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Marker group for evaluating non-alcoholic steatohepatitis

A steatohepatitis, non-alcoholic technology, applied in the field of biomedicine, can solve the problem of not systematically elucidating the function of liver EC subgroups, and achieve the effect of non-invasive and simple differentiation

Pending Publication Date: 2022-05-24
THE WEST CHINA SECOND UNIV HOSPITAL OF SICHUAN
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

However, the functional contribution of hepatic EC subsets to human cirrhosis or NASH pathology has not been systematically elucidated at the single-cell level in current clinical and preclinical models

Method used

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  • Marker group for evaluating non-alcoholic steatohepatitis
  • Marker group for evaluating non-alcoholic steatohepatitis
  • Marker group for evaluating non-alcoholic steatohepatitis

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0067] Example 1: Materials and Methods

[0068] 1. Patient and clinical samples. Liver and plasma samples of patients were collected at West China Hospital of Sichuan University with informed consent. Healthy liver tissue (without fibrosis) was obtained from patients with hepatic hemangiomas who underwent endoscopic liver resection. Cirrhotic liver tissue was obtained from patients with histologically diagnosed hepatic fibrosis. Patient information used for scRNA-Seq, liquid microarray analysis, and gene expression analysis is shown in Table 1. Plasma samples were obtained from healthy volunteers (n=21), simple fatty liver (n=16), early nonalcoholic steatohepatitis (F0-F1) (n=12), and cirrhosis / fibrosis of different pathological grades Patients (no cancer) (n=75). Fibrosis grades in non-NASH livers were determined by Fibrosis-4 Index (Fib-4) and Transient Elastography (TE) using the NAFLD Fibrosis Index (NFS), Fib-4, TE and controlled attenuation parameters ( CAP) to det...

Embodiment 2

[0111] Example 2: scRNA-Seq reveals vascular dysregulation and abnormal endothelial classification in human cirrhotic liver

[0112] NPCs were isolated from fresh normal and cirrhotic human livers and subjected to scRNA-seq (10xgenomics) ( Figure 1A , Table S1). Healthy liver tissue (without fibrosis) was obtained from a patient with hepatic hemangioma in West China Hospital, and cirrhotic liver tissue was obtained from a patient with histologically diagnosed liver cirrhosis. 22,374 NPCs from 2 healthy livers and 2 cirrhotic livers were clustered into 25 clusters ( Figure 10A -B). Seven cell lines were defined by expression of marker genes: T cells, B cells, endothelial cells (EC), macrophages (Mac), neutrophils (Neu), dendritic cells (DC), and EPCAM + cells and bile duct cells (EPCAM + )( Figure 1B -C). Experimenters of the present invention found that among all the cell types tested, ECs had the most differential genes ( Figure 1D ). The proportion of ECs in cirrho...

Embodiment 3

[0114] Example 3: Epigenetic reprogramming of liver ECs induces pro-fibrotic "sinusoidal endothelial-macrovascular endothelial dysregulation"

[0115] Epigenetic regulation (histone modification and DNA methylation) plays an important role in the progression of liver fibrosis. However, the functional roles of histone modifications and DNA methylation in different cell lines of human cirrhotic / fibrotic NPCs remain unclear. To this end, the experimenters first determined the histone modifications of parenchymal cells and NPCs in healthy livers and cirrhotic livers. Liquid-chip analysis of histone H3 and H4 modifications showed that compared with healthy livers, NPCs in human cirrhotic livers were more Histone acetylation was significantly reduced, whereas parenchymal cells (hepatocytes) were not significantly different ( Figure 1G ), suggesting epigenetic reprogramming of NPCs in human cirrhotic livers.

[0116] The experimenters further investigated epigenetic changes in dif...

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Abstract

The invention belongs to the field of biological medicine, and mainly relates to a marker group for evaluating non-alcoholic steatohepatitis. The invention provides a marker group for evaluating non-alcoholic steatohepatitis and a kit containing the marker group, and is characterized in that the marker group comprises IGFBP7 and ADAMTS1; the expression quantity of the marker group can be used for evaluating the liver fibrosis degree and the liver function impairment condition. The invention also provides a marker group for distinguishing the non-alcoholic steatohepatitis from the simple fatty liver and a kit containing the marker group, and the marker group is characterized by comprising IGFBP7 and ADAMTS1 (adenosine monophosphate-adenosine monophosphate-adenosine monophosphate-adenosine monophosphate-adenosine monophosphate-adenosine monophosphate-adenosine monophosphate). The marker group for evaluating the non-alcoholic steatohepatitis, provided by the invention, is beneficial to reliably, sensitively, simply and noninvasively evaluating the non-alcoholic steatohepatitis.

Description

technical field [0001] The invention belongs to the field of biomedicine, and mainly relates to a marker group for evaluating nonalcoholic steatohepatitis. Background technique [0002] The liver has the regenerative ability to repair itself after injury. However, in nonalcoholic steatohepatitis (NASH), liver regeneration is inhibited. Similar to diabetes and metabolic syndrome, NASH is on the rise globally. NASH can lead to liver fibrosis, cirrhosis and liver failure. Without effective anti-fibrotic treatment, liver fibrosis and liver cirrhosis caused by NASH usually lead to systemic complications and will become a major global health burden. A major obstacle to the clinical development of NASH treatments is the lack of clinical and preclinical studies of cellular and molecular networks that systematically mimic the pathogenesis of NASH. [0003] The liver is composed of parenchymal cells (hepatocytes) and non-parenchymal cells (NPCs) such as stellate cells, endothelial ...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): C12Q1/6883G01N33/68G01N33/576
CPCA61K45/06A61K31/506A61K31/706A61P1/16A61P3/10A61P3/06A61K2300/00
Inventor 丁楅森曹中炜张华马永源
Owner THE WEST CHINA SECOND UNIV HOSPITAL OF SICHUAN
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