Liver Disease
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(FIVE YEARS 22214)



2021 ◽  
Vol 12 ◽  
Yanbo Feng ◽  
Han Li ◽  
Cong Chen ◽  
Hao Lin ◽  
Guangyu Xu ◽  

The aim of this study was to investigate the hepatoprotection of Schisandra chinensis Caulis polysaccharides (SCPs) in the nonalcoholic fatty liver disease (NAFLD) induced by high-fat diet (HFD) in rats. A total of 30 Wistar rats were randomly divided into the control group (CON), model group (MOD), and Schisandra chinensis caulis polysaccharide (SCP) group. Except for those in the CON group, the other rats were fed with high-fat diet for 4 weeks to establish an NAFLD model. From the 5th week, rats in the SCP group were given SCP solution (100 mg kg−1) by gavage for 6 weeks, and those in the CON and MOD groups were given an equal volume of distilled water in the same way. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) levels in serum, the malondialdehyde (MDA) level, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) activities in the liver tissue were detected. The small molecular metabolites in the blood of rats were determined by the metabolomics method of ultra-high-performance liquid chromatography-quadrupole/electrostatic field orbitrap high-resolution mass spectrometry (UHPLC-Q-Orbitrap-MS/MS) combined with multivariate analysis. The enrichment analysis and pathway analysis of the different metabolites were carried out. The therapeutic mechanism of SCP in NAFLD rats was verified by western blot. The results showed that the levels of AST, ALT, TG, TC, and LDL-C in the serum of rats in the SCP group were significantly lower, and the levels of HDL-C were significantly higher than those in the MOD group. The screening and analysis of the metabolic pathways showed that SCP could alleviate the development of NAFLD by regulating the expression of UDP-glucose pyrophosphorylase (UGP2), UDP-glucose 6-dehydrogenase (UGDH), acetyl CoA carboxylase (ACC), and fatty acid synthase (FAS) in the liver of NAFLD rats. This study may provide a theoretical basis for the development and utilization of SCP.

2021 ◽  
Vol 11 (1) ◽  
Manal Sabry Mohamed ◽  
Tarek Mohammed Youssef ◽  
Esraa Ebrahim Abdullah ◽  
Ahmed Elmetwally Ahmed

Abstract Background Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver diseases, particularly in Egypt. It is defined as the accumulation of lipids inside the hepatocytes, in the absence of other etiologies of hepatic damage. It is frequently associated with obesity, diabetes mellitus, and metabolic syndrome. Adiponectin is an abundant adipocyte-derived protein with well-established anti-atherogenic, insulin-sensitizing, and anti-inflammatory properties. The liver is a major target organ for adiponectin especially in fatty liver diseases, and this adipocytokine has the ability to control many liver functions including metabolism, inflammation, and fibrosis. In this study, we aimed to find out the correlation between the degree of liver fibrosis in NAFLD patients and their serum adiponectin level as a future non-invasive method for the assessment of liver fibrosis to substitute liver biopsy to avoid its hazardous complication and also to study the correlation between diabetes mellitus as well as obesity and serum adiponectin level. Results Fifty patients were selected to participate in our study based on our inclusion criteria. They were recruited from the Internal Medicine Department, Gastroenterology Clinic in Al-Demerdash Hospital using a convenient sampling method. Diagnosis of NAFLD was confirmed by laboratory markers: aspartate aminotransferase (AST), alanine aminotransferase (ALT), lipid profile, ultrasound, and FibroScan examination. Analyzing the adiponectin levels showed that besides its significant correlation with body mass index (BMI), hypertension, diabetes mellitus, and dyslipidemia, it was significantly lower in the high-grade fibrosis group compared to the low-grade fibrosis group with a P-value of (0.000) and a cutoff value for stage 3/4 fibrosis of about 2.31 μg/ml which marked a promising hope of adiponectin being of protective value against liver fibrosis. Conclusion Both serum levels and hepatic adiponectin receptor expression are decreased in NAFLD. Therefore, either adiponectin itself or adiponectin-inducing agents might be of key therapeutic interest in the near future in the treatment of NAFLD.

2021 ◽  
pp. flgastro-2021-101998
Aditi Kumar ◽  
Catherine Nelson-Piercy ◽  
Christian Selinger

Zahra Sokhanvar ◽  
Ameneh Elikaei ◽  
Zohreh Sharifi

Background: Liver disease is more severe in HDV+HBV co-infected patients than HBV infected patients which seems to be related to differences in the expression of genes and other factors such as MicroRNAs (miRNAs). The aim of this study was to investigate miR-222 expression in HBV infected patients in comparison with HDV+HBV co-infected patients. Methods: First, total RNA was extracted from the serum samples and then, complementary DNA (cDNA) was produced using cDNA synthesis kit. Finally, miR-222 gene expression was measured using U6 as the internal control by quantitative PCR (qPCR). Results: The level of miR-222 expression in HDV+HBV co-infected samples was significantly up regulated. The fold change of the miR-222 expression between two groups was 3.3 (95% CI; 0.011- 17.63) with p<0.001. Conclusion: The expression of miR-222 was higher in HBV+HDV co-infected patients than HBV infected patients. Further studies should be conducted to confirm whether miR-222 can be a biomarker for prognosis of severe liver diseases.

Lucia Brodosi ◽  
Francesca Marchignoli ◽  
Giulio Marchesini ◽  
Maria Letizia Petroni

2021 ◽  
Yoon Sin Oh ◽  
Hwansu Kang ◽  
Eunhui Seo ◽  
Hee-Sook Jun

Abstract Inflammation contributes to the pathogenesis of liver disease, and inflammasome activation has been identified as a major contributor to the amplification of liver inflammation. Transforming growth factor-beta (TGF-β) is a key regulator of liver physiology, contributing to all stages of liver disease. We investigated whether TGF-β is involved in inflammasome-mediated fibrosis in hepatic stellate cells. Treatment with TGF-β increased priming of NLRP3 inflammasome signaling by increasing NLRP3 levels and activating TAK1-NF-kB signaling. Moreover, TGF-β increased the expression of p-Smad2/3-NOX4 in LX-2 cells and consequently increased ROS content, which is a trigger for NLRP3 inflammasome activation. Elevated expression of NEK7 and active caspase-1 was also shown in TGF-β-induced LX-2 cells, and this level was reduced by (5Z)-oxozeaenol, a TAK inhibitor. Finally, TGF-β-treated cells significantly increased TGF-β secretion levels, and their production was inhibited by IL-1β receptor antagonist treatment. In conclusion, TGF-β may represent an endogenous danger signal to the active NLRP3 inflammasome, by which IL-1β mediates TGF-β expression in an autocrine manner. Therefore, targeting the NLRP3 inflammasome may be a promising approach for the development of therapies for TGF-β-induced liver fibrosis.

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