis performed with 940 nm diode laser in the treatment of moderate and severe periodontitis. Twenty-five patients with 100 teeth were selected for this pilot study. The test teeth were randomly assigned to one of the four treatment groups: Group 1: scaling and root planning (SRP) (control group); and the following experimental groups: Group 2: H2O2; Group 3: 940 nm diode laser therapy; Group 4: 940 nm diode laser therapy and H2O2. Clinical examinations, like probing depth (PD), clinical attachment level (CAL) and bleeding on probing (BOP) were performed before and after the treatment. The microbiological evaluation, effectuated before and after the treatment, included nine periodontal bacteria species and investigated by means of real-time PCR assay. The clinical and bacterial differences in the tested groups, was assessed between control group and the other three experimental groups, as well as between the experimental groups. The total bacteria load was reduced for all four studied groups. Group 4 (diode laser + H2O2) showed significant bacterial reduction of the major periodontal bacteria like Pg., Tf., Td., Pi., Pm., Fn (p[0.001) than the other 3 groups (p]0.001). Also the periodontal clinical parameters, like PD, CAL and BOP showed a significant reduction after the photolysis of H2O2 with the 940 nm diode laser (p[0.001). Differences between tested groups showed a significant beneficial results in regard to Group 4.It is suggested that the photoactivation of H2O2 with the 940 nm diode laser can be used successfully in adjunctive to the non-surgical periodontal treatment as a bactericidal tool.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 132-133
Author(s):  
Genxiang Mao ◽  
Xiaogang Xu

Abstract Exosomes are one type of small-cell extracellular vesicles (sEVs), which together with the senescence-associated secretory phenotype (SASP) mainly constitute the senescent microenvironment and perform remotely intercellular communication. However, the effects of senescence on exosomes biosynthesis and secretion and its role in the cell senescence are still obscure. Here, we used human fetal lung diploid fibroblasts (2BS) passaged to PD50 to construct the senescent cells model in vitro, which were confirmed by senescence-related β-galactosidase staining, cell cycle distribution, and intracellular ROS levels. PD30 2BS was used as young control. We evaluated the exosomes derived from senescence and young control group respectively and investigated their regulation of senescence. We found that exosomes released from 2BS had typical sizes and cup-shapes morphology and their surface presented typical exosome-associated proteins. The number of exosomes secreted by senescent cells was significantly higher than that of young cells. Moreover, exosomal markers Alix, TSG101, and CD63 were all more expressed than young cells. Furthermore, we treat young cells with exosomes secreted by senescent cells, which can induce senescence-like changes in young cells, including increased SA-β-Gal activity, up-regulated p16 protein expression, and activation of the Notch signaling pathway. The above results imply that exosomes derived from senescent cells can promote cell senescence. The findings expand the current knowledge on exosomes-mediated aging and provide a novel understanding of the relationship between SASP and senescence. This study is supported by National Natural Science Foundation of China (No. 81771520 and 31702144).


Author(s):  
Joon M. Jung ◽  
Hae K. Yoon ◽  
Chang J. Jung ◽  
Soo Y. Jo ◽  
Sang G. Hwang ◽  
...  

Cold plasma can be beneficial for promoting skin wound healing and has a high potential of being effectively used in treating various wounds. Our aim was to verify the effect of cold plasma in accelerating wound healing and investigate its underlying mechanism in vitro and in vivo. For the in vivo experiments, 2 full-thickness dermal wounds were created in each mouse (n = 30). While one wound was exposed to 2 daily plasma treatments for 3 min, the other wound served as a control. The wounds were evaluated by imaging and histological analyses at 4, 7, and 11 days post the wound infliction process. Immunohistochemical studies were also performed at the same time points. In vitro proliferation and scratch assay using HaCaT keratinocytes and fibroblasts were performed. The expression levels of wound healing–related genes were analyzed by real-time polymerase chain reaction and western blot analysis. On day 7, the wound healing rates were 53.94% and 63.58% for the control group and the plasma-treated group, respectively. On day 11, these rates were 76.05% and 93.44% for the control and plasma-treated groups, respectively, and the difference between them was significant ( P = .039). Histological analysis demonstrated that plasma treatment promotes the formation of epidermal keratin and granular layers. Immunohistochemical studies also revealed that collagen 1, collagen 3, and alpha-smooth muscle actin appeared more abundantly in the plasma-treated group than in the control group. In vitro, the proliferation of keratinocytes was promoted by plasma exposure. Scratch assay showed that fibroblast exposure to plasma increased their migration. The expression levels of collagen 1, collagen 3, and alpha-smooth muscle actin were elevated upon plasma treatment. In conclusion, cold plasma can accelerate skin wound healing and is well tolerated.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Malinee Thanee ◽  
Sureerat Padthaisong ◽  
Manida Suksawat ◽  
Hasaya Dokduang ◽  
Jutarop Phetcharaburanin ◽  
...  

Abstract Background Sulfasalazine (SSZ) is widely known as an xCT inhibitor suppressing CD44v9-expressed cancer stem-like cells (CSCs) being related to redox regulation. Cholangiocarcinoma (CCA) has a high recurrence rate and no effective chemotherapy. A recent report revealed high levels of CD44v9-positive cells in CCA patients. Therefore, a combination of drugs could prove a suitable strategy for CCA treatment via individual metabolic profiling. Methods We examined the effect of xCT-targeted CD44v9-CSCs using sulfasalazine combined with cisplatin (CIS) or gemcitabine in CCA in vitro and in vivo models and did NMR-based metabolomics analysis of xenograft mice tumor tissues. Results Our findings suggest that combined SSZ and CIS leads to a higher inhibition of cell proliferation and induction of cell death than CIS alone in both in vitro and in vivo models. Xenograft mice showed that the CD44v9-CSC marker and CK-19-CCA proliferative marker were reduced in the combination treatment. Interestingly, different metabolic signatures and significant metabolites were observed in the drug-treated group compared with the control group that revealed the cancer suppression mechanisms. Conclusions SSZ could improve CCA therapy by sensitization to CIS through killing CD44v9-positive cells and modifying the metabolic pathways, in particular tryptophan degradation (i.e., kynurenine pathway, serotonin pathway) and nucleic acid metabolism.


Molecules ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 331
Author(s):  
Jung-Yun Lee ◽  
Tae Yang Kim ◽  
Hanna Kang ◽  
Jungbae Oh ◽  
Joo Woong Park ◽  
...  

Excess body weight is a major risk factor for type 2 diabetes (T2D) and associated metabolic complications, and weight loss has been shown to improve glycemic control and decrease morbidity and mortality in T2D patients. Weight-loss strategies using dietary interventions produce a significant decrease in diabetes-related metabolic disturbance. We have previously reported that the supplementation of low molecular chitosan oligosaccharide (GO2KA1) significantly inhibited blood glucose levels in both animals and humans. However, the effect of GO2KA1 on obesity still remains unclear. The aim of the study was to evaluate the anti-obesity effect of GO2KA1 on lipid accumulation and adipogenic gene expression using 3T3-L1 adipocytes in vitro and plasma lipid profiles using a Sprague-Dawley (SD) rat model. Murine 3T3-L1 preadipocytes were stimulated to differentiate under the adipogenic stimulation in the presence and absence of varying concentrations of GO2KA1. Adipocyte differentiation was confirmed by Oil Red O staining of lipids and the expression of adipogenic gene expression. Compared to control group, the cells treated with GO2KA1 significantly decreased in intracellular lipid accumulation with concomitant decreases in the expression of key transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (CEBP/α). Consistently, the mRNA expression of downstream adipogenic target genes such as fatty acid binding protein 4 (FABP4), fatty acid synthase (FAS), were significantly lower in the GO2KA1-treated group than in the control group. In vivo, male SD rats were fed a high fat diet (HFD) for 6 weeks to induced obesity, followed by oral administration of GO2KA1 at 0.1 g/kg/body weight or vehicle control in HFD. We assessed body weight, food intake, plasma lipids, levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) for liver function, and serum level of adiponectin, a marker for obesity-mediated metabolic syndrome. Compared to control group GO2KA1 significantly suppressed body weight gain (185.8 ± 8.8 g vs. 211.6 ± 20.1 g, p < 0.05) with no significant difference in food intake. The serum total cholesterol, triglyceride, and low-density lipoprotein (LDL) levels were significantly lower in the GO2KA1-treated group than in the control group, whereas the high-density lipoprotein (HDL) level was higher in the GO2KA1 group. The GO2KA1-treated group also showed a significant reduction in ALT and AST levels compared to the control. Moreover, serum adiponectin levels were significantly 1.5-folder higher than the control group. These in vivo and in vitro findings suggest that dietary supplementation of GO2KA1 may prevent diet-induced weight gain and the anti-obesity effect is mediated in part by inhibiting adipogenesis and increasing adiponectin level.


2017 ◽  
Vol 44 (4) ◽  
pp. 288-293 ◽  
Author(s):  
Shiho Yamadera ◽  
Yuya Nakamura ◽  
Masahiro Inagaki ◽  
Isao Ohsawa ◽  
Hiromichi Gotoh ◽  
...  

Aim: To examine the effects of vitamin E-coated dialyzer on oxidative stress in vitro. Methods: A dialyzer with a synthetic polymer membrane (APS-11SA) and vitamin E-coated dialyzer (VPS-11SA) were connected to a blood tubing line, and U937 cells were circulated in the device. The circulating fluid was collected at 1, 2, 5, 10, 25, and 50 cycles, which are estimated numbers of passes through the dialyzer. Intracellular reactive oxygen species (ROS) production, malondialdehyde (MDA), and Cu/Zn-superoxide dismutase (SOD) were quantified. Results: Intracellular ROS production was increased in the first cycle by APS-11SA and was decreased throughout the experiment by VPS-11SA. Intracellular ROS production in the VPS-11SA device was lower, and MDA levels were decreased. MDA levels were lower during VPS-11SA processing than during APS-11SA processing. Cu/Zn-SOD levels remained unchanged. Conclusion: Our results highlight anti-oxidative-stress effects of a vitamin E-coated dialyzer.


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