Vitamin E protects rat mesenchymal stem cells against hydrogen peroxide-induced oxidative stress in vitro and improves their therapeutic potential in surgically-induced rat model of osteoarthritis

Abstract Alzheimer's disease (AD) is the most prevalent type of dementia characterized by its progression, neurobehavioral and neuro-pathological characteristics, leading to a diverse neuronal loss. Adipose-derived mesenchymal stem cells (ADMSCs) have previously proved potential role in preventing the pathogenesis of several neurodegenerative disorders, so regarded as a promising new approach for AD regenerative therapy. Taurine was found to enhance stem cell activation and propagation yielding a higher concentration of neural progenitors and stem cells, and aid to lessen the number of activated microglia leading to down-regulated inflammation in vitro. The present study aimed to investigate the possible therapeutic potential of ADMSCs and/or taurine in treating AD rat model. It was planned to include three successive phases; induction, withdrawal, and therapeutic phases. Fifty male Wistar rats were divided into 2 main groups: control (C) group and AD model group. Behavioral changes, as manifested by the T-Maze experiment, had been recorded. β-amyloid levels had been measured in brain homogenate and serum by ELISA. Oxidative stress marker (MDA), and anti-oxidant enzymes activity (SOD, GSH, and CAT) in brain, as well as serum acetylcholine esterase activity were spectrophotometrically determined. Pro-apoptotic (p53 and Bax) and anti-apoptotic (Bcl2) gene expression in brain were evaluated using RT-qPCR. The histopathological alterations in brain tissues were also observed. The present study proved the potential therapeutic ability of ADMSCs and/or taurine in alleviating the adverse pathological changes induced by AlCl3 in AD rat model at both physiological and molecular levels.

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

Cell and Tissue Research ◽

10.1007/s00441-018-2857-3 ◽

2018 ◽

Vol 374 (1) ◽

pp. 111-120 ◽

Cited By ~ 7

Author(s):

Fazal Ur Rehman Bhatti ◽

Song Ja Kim ◽

Ae-Kyung Yi ◽

Karen A. Hasty ◽

Hongsik Cho

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Stem Cells ◽

Mesenchymal Stem Cells ◽

Adipose Tissue ◽

Vitamin E

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Peculiarities of the metabolic activity of mesenchimal stem cells under oxidative stress

Faktori eksperimental'noi evolucii organizmiv ◽

10.7124/feeo.v26.1268 ◽

2020 ◽

Vol 26 ◽

pp. 212-216

Author(s):

M. V. Kovalchuk ◽

N. S. Shuvalova ◽

V. A. Kordium

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Stem Cells ◽

Mesenchymal Stem Cells ◽

Metabolic Activity ◽

Therapeutic Potential ◽

Critical Concentration ◽

Test Results ◽

Standard Methods ◽

Mtt Test

Aim. Oxidative stress is considered to be one of the major damaging factors that limits the therapeutic potential of mesenchymal stem cells (MSCs). The purpose of our work was to study the metabolic activity of Wharton jelly-derived MSC of different donor origin under oxidative stress conditions induced by hydrogen peroxide. Methods. MSC were obtained by the explant method and cultured according to standard methods. Oxidative stress was caused by treating cells with different concentrations of hydrogen peroxide. The metabolic activity of MSCs was evaluated using the MTT test. Results. Analysis of the MTT test showed a biphasic dependence of the MSC response to the concentration of H2O2. Concentrations of hydrogen peroxide from 6.25 to 50 μM increased the level of metabolic activity of MSCs, and concentrations from 50 to 440 μM inhibited metabolic activity. The maximum stimulating effect was observed at concentrations of 12.5 μM and 25 μM depending on the donor. Conclusions. The response of cells to oxidative stress corresponded to the hormetic dependence, and the points of critical concentration and maximum stimulation were individual for each donor. Processes such as preconditioning MSCs with hydrogen peroxide to increase their survival rate during transplantation also require personalization of the approach depending on the points of maximum stimulation. Keywords: mesenchymal stem cells, hydrogen peroxide, oxidative stress.

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Antioxidant pretreatment enhances umbilical cord derived stem cells survival in response to thermal stress in vitro

Regenerative Medicine ◽

10.2217/rme-2019-0090 ◽

2020 ◽

Vol 15 (3) ◽

pp. 1441-1453

Author(s):

Ramla Ashfaq ◽

Azra Mehmood ◽

Amna Ramzan ◽

Intzar Hussain ◽

Moazzam Nazeer Tarar ◽

...

Keyword(s):

Oxidative Stress ◽

Stem Cells ◽

Wound Healing ◽

Mesenchymal Stem Cells ◽

Thermal Stress ◽

Vitamin E ◽

Vitamin C ◽

Heat Injury ◽

Injury Assessment

Aim: Pretreatment of stem cells with antioxidants accelerates their ability to counter oxidative stress and is associated with the overall therapeutic outcome of their transplantation. Material & methods: Wharton Jelly derived mesenchymal stem cells (WJMSCs) were cultured and pretreated with various doses of antioxidants; Vitamin C (Vit C), Vitamin E (Vit E), Vitamin D3 (Vit D3) and their Cocktail, followed by exposure to in vitro heat injury. Assessment of WJMSCs survival, paracrine release, in vitro wound healing and expression of angiogenic and survival markers was conducted. Results: The results displayed an enhanced survival of WJMSCs especially in the case of Cocktail priming. Conclusion: Our data suggest that antioxidant pretreatment of WJMSCs strengthens the endurance of the cells, within stress conditions.

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Geraniin protects bone marrow‑derived mesenchymal stem cells against hydrogen peroxide‑induced cellular oxidative stress in vitro

International Journal of Molecular Medicine ◽

10.3892/ijmm.2017.3276 ◽

2017 ◽

Cited By ~ 1

Author(s):

Dan Huang ◽

Li Yin ◽

Xinxin Liu ◽

Bo Lv ◽

Zulong Xie ◽

...

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Stem Cells ◽

Bone Marrow ◽

Mesenchymal Stem Cells

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Adropin-based dual treatment enhances the therapeutic potential of mesenchymal stem cells in rat myocardial infarction

Cell Death and Disease ◽

10.1038/s41419-021-03610-1 ◽

2021 ◽

Vol 12 (6) ◽

Author(s):

HuiYa Li ◽

DanQing Hu ◽

Guilin Chen ◽

DeDong Zheng ◽

ShuMei Li ◽

...

Keyword(s):

Myocardial Infarction ◽

Stem Cells ◽

Mesenchymal Stem Cells ◽

Therapeutic Potential ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Paracrine Factors ◽

Dual Treatment

AbstractBoth weak survival ability of stem cells and hostile microenvironment are dual dilemma for cell therapy. Adropin, a bioactive substance, has been demonstrated to be cytoprotective. We therefore hypothesized that adropin may produce dual protective effects on the therapeutic potential of stem cells in myocardial infarction by employing an adropin-based dual treatment of promoting stem cell survival in vitro and modifying microenvironment in vivo. In the current study, adropin (25 ng/ml) in vitro reduced hydrogen peroxide-induced apoptosis in rat bone marrow mesenchymal stem cells (MSCs) and improved MSCs survival with increased phosphorylation of Akt and extracellular regulated protein kinases (ERK) l/2. Adropin-induced cytoprotection was blocked by the inhibitors of Akt and ERK1/2. The left main coronary artery of rats was ligated for 3 or 28 days to induce myocardial infarction. Bromodeoxyuridine (BrdU)-labeled MSCs, which were in vitro pretreated with adropin, were in vivo intramyocardially injected after ischemia, following an intravenous injection of 0.2 mg/kg adropin (dual treatment). Compared with MSCs transplantation alone, the dual treatment with adropin reported a higher level of interleukin-10, a lower level of tumor necrosis factor-α and interleukin-1β in plasma at day 3, and higher left ventricular ejection fraction and expression of paracrine factors at day 28, with less myocardial fibrosis and higher capillary density, and produced more surviving BrdU-positive cells at day 3 and 28. In conclusion, our data evidence that adropin-based dual treatment may enhance the therapeutic potential of MSCs to repair myocardium through paracrine mechanism via the pro-survival pathways.

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Improved healing of critical-size femoral defect in osteoporosis rat models using 3D elastin/polycaprolactone/nHA scaffold in combination with mesenchymal stem cells

Journal of Materials Science Materials in Medicine ◽

10.1007/s10856-021-06495-w ◽

2021 ◽

Vol 32 (3) ◽

Author(s):

Fatemeh Hejazi ◽

Vahid Ebrahimi ◽

Mehrdad Asgary ◽

Abbas Piryaei ◽

Mohammad Javad Fridoni ◽

...

Keyword(s):

Stem Cells ◽

Mesenchymal Stem Cells ◽

Bone Healing ◽

Critical Size ◽

Therapeutic Potential ◽

Rna Extraction ◽

Osteotomy Site ◽

Cell Groups ◽

The Right

AbstractOsteoporosis is a common bone disease that results in elevated risk of fracture, and delayed bone healing and impaired bone regeneration are implicated by this disease. In this study, Elastin/Polycaprolactone/nHA nanofibrous scaffold in combination with mesenchymal stem cells were used to regenerate bone defects. Cytotoxicity, cytocompatibility and cellular morphology were evaluated in vitro and observations revealed that an appropriate environment for cellular attachment, growth, migration, and proliferation is provided by this scaffold. At 3 months following ovariectomy (OVX), the rats were used as animal models with an induced critical size defect in the femur to evaluate the therapeutic potential of osteogenic differentiation of bone marrow mesenchymal stem cells (BM-MSCs) seeded on 3 dimension (3D) scaffolds. In this experimental study, 24 female Wistar rats were equally divided into three groups: Control, scaffold (non-seeded BM-MSC), and scaffold + cell (seeded BM-MSC) groups. 30 days after surgery, the right femur was removed, and underwent a stereological analysis and RNA extraction in order to examine the expression of Bmp-2 and Vegf genes. The results showed a significant increase in stereological parameters and expression of Bmp-2 and Vegf in scaffold and scaffold + cell groups compared to the control rats. The present study suggests that the use of the 3D Elastin/Polycaprolactone (PCL)/Nano hydroxyapatite (nHA) scaffold in combination with MSCs may improve the fracture regeneration and accelerates bone healing at the osteotomy site in rats.

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Engineered Stem Cells Improve Neurogenic Bladder by Overexpressing SDF-1 in a Pelvic Nerve Injury Rat Model

Cell Transplantation ◽

10.1177/0963689720902466 ◽

2020 ◽

Vol 29 ◽

pp. 096368972090246 ◽

Cited By ~ 2

Author(s):

Guan Qun Zhu ◽

Seung Hwan Jeon ◽

Kyu Won Lee ◽

Hyuk Jin Cho ◽

U-Syn Ha ◽

...

Keyword(s):

Stem Cells ◽

Mesenchymal Stem Cells ◽

Growth Factor ◽

Neurogenic Bladder ◽

Rat Model ◽

Bladder Wall ◽

Bladder Function ◽

Pelvic Nerve ◽

Injured Nerve

There is still a lack of sufficient research on the mechanism behind neurogenic bladder (NB) treatment. The aim of this study was to explore the effect of overexpressed stromal cell-derived factor-1 (SDF-1) secreted by engineered immortalized mesenchymal stem cells (imMSCs) on the NB. In this study, primary bone marrow mesenchymal stem cells (BM-MSCs) were transfected into immortalized upregulated SDF-1-engineered BM-MSCs (imMSCs/eSDF-1+) or immortalized normal SDF-1-engineered BM-MSCs (imMSCs/eSDF-1−). NB rats induced by bilateral pelvic nerve (PN) transection were treated with imMSCs/eSDF-1+, imMSCs/eSDF-1−, or sham. After a 4-week treatment, the bladder function was assessed by cystometry and voiding pattern analysis. The PN and bladder tissues were evaluated via immunostaining and western blotting analysis. We found that imMSCs/eSDF-1+ expressed higher levels of SDF-1 in vitro and in vivo. The treatment of imMSCs/eSDF-1+ improved NB and evidently stimulated the recovery of bladder wall in NB rats. The recovery of injured nerve was more effective in the NB+imMSCs/eSDF-1+ group than in other groups. High SDF-1 expression improved the levels of vascular endothelial growth factor and basic fibroblast growth factor. Apoptosis was decreased after imMSCs injection, and was detected rarely in the NB+imMSCs/eSDF-1+ group. Injection of imMSCs boosted the expression of neuronal nitric oxide synthase, p-AKT, and p-ERK in the NB+imMSCs/eSDF-1+ group than in other groups. Our findings demonstrated that overexpression of SDF-1 induced additional MSC homing to the injured tissue, which improved the NB by accelerating the restoration of injured nerve in a rat model.

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