scholarly journals Melatonin-Pretreated Mesenchymal Stem Cells Improved Cognition in a Diabetic Murine Model

2021 ◽  
Vol 12 ◽  
Author(s):  
Shaimaa Nasr Amin ◽  
Nivin Sharawy ◽  
Nashwa El Tablawy ◽  
Dalia Azmy Elberry ◽  
Mira Farouk Youssef ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Stem Cells ◽  
Animal Model ◽  
Mesenchymal Stem Cells ◽  
Synaptic Plasticity ◽  
Object Recognition ◽  
Ex Vivo ◽  
Type I ◽  
Positive Effects ◽  
Tnf Α

Diabetes mellitus (DM) is a multisystem endocrine disorder affecting the brain. Mesenchymal stem cells (MSCs) pretreated with Melatonin have been shown to increase the potency of MSCs. This work aimed to compare Melatonin, stem cells, and stem cells pretreated with Melatonin on the cognitive functions and markers of synaptic plasticity in an animal model of type I diabetes mellitus (TIDM). Thirty-six rats represented the animal model; six rats for isolation of MSCs and 30 rats were divided into five groups: control, TIDM, TIDM + Melatonin, TIDM + Stem cells, and TIDM + Stem ex vivo Melatonin. Functional assessment was performed with Y-maze, forced swimming test and novel object recognition. Histological and biochemical evaluation of hippocampal Neuroligin 1, Sortilin, Brain-Derived Neurotrophic Factor (BDNF), inducible nitric oxide synthase (iNOS), toll-like receptor 2 (TLR2), Tumor necrosis factor-alpha (TNF-α), and Growth Associated Protein 43 (GAP43). The TIDM group showed a significant decrease of hippocampal Neuroligin, Sortilin, and BDNF and a significant increase in iNOS, TNF-α, TLR2, and GAP43. Melatonin or stem cells groups showed improvement compared to the diabetic group but not compared to the control group. TIDM + Stem ex vivo Melatonin group showed a significant improvement, and some values were restored to normal. Ex vivo melatonin-treated stem cells had improved spatial working and object recognition memory and depression, with positive effects on glucose homeostasis, inflammatory markers levels and synaptic plasticity markers expression.

Allogenic fetal membrane-derived mesenchymal stem cells contribute to renal repair in experimental glomerulonephritis

2010 ◽  
Vol 299 (5) ◽  
pp. F1004-F1013 ◽  
Author(s):  
Hidetoshi Tsuda ◽  
Kenichi Yamahara ◽  
Shin Ishikane ◽  
Kentaro Otani ◽  
Atsuhiro Nakamura ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Renal Diseases ◽  
Fetal Membrane ◽  
Prostaglandin E ◽  
Acute Glomerulonephritis ◽  
Type I ◽  
Paracrine Factors ◽  
Experimental Glomerulonephritis ◽  
Tnf Α

Mesenchymal stem cells (MSC) have been reported to be an attractive therapeutic cell source for the treatment of renal diseases. Recently, we reported that transplantation of allogenic fetal membrane-derived MSC (FM-MSC), which are available noninvasively in large amounts, had a therapeutic effect on a hindlimb ischemia model (Ishikane S, Ohnishi S, Yamahara K, Sada M, Harada K, Mishima K, Iwasaki K, Fujiwara M, Kitamura S, Nagaya N, Ikeda T. Stem Cells 26: 2625–2633, 2008). Here, we investigated whether allogenic FM-MSC administration could ameliorate renal injury in experimental glomerulonephritis. Lewis rats with anti-Thy1 nephritis intravenously received FM-MSC obtained from major histocompatibility complex-mismatched ACI rats (FM-MSC group) or a PBS (PBS group). Nephritic rats exhibited an increased urinary protein excretion in the PBS group, whereas the FM-MSC group rats had a significantly lower level of increase ( P < 0.05 vs. PBS group). FM-MSC transplantation significantly reduced activated mesangial cell (MC) proliferation, glomerular monocyte/macrophage infiltration, mesangial matrix accumulation, as well as the glomerular expression of inflammatory or extracellular matrix-related genes including TNF-α, monocyte chemoattractant protein 1 (MCP-1), type I collagen, TGF-β, type 1 plasminogen activator inhibitor (PAI-1) ( P < 0.05 vs. PBS group). In vitro, FM-MSC-derived conditioned medium significantly attenuated the expression of TNF-α and MCP-1 in rat MC through a prostaglandin E2-dependent mechanism. These data suggest that transplanted FM-MSC contributed to the healing process in injured kidney tissue by producing paracrine factors. Our results indicate that allogenic FM-MSC transplantation is a potent therapeutic strategy for the treatment of acute glomerulonephritis.

scholarly journals Examining Potential Type I Diabetes Mellitus Treatment Options – A Molecular Approach

2020 ◽  
Vol 5 (1) ◽  
Keyword(s):  
Diabetes Mellitus ◽  
Stem Cells ◽  
Type I Diabetes ◽  
Treatment Options ◽  
Type I Diabetes Mellitus ◽  
Type I ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Diabetic Treatment ◽  
Diabetes Mellitus Treatment

The last few decades has seen monumental strides in both technologic and scientific advances and discoveries in the field of diabetic research. This review article discusses the background behind Type I Diabetes Mellitus (T1DM), how it is an autoimmune condition with a molecular origin dysfunction before presenting discussion on recently discovered concepts. The article explores the role that stem cells play in diabetic treatment beginning with graft harvesting before discussion of newly discovered stem cells in the spleen and what that means for treatment. Tumor necrosis factor alpha (TNF- α) is believed to play a role in therapeutic options for diabetics, as there is reason to believe that TNF-α is capable of inducing apoptosis in selectively autoreactive CD8+ T-cells and data behind utilizing TNF agonists is illustrated. Ultrasensitive c-peptide assays shed light on the true functional status of islet β cells and conclude that the decline in function occurs over decades and not months as was previously thought. All these concepts and discoveries pave the way for future clinical trials and the discovery of more curative diabetic treatment options.

scholarly journals Transplantation of bone mesenchymal stem cells effectively promotes intestine regeneration to eliminate endotoxemia and reduce mortality in the animal model of acute liver failure

2020 ◽  
Author(s):  
Ting Jiang ◽  
Geng Xia ◽  
Bo Yang ◽  
Hong-wei Zhang ◽  
Yue-shan Yin ◽  
...  
Keyword(s):  
Stem Cells ◽  
Animal Model ◽  
Mesenchymal Stem Cells ◽  
Western Blot ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Epithelial Differentiation ◽  
Brdu Incorporation ◽  
Intestinal Epithelial ◽  
Tnf Α

Abstract Background Endotoxemia based on liver failure has been reported to be related to the worse clinical outcomes, but its management remains unsatisfactory. The addition of bone marrow mesenchymal stem cells (BMSCs) could promote the recovery of liver function and increase the survival with the liver failure. However, little is known about the potential of cell therapy with endotoxemia based on liver failure. Methods BMSCs were isolated from rats, and their morphology, differentiation potential, surface markers, and cell cycle were assayed. Thioacetamide-induced acute liver failure rats were randomized to groups with or without BMSCs. During the experiment, survival was recorded. Diamine oxidase (DAO), endotoxin, interleukin-6 (IL-6) and tumor necrosis factor- alpha (TNF-α) and tissue were analyzed by enzyme-linked immunosorbent assay (ELISA), histology, and western blot. Bromodeoxynucleoside uracil (BrdU) incorporation assay was performed to observe the migration of BMSCs. The intestinal epithelial differentiation of BMSCs was induced by co culture with small intestinal crypt in rats (IEC-6). Immunofluorescence was used to analyze the expression of intestinal endothelial markers. Western blot analysis was further performed to examine the differentiation effect when inhibiting the phosphoinositide kinase-3 (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway. Results BrdU-traced BMSCs targeted migrate to intestinal injury sites. Mortality was significantly decreased and intestinal damage was repaired following BMSCs transplantation. Proteomics revealed higher expression of DAO, endotoxin, IL-6 and TNF-α in the model animals, but these changes were reversed after BMSCs transplantation. In the in vitro study, the intestinal epithelial differentiation of BMSCs was exhibited following co-culture. Moreover, the blocking of PI3K/AKT/mTOR signal pathway inhibited this differentiation. Conclusions These evidences indicate that BMSCs eliminate endotoxemia and reduce mortality in the animal model of acute liver failure by reducing intestine damage.

Study a level of TNF-α and INF-Ƴ in patients with Type I and II Diabetes Mellitus in Diayla governorate

2017 ◽  
Vol 13 (3) ◽  
pp. 196-207
Author(s):  
Mohammed Abdul-Daim Saleh ◽  
◽  
Shahrazad Ahmed Khalaf
Keyword(s):  
Diabetes Mellitus ◽  
Type I ◽  
Tnf Α
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