scholarly journals Effects of Lipid Deposition on Viscoelastic Response in Human Hepatic Cell Line HepG2

2021 ◽  
Vol 12 ◽  
Author(s):  
Rui Li ◽  
Yang Bu ◽  
Chendong Yang ◽  
Jizeng Wang
Keyword(s):  
Mechanical Properties ◽  
Hepatic Steatosis ◽  
Early Stage ◽  
Relaxation Modulus ◽  
Liver Lesion ◽  
Lipid Deposition ◽  
Pathological Feature ◽  
Quantitative Changes ◽  
Power Law Creep

Hepatic steatosis is associated with various liver diseases. The main pathological feature of steatosis is the excessive lipid accumulation. Ultrasound has been extensively used for the diagnosis of hepatic steatosis. However, most ultrasound-based non-invasive methods are still not accurate enough for cases with light lipid infiltration. One important reason is that the extent to which lipid infiltration may affect mechanical properties of hepatocytes remains unknown. In this work, we used atomic force microscope and in vitro dose-dependent lipid deposition model to detect the quantitative changes of mechanical properties under different degrees of steatosis in a single-cell level. The results show that hepatic cells with lipid deposition can be treated as linear viscoelastic materials with the power law creep compliance and relaxation modulus. Further analysis showed that even slight accumulation of lipid can lead to measurable decrease of stiffness and increased fluidity in liver cells. The accurate detection of viscoelastic properties of hepatocytes and the analysis methods may provide novel insights into hepatic steatosis grading, especially in the very early stage with reversible liver lesion. The application of viscoelasticity index for grading fat deposition might be a new detection indicator in future clinical diagnosis.

Novel Strategy of the Determination of Mechanical Properties of Human Carotid Atherosclerotic Plaques

2012 ◽  
Author(s):  
Renate W. Boekhoven ◽  
Richard G. P. Lopata ◽  
Marcel C. M. Rutten ◽  
Marc R. H. M. van Sambeek ◽  
Frans N. van de Vosse
Keyword(s):  
Mechanical Properties ◽  
Carotid Endarterectomy ◽  
Early Stage ◽  
Three Dimensions ◽  
Atherosclerotic Plaques ◽  
Ct Data ◽  
Novel Strategy ◽  
Unstable Plaques ◽  
Set Up

Carotid endarterectomy is the procedure of choice in patients with a recent symptomatic stenosis of 70–99%. Currently, the selection of candidates eligible for carotid endarterectomy is based on stenosis size only. However, the treatment is only beneficial for patients with unstable plaques, which comprises only 16% of the patient population [1]. Hence, identifying plaque stability at an early stage would permit timely intervention, while substantially reducing overtreatment of stable plaques. The objective of this study is to distinguish between stable and unstable carotid atherosclerotic plaques by determining the plaque geometry, the plaque composition and the mechanical properties of plaque components in three dimensions (3D). Mechanical properties from healthy vessels were assessed earlier by van den Broek et al. [2] using ultrasound (US) imaging. They obtained a dynamic dataset in 2D + t. When blood pressure and vessel wall movement are known, mechanical properties can be extracted from these data using a constitutive model. However, atherosclerotic plaques are mostly asymmetric, and present calcifications will cause unfavorable acoustic shadowing when using US. In this study, the focus is on the assessment of plaque geometry, from in vitro echo-CT data, overcoming the aforementioned problems. In an experimental set-up (Fig. 1) both healthy and endarterectomy specimens were mounted, and exposed to physiological intraluminal pressures. Echo-CT was used to image the arterial segments in 3D+t. Automated geometry assessment of the arterial segments will be demonstrated and validated using microCT (μCT).

In Vitro Three Dimensional Imaging of Human Carotid Atherosclerotic Plaques Using Ultrasonography

2011 ◽  
Author(s):  
Renate W. Boekhoven ◽  
Marcel C. M. Rutten ◽  
Marc R. H. M. van Sambeek ◽  
Frans N. van de Vosse
Keyword(s):  
Mechanical Properties ◽  
Carotid Artery ◽  
Carotid Endarterectomy ◽  
Early Stage ◽  
Three Dimensional ◽  
Atherosclerotic Plaques ◽  
Unstable Plaques ◽  
Human Carotid ◽  
Selection Of

Ruptured atherosclerotic plaques in the carotid artery are the main cause of stroke (70–80%). To prevent it, carotid endarterectomy is the procedure of choice in patients with a recent symptomatic 70–99% stenosis. Today, the selection of candidates is based on stenosis size only. However, endarterectomy is beneficial for only 1 out of 6 patients [1], the patients with unstable plaques (Fig. 1). Knowledge of mechanical properties of different components in the atherosclerotic arteries is important, because it will allow the identification of plaque stability at an early stage.

scholarly journals Ginsenoside Rg1 Ameliorates Palmitic Acid-Induced Hepatic Steatosis and Inflammation in HepG2 Cells via the AMPK/NF-κB Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Qing Xiao ◽  
Shujun Zhang ◽  
Cheng Yang ◽  
Ruoyang Du ◽  
Jinqiu Zhao ◽  
...  
Keyword(s):  
Palmitic Acid ◽  
Hepatic Steatosis ◽  
Proinflammatory Cytokines ◽  
Hepg2 Cells ◽  
Nuclear Translocation ◽  
Lipid Deposition ◽  
Ginsenoside Rg1 ◽  
Oil Red O Staining ◽  
Oil Red O

Nonalcoholic fatty liver disease (NAFLD) is one of the common diseases in the world, and it can progress from simple lipid accumulation to sustained inflammation. The present study was designed to investigate the effects and underlying mechanisms of ginsenoside Rg1 (G-Rg1) treatment on NAFLD in vitro. HepG2 cells were treated with palmitic acid (PA) to induce steatosis and inflammation and then successively incubated with G-Rg1. Lipids accumulation was analyzed by Oil Red O staining and intracellular triglyceride (TG) quantification. Inflammatory conditions were examined by quantifying the levels of cell supernatant alanine transaminase/aspartate aminotransferase (ALT/AST) and secretory proinflammatory cytokines, including IL-1β, IL-6, and TNF-α in the cell supernatants. Quantitative RT-PCR and western blotting were used to measure the expressions of genes and proteins associated with lipogenic synthesis and inflammation, including AMP-activated protein kinase (AMPK) and nuclear factor-kappa B (NF-κB) pathways. HepG2 cells were pretreated with an AMPK inhibitor; then, Oil Red O staining and TG quantification were performed to study the lipid deposition. Phospho-AMPK (Thr172) (p-AMPK) and phospho-acetyl-CoA carboxylase (Ser79) (p-ACCα) were quantified by immunoblotting. Immunofluorescence was performed to demonstrate the nuclear translocation of NF-κB P65. The present study showed that PA markedly increased the intracellular lipid droplets accumulation and TG levels, but decreased AMPK phosphorylation and the expressions of its downstream lipogenic genes. However, G-Rg1 alleviated hepatic steatosis and reduced the intracellular TG content; these changes were accompanied by the activation of the AMPK pathway. In addition, blocking AMPK by using the AMPK inhibitor markedly abolished the G-Rg1-mediated protection against PA-induced lipid deposition in HepG2 cells. Furthermore, G-Rg1 reduced the ALT/AST levels and proinflammatory cytokines release, which were all enhanced by PA. These effects were correlated with the inactivation of the NF-κB pathway and translocation of P65 from the cytoplasm to the nucleus. Overall, these results suggest that G-Rg1 effectively ameliorates hepatic steatosis and inflammation, which might be associated with the AMPK/NF-κB pathway.

Resveratrol Ameliorates Alcoholic Fatty Liver by Inducing Autophagy

2016 ◽  
Vol 44 (06) ◽  
pp. 1207-1220 ◽  
Author(s):  
Liying Tang ◽  
Fengli Yang ◽  
Zhirui Fang ◽  
Chengmu Hu
Keyword(s):  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Lipid Accumulation ◽  
Early Stage ◽  
Low Density Lipoprotein ◽  
Specific Inhibitor ◽  
Density Lipoprotein ◽  
Protective Effects ◽  
Alcoholic Fatty Liver

Alcoholic fatty liver (AFL) is early stage of alcoholic liver disease, which can progress to steatohepatitis, fibrosis, and cirrhosis if alcohol consumption is continued. The pathogenesis of AFL is associated with excessive lipid accumulation in hepatocytes. Resveratrol (RES), a dietary polyphenol found in red wines and grapes, has been shown to have a hepatoprotective effect. Autophagy is a crucial physiological process in cellular catabolism that involves the regulation of lipid droplets. Autophagy maintains a balance between protein synthesis, degradation and self-recycling. In the present study, we evaluated the protective effects of RES (10[Formula: see text]mg/kg, 30[Formula: see text]mg/kg, 100[Formula: see text]mg/kg) on AFL mice fed with an ethanol Lieber-DeCarli liquid diet, and HepG2 cells in the presence of oleic acid and alcohol to investigate whether resveratrol could induce autophagy to attenuate lipid accumulation. The results showed that RES (30[Formula: see text]mg/kg and 100[Formula: see text]mg/kg) treatment significantly attenuated hepatic steatosis and lowered the activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), low density lipoprotein cholesterol (LDL-C). H&E staining showed that RES reduced hepatic lipid accumulation. Transmission electron microscopy (TEM) images showed that RES treatment increased the number of autophagosomes and promoted the formation of autophagy. Western blot analysis showed that RES treatment increased the levels of microtubule-associated protein light chain3- II (LC3-II) and Beclin1, decreased expression of p62 protein. In addition, in vitro studies also demonstrated that RES led to the formation of acidic vesicular organelles (AVOs), however, 3-Methyladenine (3-MA), a specific inhibitor of autophagy, obviously inhibited the above effects of RES. In conclusion, RES has protective effects on alcoholic hepatic steatosis, and the potential mechanism might be involved in inducing autophagy.

scholarly journals Inhibition of Semaphorin 4D/Plexin-B1 Signal Inhibits the Subchondral Bone Loss in Early-Stage Osteoarthritis of Temporomandibular Joint

2021 ◽  
Author(s):  
Zhaoyichun Zhang ◽  
Lei Lu ◽  
Tao Ye ◽  
Shibin Yu ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Formation ◽  
Temporomandibular Joint ◽  
Subchondral Bone ◽  
Early Stage ◽  
Cartilage Degeneration ◽  
Pathological Feature ◽  
Semaphorin 4D ◽  
New Therapeutic Approaches

Subchondral bone loss is an important pathological feature of early-stage temporomandibular joint (TMJ) osteoarthritis (OA). Previous studies focused mainly on the bone resorption by osteoclasts in early-stage OA, but the bone formation feature has not drawn enough attention. Sema4D/Plexin-B1 is a pair of molecules expressed by osteoclast/osteoblast, which is capable of inhibiting bone formation by osteoblasts. The present study found that subchondral bone loss in early-stage TMJ OA was accompanied by up-regulated expression of Sema4D in cartilage and subchondral bone and Plexin-B1 in subchondral bone. Reducing Sema4D level could inhibit the subchondral bone loss and cartilage degeneration of early-stage TMJ OA. In vitro, results revealed that Sema4D could reduce the expression of osteocalcin (OCN) and alkaline phosphatase (ALP), and increase the migrating capability of Plexin-B1-positive osteoblasts. Our results revealed that elevated Sema4D expression in early-stage TMJ OA might decrease the bone formation activity of osteoblasts in the subchondral bone by binding to Plexin-B1 expressed by osteoblasts. Inhibiting Sema4D/Plexin-B1 signaling in the early-stage OA holds promise as a strategy for new therapeutic approaches to osteoarthritis.

Cytocompatibility and Material Properties of Poly-carbonate Urethane/Carbon Nanofiber Composites for Neural Applications

2003 ◽  
Vol 774 ◽  
Author(s):  
Janice L. McKenzie ◽  
Michael C. Waid ◽  
Riyi Shi ◽  
Thomas J. Webster
Keyword(s):  
Mechanical Properties ◽  
Carbon Nanofibers ◽  
Material Properties ◽  
Carbon Nanofiber ◽  
Scar Tissue ◽  
Tissue Response ◽  
Positive Interactions ◽  
Weight Percentage ◽  
Poly Carbonate

AbstractCarbon nanofibers possess excellent conductivity properties, which may be beneficial in the design of more effective neural prostheses, however, limited evidence on their cytocompatibility properties exists. The objective of the present in vitro study was to determine cytocompatibility and material properties of formulations containing carbon nanofibers to predict the gliotic scar tissue response. Poly-carbonate urethane was combined with carbon nanofibers in varying weight percentages to provide a supportive matrix with beneficial bulk electrical and mechanical properties. The substrates were tested for mechanical properties and conductivity. Astrocytes (glial scar tissue-forming cells) were seeded onto the substrates for adhesion. Results provided the first evidence that astrocytes preferentially adhered to the composite material that contained the lowest weight percentage of carbon nanofibers. Positive interactions with neurons, and, at the same time, limited astrocyte functions leading to decreased gliotic scar tissue formation are essential for increased neuronal implant efficacy.

MiR-485-5p Promotes Neuron Survival through Mediating Rac1/Notch2 Signaling Pathway after Cerebral Ischemia/Reperfusion

2020 ◽  
Vol 17 (3) ◽  
pp. 259-266 ◽  
Author(s):  
Xuan Chen ◽  
Sumei Zhang ◽  
Peipei Shi ◽  
Yangli Su ◽  
Dong Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Therapeutic Option ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Small Gtpase ◽  
Luciferase Reporter ◽  
Pathological Feature ◽  
In Cells

Objective: Ischemia-reperfusion (I/R) injury is a pathological feature of ischemic stroke. This study investigated the regulatory role of miR-485-5p in I/R injury. Methods: SH-SY5Y cells were induced with oxygen and glucose deprivation/reoxygenation (OGD/R) to mimic I/R injury in vitro. Cells were transfected with designated constructs (miR-485- 5p mimics, miR-485-5p inhibitor, lentiviral vectors overexpressing Rac1 or their corresponding controls). Cell viability was evaluated using the MTT assay. The concentrations of lactate dehydrogenase, malondialdehyde, and reactive oxygen species were detected to indicate the degree of oxidative stress. Flow cytometry and caspase-3 activity assay were used for apoptosis assessment. Dual-luciferase reporter assay was performed to confirm that Rac family small GTPase 1 (Rac1) was a downstream gene of miR-485-5p. Results: OGD/R resulted in decreased cell viability, elevated oxidative stress, increased apoptosis, and downregulated miR-485-5p expression in SH-SY5Y cells. MiR-485-5p upregulation alleviated I/R injury, evidenced by improved cell viability, decreased oxidative markers, and reduced apoptotic rate. OGD/R increased the levels of Rac1 and neurogenic locus notch homolog protein 2 (Notch2) signaling-related proteins in cells with normal miR-485-5p expression, whereas miR- 485-5p overexpression successfully suppressed OGD/R-induced upregulation of these proteins. Furthermore, the delivery of vectors overexpressing Rac1 in miR-485-5p mimics-transfected cells reversed the protective effect of miR-485-5p in cells with OGD/R-induced injury. Conclusion: This study showed that miR-485-5p protected cells following I/R injury via targeting Rac1/Notch2 signaling suggest that targeted upregulation of miR-485-5p might be a promising therapeutic option for the protection against I/R injury.

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