scholarly journals Effectiveness of Mesenchymal Stem Cells and Bovine Colostrum on Decreasing Tumor Necrosis Factor-Α Levels and Enhancement of Macrophages M2 in Remnant Liver

2021 ◽  
Vol 9 (A) ◽  
pp. 1195-1202
Author(s):  
Ezra Endria Gunadi ◽  
Yan Wisnu Prajoko ◽  
Agung Putra
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Tumor Necrosis ◽  
Wistar Rats ◽  
Tumor Necrosis Factor Α ◽  
Bovine Colostrum ◽  
Control Group ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

BACKGROUND: Mesenchymal stem cells (MSCs) and bovine colostrum are potential therapies for the treatment of various degenerative and immune diseases. AIM: This study aimed to analyze the effect of MSCs on levels of tumor necrosis factor-Α (TNF-α) and macrophages M2 in the liver fibrosis of Wistar rats after 50% resection. METHODS: This study is a quasi-experimental post-test-only control group design to analyze the effect of giving bovine colostrum and MSCs to test animals on the process of regeneration of the remaining 50% liver with fibrosis. The study was conducted at the Stem Cell and Cancer Research Universitas Sultan Agung. The number of samples used was 40 male Wistar rats. The independent variables included MSC 1.000.0000 cells and bovine colostrum at a dose of 15 μL/g. Dependent variables used were macrophages M2 and levels of TNF-α ELISA. RESULTS: TNF-α levels on day 3 were (p = 0.001), day 7 were (p = 0.01), and day 10 were (p = 0.01) in liver tissue in various study groups analyzed using ELISA on day three*. The results showed differences which were significant between the control and treatment groups (p < 0.05). The expression of CD163 marked brown in liver tissue had more expression than the control group. CONCLUSION: The combination of MSCs and bovine colostrum can reduce TNF-α levels and significantly increase macrophages expression in the liver fibrosis of Wistar rats after 50% resection on the 3th, 7th, and 10th days.

The let-7f-5p–Nme4 pathway mediates tumor necrosis factor α-induced impairment in osteogenesis of bone marrow-derived mesenchymal stem cells

2021 ◽  
pp. 1-11
Author(s):  
Ying-Jie Zhao ◽  
Zheng-Chao Gao ◽  
Xi-Jing He ◽  
Jing Li
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Tumor Necrosis Factor ◽  
Osteogenic Differentiation ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Although tumor necrosis factor α (TNF-α)-mediated inflammation significantly impacts osteoporosis, the mechanisms underlying the osteogenic differentiation defects of bone marrow-derived mesenchymal stem cells (BM-MSCs) caused by TNF-α remain poorly understood. We found that TNF-α stimulation of murine BM-MSCs significantly upregulated the expression levels of several microRNAs (miRNAs), including let-7f-5p, but this increase was significantly reversed by treatment with the kinase inhibitor BAY 11-7082. To study gain- or loss of function, we transfected cells with an miRNA inhibitor or miRNA mimic. We then demonstrated that let-7f-5p impaired osteogenic differentiation of BM-MSCs in the absence and presence of TNF-α, as evidenced by alkaline phosphatase and alizarin red staining as well as quantitative assays of the mRNA levels of bone formation marker genes in differentiated BM-MSCs. Moreover, let-7f-5p targets the 3′ untranslated region of Nucleoside diphosphate kinase 4 (Nme4) mRNA and negatively regulates Nme4 expression in mouse BM-MSCs. Ectopic expression of Nme4 completely reversed the inhibitory effects of the let-7f-5p mimic on osteogenic differentiation of mouse BM-MSCs. Furthermore, inhibition of let-7f-5p or overexpression of Nme4 in BM-MSCs restored in-vivo bone formation in an ovariectomized animal model. Collectively, our work indicates that let-7f-5p is involved in TNF-α-mediated reduction of BM-MSC osteogenesis via targeting Nme4.

The change of proinflammatory cytokine tumor necrosis factor α level in the use of meloxicam in rat model of osteoarthritis

2019 ◽  
Vol 30 (6) ◽  
Author(s):  
Junaidi Khotib ◽  
Naning Windi Utami ◽  
Maria Apriliani Gani ◽  
Chrismawan Ardianto
Keyword(s):  
Tumor Necrosis Factor ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Treatment Groups ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background Osteoarthritis (OA) is a chronic disease in the joints. One of the proinflammatory cytokines that is thought to have a major role in the inflammatory process, the emergence of pain, and cartilage damage in OA is tumor necrosis factor α (TNF-α). Meloxicam is a nonsteroidal anti-inflammatory drug class of drugs that is relatively selective in inhibiting the activity of cyclooxygenase 2 (COX-2) formation. This study is conducted to prove the change in TNF-α level in the use of meloxicam with model in animals suffering from OA. Methods The OA rat model was induced with sodium monoiodoacetate intra-articularly. Rats were divided into 5 groups: negative control group, positive control group, and treatment groups with various doses of meloxicam. Hyperalgesia effect was evaluated using a warm plate test, and TNF-α level was determined using enzyme-linked immunosorbent assay. Results The treatment groups that received meloxicam at a dose of 1.0, 3.0, or 10.0 mg/kg body weight (BW) did not show significant differences in rat knee joint diameter (p = 0.99), but showed a significant difference in sensitivity to heat stimulation (p = 0.02) compared to the control group. Osteoarthritis rats experienced a significant reduction in TNF-α level after being given meloxicam at a dose of 10 mg/kg BW compared with the control group. This shows that the 10 mg/kg BW of meloxicam is a potential dose in reducing the TNF-α level in OA rat models. Conclusions Based on these data, it can be concluded that the inhibition of pain and the development of OA by meloxicam in animal models may be assigned to a decreased level of TNF-α.

scholarly journals TINGGINYA KADAR TUMOR NECROSIS FACTOR-α (TNF-α) PLASMA PADA MENCIT BUNTING YANG TERINFEKSI PLASMODIUM BERGHEI BERHUBUNGAN KUAT DENGAN KADAR HEMOGLOBIN YANG RENDAH TETAPI TIDAK BERHUBUNGAN DENGAN BERAT BADAN JANIN RENDAH

2013 ◽  
Vol 2 (1) ◽  
pp. 51-64
Author(s):  
Yuliyanik Yuliyanik
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Placental Tissue ◽  
Control Group ◽  
Study Group ◽  
Low Weight ◽  
Tnf Α ◽  
Pregnant Mice ◽  
Factor Α ◽  
Necrosis Factor

Malaria infection in pregnancy may increase the morbidity and mortality of both mother and fetus. In pregnant women, it can lead to severe anemia, cerebral malaria, pulmonary edema, renal failure and even death, while in the fetus it can cause abortion, premature birth, low birth weight, and fetal death. Elevated levels of tumor necrosis factor-α(TNF-α ) is associated with low birth weight and anemia in pregnant women. This study was conducted to measure the levels of TNF-α in plasma and placental tissue, and hemoglobin levels as well as fetal weight to determine the relationship between them in P. berghei infected pregnant mice and normal pregnant mice. Seventeen BALB/c mice used in this study were divided into two groups, those were the study group (9 pregnant mice infected with P. berghei) and control group (8 pregnant mice not infected with P. berghei). Level of TNF-α were measured using Enzyme Linked Immunosorbent assay (R&D Systems, catalog A00B MT). Hemoglobin levels were determined using flowcytometri, whereas fetal weight were performed with Mettler analytical balance AE 50. T-test statistical analysis showed that the levels of TNF-α in plasma and placental tissue in study group were higher than control group (p=0.000, p=0.034). Hemoglobin levels in the study group were lower than control group (p=0.025). Fetal weights were also lower in fetuses of infected mice than fetuses of uninfected mice (p=0.002). Pearson correlation test showed increasing plasma levels of TNF-α in infected P. berghei pregnant mice were related with the decreasing levels of Hb, (r=-0.748; p=0.020,), whereas levels of placental TNF-α were not associated with hemoglobin level (p=0.337). Both plasma and placental levels of TNF-α were not associated with the incidence of fetal low weight (p=0.380, and p=0.365). It can be concluded that the increased levels of TNF-α is associated with decreased levels of hemoglobin (Hb), but not associated with fetal low weight.

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