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自噬在小儿肝脂肪变性发病机制中的作用

Does Autophagy have a Role in the Pathogenesis of Pediatric Hepatic Steatosis?

机构信息

Pathology Department, Faculty of Medicine, Menoufia University, Shebin El-Kom, Egypt.

Pediatric Department, National Liver Institute, Menoufia University, Shebin El-Kom, Egypt.

出版信息

Asian Pac J Cancer Prev. 2024 May 1;25(5):1753-1761. doi: 10.31557/APJCP.2024.25.5.1753.

DOI:10.31557/APJCP.2024.25.5.1753
PMID:38809648
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11318833/
Abstract

UNLABELLED

Hepatic steatosis has become the most common cause of chronic liver disease among children worldwide.  Lipophagy has been considered as a pathway affecting steatosis development and progression.

OBJECTIVE

this study aimed to evaluate the immunohistochemical expression of Beclin1 and LC3A in pediatric hepatic tissues with steatosis and to correlate their expression with clinicopathological parameters.

METHODS

this study included 81 Egyptian pediatric patients with hepatic steatosis and 21 pediatric cases without hepatic steatosis. All specimens were stained by Beclin1 and LC3A antibodies. According to final diagnosis obtained from Pediatric Hepatology department, patients were divided into two groups: chronic liver disease (CLD) group that included 45 cases and inborn error of metabolism (IEM) group that included 36 cases.

RESULTS

higher beclin1 expression was significantly correlated with higher stages of fibrosis and distorted liver architecture in CLD group, (P=0.043) for both. The control group showed higher positivity, percentage, as well as the median values of the H score of LC3A expression than did the CLD group or the IEM group (P=0.055, 0.001, and 0.008, respectively). Higher positivity of LC3A was significantly associated with higher stages of fibrosis and distorted liver architecture in the studied IEM group (P=0.021) for both.

CONCLUSIONS

Varying intensity grades of LC3A and Beclin 1 immunohistochemical expression demonstrate the variation of autophagy at different phases of pediatric hepatic steatosis and varied disease etiology.

摘要

未加标签

肝脂肪变性已成为世界范围内儿童慢性肝病的最常见原因。脂噬作用被认为是影响脂肪变性发展和进展的途径。

目的

本研究旨在评估 Beclin1 和 LC3A 在伴有脂肪变性的小儿肝组织中的免疫组织化学表达,并将其表达与临床病理参数相关联。

方法

本研究包括 81 例埃及小儿肝脂肪变性患者和 21 例无小儿肝脂肪变性患者。所有标本均用 Beclin1 和 LC3A 抗体染色。根据儿科肝病科获得的最终诊断,患者被分为两组:慢性肝病 (CLD) 组,包括 45 例,先天性代谢错误 (IEM) 组,包括 36 例。

结果

Beclin1 表达较高与 CLD 组肝纤维化分期较高和肝结构扭曲显著相关(P=0.043)。对照组的 LC3A 表达阳性率、百分率以及 H 评分中位数均高于 CLD 组或 IEM 组(P=0.055,0.001,0.008)。LC3A 表达阳性率较高与 IEM 组肝纤维化分期较高和肝结构扭曲显著相关(P=0.021)。

结论

LC3A 和 Beclin 1 的免疫组织化学表达强度不同,表明小儿肝脂肪变性的不同阶段和不同病因的自噬存在差异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f843/11318833/f0c4cd97b53f/APJCP-25-1753-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f843/11318833/47e394656015/APJCP-25-1753-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f843/11318833/f0c4cd97b53f/APJCP-25-1753-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f843/11318833/47e394656015/APJCP-25-1753-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f843/11318833/f0c4cd97b53f/APJCP-25-1753-g002.jpg

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Reduced Liver Autophagy in High-Fat Diet Induced Liver Steatosis in New Zealand Obese Mice.高脂饮食诱导新西兰肥胖小鼠肝脏脂肪变性过程中肝脏自噬的降低
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