Angiogenesis and Full-Thickness Wound Healing Efficiency of a Copper-Doped Borate Bioactive Glass/Poly(lactic- co-glycolic acid) Dressing Loaded with Vitamin E in Vivo and in Vitro

Hu H, Tang Y, Pang L, Lin C, Huang W, Wang D, Jia W

Send to ACS Appl Mater Interfaces. 2018 Jul 11;10(27):22939-22950. doi: 10.1021/acsami.8b04903. Epub 2018 Jun 28.

Abstract

There is an urgent demand for wound healing biomaterials because of the increasing frequency of traffic accidents, industrial contingencies, and natural disasters. Borate bioactive glass has potential applications in bone tissue engineering and wound healing; however, its uncontrolled release runs a high risk of rapid degradation and transient biotoxicity. In this study, a novel organic-inorganic dressing of copper-doped borate bioactive glass/poly(lactic- co-glycolic acid) loaded with vitamin E (0-3.0 wt % vitamin E) was fabricated to evaluate its efficiency for angiogenesis in cells and full-thickness skin wounds healing in rodents. In vitro results showed the dressing was an ideal interface for the organic-inorganic mixture and a controlled release system for Cu2+ and vitamin E. Cell culture suggested the ionic dissolution product of the copper-doped and vitamin E-loaded dressing showed the best migration, tubule formation, and vascular endothelial growth factor (VEGF) secretion in human umbilical vein endothelial cells (HUVECs) and higher expression levels of angiogenesis-related genes in fibroblasts in vitro. Furthermore, this dressing also suggested a significant improvement in the epithelialization of wound closure and an obvious enhancement in vessel sprouting and collagen remodeling in vivo. These results indicate that the copper-doped borate bioactive glass/poly(lactic- co-glycolic acid) dressing loaded with vitamin E is effective in stimulating angiogenesis and healing full-thickness skin defects and is a promising wound dressing in the reconstruction of full-thickness skin injury.

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Impacts of selenium and vitamin E supplementation on mRNA of heat shock proteins, selenoproteins and antioxidants in broilers exposed to high temperature.

Kumbhar S, Khan AZ, Parveen F, Nizamani ZA, Siyal FA, El-Hack MEA, Gan F, Liu Y, Hamid M, Nido SA, Huang K

AMB Express. 2018 Jul 10;8(1):112. doi: 10.1186/s13568-018-0641-0.

Abstract

The study was carried out to investigate the effect of dietary selenium (Se) and vitamin E (VE) supplementation on mRNA level of heat shock proteins, selenoproteins, and antioxidant enzyme activities in the breast meat of broilers under summer heat stress conditions. A total of 200 male broilers (Ross 308) of 1 day age were randomly separated into 4 groups in a complete randomized design and were given a basal diet (Control, 0.08 mg Se/kg diet) or basal diet supplemented with VE (250 mg/kg VE), sodium selenite (0.2 mg/kg Se), or Se + VE (0.2 mg/kg Se + 250 mg/kg VE) to investigate the expression of key antioxidant and heat shock protein (HSP) genes under high temperature stress. Dietary Se, VE and Se + VE significantly enhanced the activities and mRNA levels of catalase as well as superoxide dismutase (SOD) but decreased the mRNA levels of HSP70 and HSP90. Se alone or combined with VE increased the concentration of selenoprotein P and selenoproteins mRNA level and decreased the expression of HSP60. In addition, Se and Se + VE significantly enhanced the glutathione peroxidase (GPx) activity and the expression of GPx1 and GPx4 in breast muscle tissues. It is noteworthy that all the treatments significantly decreased malondialdehyde (MDA) level in the breast meat. Overall results showed that Se in combination with VE has maximal effects to mitigate heat stress. Based on given results it can be recommended that Se + VE are a suitable dietary supplement for broilers to ameliorate the negative effects of summer heat stress conditions.

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A Review on the Relationship between Tocotrienol and Alzheimer Disease

Chin KY, Tay SS

Nutrients. 2018 Jul 9;10(7). pii: E881. doi: 10.3390/nu10070881.

Abstract

Alzheimer’s disease (AD) is plaguing the aging population worldwide due to its tremendous health care and socioeconomic burden. Current treatment of AD only offers symptomatic relief to patients. Development of agents targeting specific pathologies of AD is very slow. Tocotrienol, a member of the vitamin E family, can tackle many aspects of AD, such as oxidative stress, mitochondrial dysfunction and abnormal cholesterol synthesis. This review summarizes the current evidence on the role of tocotrienol as a neuroprotective agent. Preclinical studies showed that tocotrienol could reduce oxidative stress by acting as a free-radical scavenger and promoter of mitochondrial function and cellular repair. It also prevented glutamate-induced neurotoxicity in the cells. Human epidemiological studies showed a significant inverse relationship between tocotrienol levels and the occurrence of AD. However, there is no clinical trial to support the claim that tocotrienol can delay or prevent the onset of AD. As a conclusion, tocotrienol has the potential to be developed as an AD-preventing agent but further studies are required to validate its efficacy in humans.

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a-Tocopherol modifies the expression of genes related to oxidative stress and apoptosis during invitro maturation and enhances the developmental competence of rabbit oocytes

Arias-Álvarez M, García-García RM, López-Tello J, Rebollar PG, Gutiérrez-Adán A, Lorenzo PL

Reprod Fertil Dev. 2018 Jul 3. doi: 10.1071/RD17525. [Epub ahead of print]

Abstract

The developmental competence of invitro maturation (IVM) oocytes can be enhanced by antioxidant agents. The present study investigated, for the first time in the rabbit model, the effect of adding α-tocopherol (0, 100, 200 and 400µM) during IVM on putative transcripts involved in antioxidant defence (superoxide dismutase 2, mitochondrial (SOD2), glutathione peroxidase 1 (GPX1), catalase (CAT)), cell cycle regulation and apoptosis cascade (apoptosis tumour protein 53 (TP53), caspase 3, apoptosis-related cysteine protease (CASP3)), cell cycle progression (cellular cycle V-Akt murine thymoma viral oncogene homologue 1 (AKT1)), cumulus expansion (gap junction protein, alpha 1, 43 kDa (GJA1) and prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclo-oxygenase) (PTGS2)) and metabolism (glucose-6-phosphate dehydrogenase (G6PD)). Meiotic progression, mitochondrial reallocation, cumulus cell apoptosis and the developmental competence of oocytes after IVF were also assessed. Expression of SOD2, CAT, TP53, CASP3 and GJA1 was downregulated in cumulus-oocyte complexes (COCs) after IVM with 100μM α-tocopherol compared with the group without the antioxidant. The apoptotic rate and the percentage of a non-migrated mitochondrial pattern were lower in COCs cultured with 100μM α-tocopherol, consistent with better-quality oocytes. In fact, early embryo development was improved when 100μM α-tocopherol was included in the IVM medium, but remained low compared with invivo-matured oocytes. In conclusion, the addition of 100μM α-tocopherol to the maturation medium is a suitable approach to manage oxidative stress and apoptosis, as well as for increasing the in vitro developmental competence of rabbit oocytes.

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Vitamin E as alternative local treatment in genitourinary syndrome of menopause: a randomized controlled trial

Golmakani N, Parnan Emamverdikhan A, Zarifian A, Sajadi Tabassi SA, Hassanzadeh M

Int Urogynecol J. 2018 Jul 3. doi: 10.1007/s00192-018-3698-z. [Epub ahead of print]

Abstract

INTRODUCTION AND HYPOTHESIS:

Genitourinary syndrome of menopause is a major health concern in postmenopausal women. This study was aimed at comparing the effect of a vitamin E vaginal suppository with that of conjugated estrogen vaginal cream on sexual function in postmenopausal women with genitourinary syndrome of menopause.

METHODS:

This survey was carried out on 52 postmenopausal women aged 40-65 years who had been referred to gynecology clinics in Mashhad city, during 2013-2014. Keeping β = 0.1, the power was calculated to be 90%. The patients were randomly divided into two groups: vitamin E vaginal suppository and conjugated estrogen vaginal cream. Participants used the medications for 12 weeks. They were visited at the 4th, 8th, and 12th weeks. Validated Abbreviated Sexual Function Questionnaire (ASFQ), as the primary outcome measure, and a demographic information questionnaire, were used to collect data at each visit. Data were analyzed using SPSS and p < 0.05 was considered statistically significant.

RESULTS:

Mean overall scores of the ASFQ were increased significantly in both groups during the course of the study, compared with baseline (p < 0.001). However, the mean ASFQ scores of the two treatments did not differ significantly.

CONCLUSION:

Improved scores of ASFQ after the 12th week showed that the treatment was successful in both groups. Therefore, a vitamin E vaginal suppository may be an alternative to vaginal estrogen in relieving the symptoms of vaginal atrophy in postmenopausal women, especially those not able to use hormone therapy or have low compliance.

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Vitamin E and vitamin C attenuate Di-(2-ethylhexyl) phthalate-induced blood-testis barrier disruption by p38 MAPK in immature SD rats

Shen L, Tang X, Wei Y, Long C, Tan B, Wu S, Sun M, Zhou Y, Cao X, Wei G

Reprod Toxicol. 2018 Jun 27;81:17-27. doi: 10.1016/j.reprotox.2018.06.015. [Epub ahead of print]

Abstract

As an environmental endocrine disruptor, Di-(2-ethylhexyl) phthalate (DEHP) affects blood-testis barrier (BTB)-associated proteins expression, which compromises BTB integrity and causes infertility. Notably, DEHP-induced testicular toxicity is related to oxidative stress, but the specific mechanism remains unclear. Therefore, we sought to investigate this mechanism and determine whether vitamin C and vitamin E administration would attenuate the BTB impairment induced by DEHP in vivo and by Mono-(2-Ethylhexyl) Phthalate (MEHP) in vitro, respectively. HE staining and EM found that DEHP exposure led to spermatogenesis dysfunction and BTB disruption, respectively. The Western blot and immunofluorescence results showed that DEHP exposure caused BTB impairment through oxidative stress-mediated p38 mitogen-activated protein kinase (MAPK) signaling pathway. Furthermore, Vitamin E and vitamin C could alleviate the oxidative stress, block DEHP-induced spermatogenesis dysfunction and BTB disruption by inhibiting p38 MAPK signaling pathway. In summary, vitamin E and vitamin C are good candidates for the treatment of DEHP-induced male infertility.

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Cytoprotective role of vitamin E in porcine adipose-tissue-derived mesenchymal stem cells against hydrogen-peroxide-induced oxidative stress

Bhatti FUR, Kim SJ, Yi AK, Hasty KA, Cho H

Cell Tissue Res. 2018 Jun 27. doi: 10.1007/s00441-018-2857-3. [Epub ahead of print]

Abstract

Survival of mesenchymal stem cells (MSCs) against oxidative stress and inflammation is vital for effective stem cell therapy. The reactive oxygen species (ROS) result in apoptosis and release of inflammatory mediators. Adipose-derived stem cells (ASCs) have shown promise for stem cell therapy owing to their anti-inflammatory and anti-oxidant activity. Previously, we showed the benefits of vitamin E against hydrogen peroxide (H2O2)-induced oxidative stress in rat bone marrow-derived MSCs. In this study, we aim to evaluate the effect of vitamin E treatment on porcine adipose-derived mesenchymal stem cells (pASCs) against H2O2-induced oxidative stress. The oxidative stress was induced by treating pASCs with 500 μM H2O2 with or without vitamin E. Viability of pASCs is enhanced after vitamin E treatment. In addition, reduced cellular toxicity, total NO level, PGE2 production and caspase-3 activity were observed after vitamin E treatment. Gene expression analysis of vitamin E-treated pASCs showed down-regulated expression for the genes associated with oxidative stress and apoptosis, viz., NOS2, Casp3, p53, BAX, MDM2, NFκB, HIF1α and VEGF-A genes. On the other hand, expression of anti-apoptotic and survival genes was up-regulated, viz., BCL2, BCL2L1 and MCL1. Furthermore, phosphorylation of Akt was attenuated following vitamin E treatment. The findings of this study may help in developing effective stem cell therapy for the diseases characterized by the oxidative stress and inflammation.

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Incorporation of tocopherol-rich extracts from mushroom mycelia into yogurt

Bouzgarrou C, Amara K , Reis FS , Barreira JCM , Skhiri F , Chatti N , Martins A , Barros L , Ferreira ICFR

Food Funct. 2018 Jun 20;9(6):3166-3172. doi: 10.1039/c8fo00482j.

Abstract

Consumers are well-informed about food additives and it is likely that they prefer natural additives over their synthetic analogues. Antioxidants represent a major class of food preservatives, among which tocopherols stand out as one of the most important examples. Interestingly, these compounds are present in relevant amounts in the mycelia of in vitro cultured mushrooms. Accordingly, the mycelia from Ganoderma lucidum, Pleurotus ostreatus and Pleurotus eryngii were used as alternative sources of tocopherols. These extracts were incorporated into different yogurt formulations, which were further compared among each other and with yogurts containing commercial α-tocopherol (E307), regarding their nutritional parameters, fatty acid profile and antioxidant activity. The proposed approach was validated as an effective functionalization strategy, particularly in the case of the G. lucidum mycelium, which showed the highest antioxidant potential, most likely as a result of its tocopherol profile. Furthermore, yogurts prepared with each mycelium extract allowed maintaining the nutritional properties observed in the “blank” yogurt formulation.

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Combined use of Vitamins E and C improve nephrotoxicity induced by colistin in rats

Ghlissi Z, Hakim A, Mnif H, Zeghal K, Rebai T, Boudawara T, Sahnoun Z

Saudi J Kidney Dis Transpl. 2018 May-Jun;29(3):545-553. doi: 10.4103/1319-2442.235168.

Abstract

This study was performed to investigate the protective effect of combined use of Vitamins E and C on colistin-induced tubular damage in rat. Animals were treated with sterile saline, colistin methanesulfonate (CMS), CMS + Vitamin E + Vitamin C, and Vitamin E + vitamin C, respectively, for seven days. Thereafter, animals were sacrificed and the urine N-acetyl-b-D-glucosaminidase (NAG) and gamma-glutamyl transferase (GGT) levels, plasma level of creatinine (Cr), vitamin E and vitamin C, and renal tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as renal histology were performed. CMS induced acute tubular necrosis, increased the NAG, GGT, and MDA levels, and reduced the Vitamin E, Vitamin C, SOD, CAT, and GPx activities. Co-treatment with vitamins E and C restored all biochemical parameters cited above and improved the histopathological damage. Tubular damage induced by colistin is at least partly due to oxidative stress. Nephroprotective effect of Vitamins E and C is partially mediated through its antioxidant properties, and the higher protection by the combination of these vitamins is related to its synergistic effects.

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Arsenic-induced oxidative stress, cholinesterase activity in the brain of Swiss albino mice, and its amelioration by antioxidants Vitamin E and Coenzyme Q10

Sharma A, Kshetrimayum C, Sadhu HG, Kumar S

Environ Sci Pollut Res Int. 2018 Jun 8. doi: 10.1007/s11356-018-2398-z. [Epub ahead of print]

Abstract

Arsenic toxicity becomes one of the major public health issues in several countries. Chronic and acute exposure to arsenic has been reported to be toxic to various systems of the human body and also observed in controlled experimental studies. The study was conducted to evaluate the neurotoxic effect of arsenic in Swiss albino mice and its amelioration by Vitamin E, Coenzyme Q10 and their combination. Swiss albino mice were treated with arsenic of 136 ppm for 15 days. The daily dose is 1/3 of LD 50 (acute) reported dose of arsenic. Thereafter, the animals were maintained either on drinking water or treated with Vitamin E (50 mg/kg bwt), Coenzyme Q10 (10 mg/kg bwt), and their combination by i.p.daily for 15 days. After the treatment, animals were sacrificed. The weight of the brain was marginally lower (ns), in arsenic-treated group as compared to control and antioxidant-protected groups. The LPO (lipid peroxidation) level was higher in arsenic-treated group, and this elevation was checked to some extent by the selected antioxidants which were statistically significant in combination of antioxidant-protected group. A significant reduction was found in GSH (reduced glutathione) level in the brain of arsenic-treated mice whereas GSH level was considerably higher in antioxidant-protected groups. Further, total thiol and total protein level were lower in arsenic-treated group. However, total thiol was significantly higher in antioxidant-protected groups. CAT (catalase) activity was significantly lower while SOD (superoxide dismutase) activity was marginally lowered in arsenic-treated group, and it was slightly higher in antioxidant-protected groups. Further, reduction in AChE (acetylcholinesterase) and BChE (butyrylcholinesterase) and motor coordination activity were also observed in arsenic-treated groups. Whereas, a higher AChE, BChE, and motor coordination activity was observed in antioxidant-protected group. These data indicate a positive role of selected antioxidant against the toxicity of arsenic in the brain of mice.

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