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Abstract

 

Objectives

 

Transfusion of umbilical cord‐derived mesenchymal stem cells (UC‐MSCs) is a novel strategy for treatment of various liver diseases. However, the therapeutic effect of UC‐MSCs is limited because only a few UC‐MSCs migrate towards the damaged regions. In this study, we observed the effects of autophagy on the migration of UC‐MSCs in vitro and in a model of liver ischaemia/reperfusion (I/R) injury.

 

Materials and Methods

 

We investigated the effects of autophagy on the status of the cell, release of anti‐inflammatory factors and migration of UC‐MSCs in vitro. The therapeutic effects and in vivo migration of rapamycin‐preconditioned UC‐MSCs were observed in a C57/B6 mouse model of liver I/R injury.

 

Results

 

Induction of autophagy by rapamycin enhanced the ability of UC‐MSCs to migrate and release anti‐inflammatory cytokines as well as increased expression of CXCR4 without affecting cell viability. Inhibition of CXCR4 activation markedly decreased migration of these cells. In a mouse model of liver I/R injury, we found significantly upregulated expression of CXCR12 in the damaged liver. More rapamycin‐preconditioned UC‐MSCs migrated towards the ischaemic regions than 3‐methyladenine‐preconditioned or non‐preconditioned UC‐MSCs, leading to improvement in hepatic performance, pathological changes and levels of inflammatory cytokines. These effects were abolished by AMD3100.

 

Conclusions

 

Preconditioning of UC‐MSCs by rapamycin afforded increased protection against liver I/R injury by enhancing immunosuppression and strengthening the homing and migratory capacity of these cells via the CXCR4/CXCL12 axis.


The negative effect of ANGPTL8 on HDL-mediated cholesterol efflux capacity

Posted by MD Luo, ZY Zhang, S Wang, et al. on 2018-12-27 15:20:00

Abstract

 

Background

 

It is well known that angiopoietin-like protein 8 (ANGPTL8) exerts its effects on lipid metabolism through the inhibition of lipoprotein lipase and subsequent elevation of plasma triglyceride. However, it is not clear whether ANGPTL8 could affect lipid metabolism via other pathways. The study was aimed to investigate the effects of ANGPTL8 on the function of high-density lipoprotein (HDL), which plays a protective role in atherosclerosis progression.

 

Methods

 

Two hundred and ten subjects were recruited. Plasma ANGPTL8 was measured by enzyme-linked immunosorbent assays. Cholesterol efflux capacity was chosen as the biomarker of HDL function and measured via H3-cholesterol loading THP-1 cell models.

 

Results

 

ANGPTL8 exhibited no significant difference between CAD group and nonCAD group, but ANGPTL8 in DM group was significantly higher than that in the nonDM group [568.3 (406.2–836.8) vs 458.2 (356.8–755.6), P?=?0.023]. Compared to controls, subjects in CAD group and DM group exhibited significantly lower cholesterol efflux capacity [CAD: 14.58?±?2.06 vs 12.51?±?2.83%, P?<?0.0001; DM: 13.62?±?2.57 vs 12.34?±?3.16%, P?=?0.0099]. ANGPTL8 was inversely correlated with cholesterol efflux capacity (r?=???0.188, P?<?0.01). Regression analysis revealed that plasma ANGPTL8 was an independent contributor to cholesterol efflux capacity (standardized β?=???0.143, P?=?0.023).

 

Conclusion

 

ANGPTL8 presents a negative effect on HDL-mediated cholesterol efflux capacity.

 

Keywords

ANGPTL8 Cholesterol efflux capacity Coronary artery disease Diabetes

Protective role of chrysin on thioacetamide-induced hepatic encephalopathy in rats

Posted by S A. El-Marasy, S A. El Awdan, R M. Abd-Elsalam. on 2018-12-27 10:36:00

Abstract

Hepatic encephalopathy (HE) is a serious neuropsychiatric syndrome due to either acute or chronic hepatic failure. This study aimed to investigate the possible neuroprotective effect of chrysin, a natural flavenoid on thioacetamide (TAA)-induced hepatic encephalopathy in rats. Also the effect of chrysin on motor impairment, cognitive deficits, oxidative stress, neuroinflammation, apoptosis and histopathological damage was assessed. HE was induced in Wistar rats by intraperitoneal (i.p.) injection of TAA (200?mg/kg) for three alternative days. Normal and control groups received the vehicle for 21 days. Chrysin was administered orally for 21 days (25, 50, 100?mg/kg) and starting from day 17, rats received i.p. dose of TAA (200?mg/kg) at three alternative days. Then behavioral, biochemical, histopathological and immunohistochemical analyses were conducted. Chrysin improved TAA-induced motor incoordination as it reduced final falling latency time in rotarod test, ameliorated cognitive deficits in object recognition test (ORT) and attenuated serum ammonia, hepatic liver enzymes namely, aspartate aminotransferase (AST) and alanine aminotransferase (ALT), reduced malondialdehyde (MDA), elevated reduced glutathione (GSH), reduced nuclear factor kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) brain contents. Chrysin administration also reduced Toll-4 receptor (TLR-4) gene expression, caspase-3 protein expression, hepatic necrosis and astrocyte swelling. This study depicts that chrysin exerted neuroprotective effect in TAA-induced HE rats, evidenced by improvement of cognitive deficits, motor incoordination and histopathological changes such as astrocyte swelling and vacuolization; hallmarks in HE, via reducing hyperammonia, ameliorating hepatic function, in addition to its anti-oxidant, inactivation of TLR-4/NF-κB inflammatory pathway, and anti-apoptotic effects.


Beta-caryophyllene alleviates diet-induced neurobehavioral changes in rats: The role of CB2 and PPAR-γ receptors

Posted by D A. Youssef, H M. El-Fayoumi, M F. Mahmoud. on 2018-11-30 10:59:00

Abstract

 

Background and purpose: Insulin resistance (IR) and obesity predispose diseases such as diabetes, cardiovascular and neurodegenerative disorders. Beta-caryophyllene (BCP), a natural sesquiterpene, exerts neuroprotective, anxiolytic and antidepressant effects via its selective agonism to cannabinoid receptor 2 (CB2R). BCP was shown to have an anti-diabetic effect, however, the implication of CB2R is yet to be elucidated. A link between CB2R agonism and PPAR-γ activation has been discussed, but the exact mechanism is not well-defined. This study was designed to examine the role of BCP in improving diet-induced metabolic (insulin resistance), neurobehavioral (anxiety, depression and memory deficit), and neurochemical (oxidative, inflammatory and neurotrophic factor) alterations in the prefrontal cortex of obese rats’ brain. The involvement of CB2R and/or PPAR-γ dependent activity was also investigated.

 

Experimental approach: Male Wistar rats were fed a high fat/fructose diet (HFFD) for 12 weeks to induce IR and obesity. Rats were treated with BCP for the last 4 weeks. Either CB2R antagonist AM630 or PPAR-γ antagonist BADGE was administered before BCP treatment to study the mechanism of BCP actions.

 

Key results: Beta-caryophyllene alleviated HFFD-induced IR, oxidative-stress, neuroinflammation and behavioral changes. The anxiolytic, anti-oxidant and anti-inflammatory effects of BCP were mediated by both PPAR-γ and CB2R. The effects of BCP on glycemic parameters seem to be CB2R-dependent with the non-significant role of PPAR-γ. Furthermore, BCP-evoked antidepressant and memory improvement are likely mediated only via CB2R, mainly by upregulation of PGC-1α and BDNF.

 

Conclusion: This study suggests the potential effect of BCP in treating HFFD-induced metabolic and neurobehavioral alterations. BCP seems to activate PPAR-γ in a ligand-independent manner, via upregulation and activation of PGC-1α. The BCP activation of PPAR--γ seems to be CB2R-dependent.

Abstract

Acetochlor (ACT) is a chiral chloroacetamide pesticide that has been heavily used around the world, resulting in its residues being frequently found in surface waters. It has been reported that ACT is an endocrine disrupting chemical (EDC) with strong thyroid hormone-disrupting activity in aquatic organisms. However, the enantioselectivity underlying thyroid disruption has yet to be understood. In this study, using a zebrafish embryo-larvae model, the enantioselective thyroid disruption of ACT was investigated at a series of environmentally relevant concentrations (1, 2, 10 and 50?μg/L). Our results showed that both racemic ACT and its enantiomers significantly increased the malformation rates of embryos at 72?h postfertilization (hpf). Decreased thyroxine (T4) contents and increased triiodothyronine (T3) contents were found in larvae at 120?hpf, with (+)-S-ACT exhibiting a greater effect than (?)-R-enantiomer. Similarly, (+)-S-ACT also showed a stronger effect on the mRNA expressions of thyroid hormone receptors (TRα and TRβ), deiodinase2 (Dio2) and thyroid-stimulating hormone-β (TSHβ) genes. The observed enantioselectivity in TR expressions was consistent with that of in silico binding analysis, which suggested that (+)-S-enantiomer binds more potently to the TRs than (?)-R-enantiomer. In general, ACT enantiomers showed different influences on the secretion of THs, expression of TH-related key genes and binding affinity to TRs. Considering the different toxicity of different enantiomers, our study highlights the importance of enantioselectivity in understanding of thyroid disruption effects of chiral pesticides.


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