Angelica polysaccharide alleviates TNF‐α‐induced MIN6 cell damage a through the up‐regulation microRNA‐143

BioFactors ◽  
2019 ◽  
Author(s):  
Yingying Zhao ◽  
Chuanqian Liu ◽  
Xueting Zhang ◽  
Xipeng Yan
Keyword(s):  
Cell Damage ◽  
Min6 Cell ◽  
Tnf Α

Alteration of intrapancreatic serotonin, homocysteine, TNF-α, and NGF levels as predisposing factors for diabetes following exposure to 900-MHz waves

2021 ◽  
pp. 074823372110226
Author(s):  
Gholamali Jelodar ◽  
Mansour Azimzadeh ◽  
Fatemeh Radmard ◽  
Narges Darvishhoo
Keyword(s):  
Cell Damage ◽  
Pancreatic Beta Cell ◽  
Predisposing Factors ◽  
Male Rats ◽  
Control Group ◽  
Predisposing Factor ◽  
Time Exposure ◽  
Tnf Α ◽  
Long Time ◽  
Short Time

Exposure to mobile phone radiation causes deleterious health effects on biological systems. The objects of this study were to investigate the effect of 900-MHz radiofrequency waves (RFW) emitted from base transceiver station antenna on intrapancreatic homocysteine (Hcy), tumor necrosis factor-α (TNF-α), and nerve growth factor (NGF) as predisposing factors involved in pancreatic beta cell damage. Thirty male rats (Sprague-Dawley, 200 ± 10 g) were randomly divided into the control (without any exposure) and exposed groups: short time (2 h/day), long time (4 h/day), and exposed to 900-MHz RFW for 30 consecutive days. On the last days of the experiment, animals were killed and pancreas tissue was dissected out for evaluation of serotonin, Hcy, TNF-α, and NGF. There was a significant decrease in the serotonin and NGF levels in the pancreatic tissue of exposed groups compared to the control group ( p < 0.05). Also, the levels of serotonin and NGF in the long-time exposure were significantly lower than the short-time exposure ( p < 0.05). However, levels of Hcy and TNF-α were significantly increased in the pancreas of exposed groups compared to the control groups ( p < 0.05). Exposure to 900-MHz RFW decreased pancreatic NGF and serotonin levels and increased the proinflammatory markers (Hcy and TNF-α), which can be a predisposing factor for type 2 diabetes.

Tetrahydroxystilbene Glucoside Improves TNF-α-Induced Endothelial Dysfunction: Involvement of TGFβ/Smad Pathway and Inhibition of Vimentin Expression

2015 ◽  
Vol 43 (01) ◽  
pp. 183-198 ◽  
Author(s):  
Wenjuan Yao ◽  
Chengjing Gu ◽  
Haoran Shao ◽  
Guoliang Meng ◽  
Huiming Wang ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Nuclear Translocation ◽  
Cell Damage ◽  
Umbilical Vein ◽  
Polygonum Multiflorum ◽  
Vimentin Expression ◽  
Smad Signaling ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells

Endothelial dysfunction plays an important role in the pathogenesis of atherogenesis. 2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside (TSG), an active component of the rhizome extract from Polygonum multiflorum (PM), exhibits significant anti-atherosclerotic activity. Here, we used human umbilical vein endothelial cells (HUVECs) induced by tumor necrosis factor-α (TNF-α) in vitro to investigate the cytoprotective effects of TSG on TNF-α-induced endothelial injury and the related mechanisms. Pretreatment with 50 and 100 μM TSG markedly attenuated TNF-α-induced loss of cell viability and release of lactate dehydrogenase (LDH) and inhibited TNF-α-induced cell apoptosis. The inhibition of vimentin expression was involved in the cytoprotection afforded by TSG. Using inhibitors for PI3K and TGFβ or siRNA for Akt and Smad2, we found that vimentin production in HUVECs is regulated by TGFβ/Smad signaling, but not by PI3K–Akt–mTOR signaling. Meanwhile, TSG inhibited both the expression of TGFβ1 and the phosphorylation of Smad2 and Smad3, and TSG suppressed the nuclear translocation of Smad4 induced by TNF-α. These results suggest that TSG protects HUVECs against TNF-α-induced cell damage by inhibiting vimentin expression via the interruption of the TGFβ/Smad signaling pathway.

scholarly journals Biocompatibility of Bone Marrow-Derived Mesenchymal Stem Cells in the Rat Inner Ear following Trans-Tympanic Administration

2020 ◽  
Vol 9 (6) ◽  
pp. 1711 ◽  
Author(s):  
Adrien A. Eshraghi ◽  
Emre Ocak ◽  
Angela Zhu ◽  
Jeenu Mittal ◽  
Camron Davies ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Inner Ear ◽  
Cell Damage ◽  
Tunel Staining ◽  
Tnf Α ◽  
Rat Cochlea ◽  
Necrosis Factor

Recent advancements in stem cell therapy have led to an increased interest within the auditory community in exploring the potential of mesenchymal stem cells (MSCs) in the treatment of inner ear disorders. However, the biocompatibility of MSCs with the inner ear, especially when delivered non-surgically and in the immunocompetent cochlea, is not completely understood. In this study, we determined the effect of intratympanic administration of rodent bone marrow MSCs (BM-MSCs) on the inner ear in an immunocompetent rat model. The administration of MSCs did not lead to the generation of any oxidative stress in the rat inner ear. There was no significant production of proinflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and IL-12, due to BM-MSCs administration into the rat cochlea. BM-MSCs do not activate caspase 3 pathway, which plays a central role in sensory cell damage. Additionally, transferase dUTP nick end labeling (TUNEL) staining determined that there was no significant cell death associated with the administration of BM-MSCs. The results of the present study suggest that trans-tympanic administration of BM-MSCs does not result in oxidative stress or inflammatory response in the immunocompetent rat cochlea.

The role of protein kinase C isozymes in TNF-α-induced cytotoxicity to a rat intestinal epithelial cell line

2001 ◽  
Vol 280 (4) ◽  
pp. G572-G583 ◽  
Author(s):  
Q. Chang ◽  
B. L. Tepperman
Keyword(s):  
Epithelial Cell ◽  
Caspase 3 ◽  
Cell Injury ◽  
Cell Damage ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial ◽  
Kinase C ◽  
Pkc Isoforms ◽  
Tnf Α

Tumor necrosis factor (TNF)-α can induce cytotoxicity and apoptosis in a number of cell types and has been implicated in the regulation of many inflammatory processes. It has been suggested that protein kinase C (PKC) is one of the intracellular mediators of the actions of TNF-α. In the present study, the role of PKC isoforms in TNF-α-mediated cytotoxicity and apoptosis in intestinal cells was investigated using the rat epithelial cell line, IEC-18. Cells were incubated with TNF-α in the presence or absence of the transcription inhibitor actinomycin D (AMD). The extent of cell damage was enhanced when AMD was added to incubation medium, suggesting that new protein synthesis plays a role in the cytotoxic action of TNF. TNF-α also induced the translocation of PKC-α, -δ, and -ε from cytosol to the membrane fraction of the intestinal cells. Furthermore, the cytotoxic and apoptotic effects of TNF were reduced by pretreating the cells with the PKC-ε translocation inhibitor, PKC-εV1–2. In contrast, although cells incubated with the phorbol ester phorbol 12-myristate 13-acetate (PMA) also displayed an increase in cell injury, the extent of cytotoxicity and apoptosis was not enhanced by AMD. Furthermore, PMA-induced cell damage was reduced by rottlerin, a PKC-δ inhibitor. Caspase-3, an enzyme implicated in the mediation of apoptosis, was activated in cells in response to either TNF-α or PMA stimulation, and its effects on this activity were reduced by selective inhibition of PKC-ε and -δ, respectively. Furthermore, inhibition of caspase-3 activity reduced apoptosis. These data suggest that activation of selective PKC isoforms mediate the effects of TNF-α on intestinal epithelial cell injury.

scholarly journals Tripterine up-regulates miR-223 to alleviate lipopolysaccharide-induced damage in murine chondrogenic ATDC5 cells

2019 ◽  
Vol 33 ◽  
pp. 205873841882452 ◽  
Author(s):  
Xuefu Li ◽  
Wei Wei ◽  
Zhongquan Zhao ◽  
Shuzhen Lv
Keyword(s):  
Western Blot ◽  
Therapeutic Potential ◽  
Cell Damage ◽  
Quantitative Polymerase Chain Reaction ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inhibitory Effects ◽  
Tnf Α ◽  
Associated Proteins ◽  
Regulatory Effects ◽  
Induced Apoptosis

Tripterine, also known as celastrol, is a main natural ingredient in Tripterygium wilfordii. Tripterine has a variety of pharmacological functions, and the therapeutic potential of tripterine in many kinds of inflammation-linked diseases has been revealed. However, the function of tripterine on osteoarthritis still remains unclear. The objective of this study was to study the function of tripterine (TPR) on lipopolysaccharide (LPS)-injured chondrocyte. ATDC5 cells were treated with tripterine after LPS stimulation and then cell survival, the release of pro-inflammatory cytokines, and the expression of chondrogenic differentiation-associated proteins were assessed by performing CCK-8, flow cytometry, reverse transcription quantitative polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and Western blot. Moreover, the expression of miR-223 and core factors in PI3K/AKT and nuclear factor kappa B (NF-κB) signaling was tested by RT-qPCR/Western blot. LPS stimulation significantly reduced ATDC5 cells viability, induced apoptosis, and increased the release of interleukin (IL)-6 and tumor necrosis factor (TNF)-α. Tripterine protected ATDC5 cells against LPS-induced chondrocyte loss and the release of IL-6 and TNF-α. miR-223 was down-regulated by LPS, while was up-regulated by tripterine. The protective actions of tripterine were eliminated when miR-223 was silenced. Besides, tripterine inhibited hypertrophic differentiation induced by LPS, and the inhibitory effects of tripterine on hypertrophic differentiation could be abolished when miR-223 was silenced. Furthermore, tripterine activated PI3K/AKT pathway and deactivated NF-κB pathway. And the regulatory effects of tripterine on these two pathways were abolished by miR-223 silence. This study revealed that tripterine protected ATDC5 cells against LPS-induced cell damage possibly via up-regulation of miR-223 and modulation of NF-κB and PI3K/AKT pathways.

scholarly journals An Immuno-Cardiac Model for Macrophage-Mediated Inflammation in COVID-19 Hearts

2021 ◽  
Author(s):  
Liuliu Yang ◽  
Yuling Han ◽  
Fabrice Jaffre ◽  
Benjamin E Nilsson-Payant ◽  
Yaron Bram ◽  
...  
Keyword(s):  
Cell Damage ◽  
Case Reports ◽  
Cardiac Injury ◽  
Cardiac Complications ◽  
Rna Seq ◽  
Inflammatory Infiltration ◽  
Drug Candidates ◽  
Cardiac Model ◽  
Tnf Α ◽  
Clinically Significant

Rationale: While respiratory failure is a frequent and clinically significant outcome of COVID-19, cardiac complications are a common feature in hospitalized COVID-19 patients and are associated with worse patient outcomes. The cause of cardiac injury in COVID-19 patients is not yet known. Case reports of COVID-19 autopsy heart samples have demonstrated abnormal inflammatory infiltration of macrophages in heart tissues. Objective: Generate an immuno-cardiac co-culture platform to model macrophage-mediated hyper-inflammation in COVID-19 hearts and screen for drugs that can block the macrophage-mediated inflammation. Methods and Results: We systematically compared autopsy samples from non-COVID-19 donors and COVID-19 patients using RNA-seq and immunohistochemistry. We observed strikingly increased expression levels of CCL2 as well as macrophage infiltration in heart tissues of COVID-19 patients. We generated an immuno-cardiac co-culture platform containing human pluripotent stem cell (hPSC)-derived cardiomyocytes (CMs) and macrophages. We found that macrophages induce increased reactive oxygen species (ROS) and apoptosis in CMs by secreting IL-6 and TNF-α after SARS-CoV-2 exposure. Using this immuno-cardiac co-culture platform, we performed a high content screen and identified ranolazine and tofacitinib as compounds that protect CMs from macrophage-induced cardiotoxicity. Conclusions: We established an immuno-host co-culture system to study macrophage-induced host cell damage following SARS-CoV-2 infection and identified FDA-approved drug candidates that alleviate the macrophage-mediated hyper-inflammation and cellular injury.

scholarly journals Biomechanical signals upregulate myogenic gene induction in the presence or absence of inflammation

2007 ◽  
Vol 293 (1) ◽  
pp. C267-C276 ◽  
Author(s):  
Ravi Chandran ◽  
Thomas J. Knobloch ◽  
Mirela Anghelina ◽  
Sudha Agarwal
Keyword(s):  
Cell Differentiation ◽  
Muscle Cell ◽  
Kinase Inhibitor ◽  
Cell Damage ◽  
Myogenic Differentiation ◽  
C2c12 Cell ◽  
Gene Induction ◽  
C2c12 Cells ◽  
Proinflammatory Mediators ◽  
Tnf Α

Inflammation of the muscle invariably leads to muscle cell damage and impaired regeneration. Biomechanical signals play a vital role in the regulation of myogenesis in healthy and inflamed muscle. We hypothesized that biomechanical signals counteract the actions of proinflammatory mediators and upregulate the basic helix-loop-helix and MADS box transcription enhancer factor 2 (MEF2) families of transcription factors, leading to increased myogenesis in inflamed muscle cells. For this purpose, C2C12 cells plated on collagenized silastic membranes were subjected to equibiaxial cyclic tensile strain (CTS) in the presence or absence of TNF-α, and the myogenic gene induction was examined over a period of 72 h. Exposure of cells to CTS resulted in a significant upregulation of mRNA expressions and synthesis of myogenic regulatory factors, MYOD1, myogenin (MYOG), MEF2A, and cyclin-dependent kinase inhibitor 1A (CDKN1A; p21) as well as muscle structural proteins like myosin heavy chain (MYHC) isoforms (MYH1, MYH2, and MYH4) and α-tropomyosin (TPM1), eventually leading to an increase in myotube formation. Contrarily, TNF-α suppressed the expression of all of the above differentiation-inducing factors in C2C12 cells. Further results revealed that simultaneous exposure of C2C12 cells to CTS and TNF-α abrogated the TNF-α-mediated downregulation of myogenic differentiation. In fact, the mRNA expression and protein synthesis of all myogenic factors ( Myod1, Myog, Mef2a, Cdkn1a, Myh1, Myh2, Myh4, and Tpm1) were increased in stretched C2C12 cells despite the sustained presence of TNF-α. These results demonstrate that mechanotransduction regulates multiple signaling molecules involved in C2C12 cell differentiation. On one hand, these signals are potent transducers of myotube phenotype in myoblasts; on the other, these signals counteract catabolic actions of proinflammatory cytokines like TNF-α and allow the expression of myogenic genes to upregulate muscle cell differentiation.

Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation

2005 ◽  
Vol 288 (2) ◽  
pp. L317-L325 ◽  
Author(s):  
Branislava Janic ◽  
Todd M. Umstead ◽  
David S. Phelps ◽  
Joanna Floros
Keyword(s):  
Immune Cells ◽  
Cytokine Production ◽  
Cell Damage ◽  
Surfactant Protein ◽  
Proinflammatory Cytokine Production ◽  
Tnf Α ◽  
In Vitro Systems ◽  
Alveolar Proteinosis

Ozone (O3), a major component of air pollution and a strong oxidizing agent, can lead to lung injury associated with edema, inflammation, and epithelial cell damage. The effects of O3on pulmonary immune cells have been studied in various in vivo and in vitro systems. We have shown previously that O3exposure of surfactant protein (SP)-A decreases its ability to modulate proinflammatory cytokine production by cells of monocyte/macrophage lineage (THP-1 cells). In this report, we exposed THP-1 cells and/or native SP-A obtained from bronchoalveolar lavage of patients with alveolar proteinosis to O3and studied cytokine production and NF-κB signaling. The results showed 1) exposure of THP-1 cells to O3significantly decreased their ability to express TNF-α in response to SP-A; TNF-α production, under these conditions, was still significantly higher than basal (unstimulated) levels in filtered air-exposed THP-1 cells; 2) exposure of both THP-1 cells and SP-A to O3did not result in any significant differences in TNF-α expression compared with basal levels; 3) O3exposure of SP-A resulted in a decreased ability of SP-A to activate the NF-κB pathway, as assessed by the lack of significant increase and decrease of the nuclear p65 subunit of NF-κB and cytoplasmic IκBα, respectively; and 4) O3exposure of THP-1 cells resulted in a decrease in SP-A-mediated THP-1 cell responsiveness, which did not seem to be mediated via the classic NF-κB pathway. These findings indicate that O3exposure may mediate its effect on macrophage function both directly and indirectly (via SP-A oxidation) and by involving different mechanisms.

scholarly journals Gastric Cytoprotection as Basis of Gastrointestinal Mucosa Protection and Repair in Erosive Ulcerative Lesions of Various Aetiologies

2020 ◽  
Vol 30 (5) ◽  
pp. 7-17
Author(s):  
K. V. Ivashkin ◽  
E. A. Izatullaev ◽  
V. R. Korneeva
Keyword(s):  
Cell Damage ◽  
Current Treatment ◽  
Gastrointestinal Mucosa ◽  
Gastroduodenal Mucosa ◽  
Gastric Cytoprotection ◽  
Tnf Α ◽  
Vitamin U ◽  
Ulcerative Lesions ◽  
Mucin Release ◽  
Treatment Settings

Aim. Assessment of efficacy and the mechanism of action of gastrointestinal mucosa (GM) protection in current treatment settings with methylmethionine-sulfonium chloride (vitamin U) to illustrate its applicability in erosive ulcerative lesions of various aetiologies.Key points. Aside to damage prevention in exposure to aggressive agents, gastroprotection implies healing promotion under the preserved level of hydrochloric acid secretion. Prostaglandins (PG) and SH-antioxidants are key mediators of gastroprotection in acute and chronic damage. SH-containing endogenous substances (L-cysteine, D,L-methionine, GSH) and exogenous molecules (methylmethionine-sulfonium chloride (MMSC), N-acetylcysteine) prevent damage due to the ability to absorb/neutralise free radicals released in xenobiotic-triggered cell damage, inhibit TNF-α expression, reduce the aspirin-induced leukocyte-endothelium adhesion and stimulate mucin release. In experiment, MMSC prevented the ethanol-induced GM damage, stimulated mucin release and its redistribution on the GM surface; in clinical trials, MMSC effectively facilitated remission in duodenal ulcer.Conclusion. Preparations exerting a protective effect on gastroduodenal mucosa, such as methylmethionine-sulfonium chloride (vitamin U), may improve basic treatment settings and facilitate remission in erosive ulcerative lesions of upper gastrointestinal tract.

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