Effects of LSS function deficiency on intestinal function in NAFLD model mice
10.19405/j.cnki.issn1000-1492.2025.09.012
- VernacularTitle:LSS 功能缺失对 NAFLD 模型小鼠肠道功能的影响
- Author:
Hongmei Bai
1
;
Zhen Yang
1
;
Weikang Hu
1
;
Zihan Wang
1
;
Wenjing Zhou
1
;
Qingya He
1
;
Jian Zhong
1
;
Mingcong Li
2
;
Li Liu
3
;
Chaoyang Zhang
3
;
Sumei Zhang
1
;
Shengquan Zhang
1
Author Information
1. Dept of Biochemistry and Molecular Biology，School of Basic Medicine,Anhui Medical University，Hefei 230032
2. Dept of Pathology，Affiliated Hefei Hospital of Anhui Medical University( The Second People 's Hospital of Hefei) ，Hefei 230011
3. Research and Experiment Center， Anhui Medical University，Hefei 230032
- Publication Type:Journal Article
- Keywords:
lanosterol synthase;
cholesterol metabolism;
non-alcoholic fatty liver disease;
intestinal permeability;
tight junction protein;
intestinal barrier function
- From:
Acta Universitatis Medicinalis Anhui
2025;60(9):1653-1660
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of loss of function of lanosterol synthase( LSS) gene on intestinal function in a mouse model of non-alcoholic fatty liver disease( NAFLD) induced by a high-fat diet．
Methods:LSS gene heterozygous knockout C57 mice ( LSS + / －) were established using the CRISRP / Cas9 system．After being fed a high-fat diet with 60% fat content for 6 months，the fat deposition in liver tissues was detected by HE and Oil red O staining，the morphological changes of small intestine tissue were detected by HE staining．The changes in total cholesterol content in intestinal tissue were detected by kits．The gastrointestinal motility function of mice was detected by phenol red paste．The intestinal permeability was detected by Evans blue staining，and the expression of LSS，tight junction protein ( Claudin) -1，Claudin-5，cluster of differentiation 36 ( CD36) ，and Niemann-Pick type C1-like 1 protein ( NPC1L1) proteins in small intestinal tissues were detected by Western blot．
Results :The results of HE and Oil red O staining of liver tissues showed that liver fat deposition in LSS gene heterozygous knockout mice was lower than that in wild-type mice in the high-fat diet group．The total cholesterol content in intestinal tis- sue of LSS gene heterozygous knockout mice decreased ( P ＜0. 01) ，but no morphological differences were ob- served between the two groups of mice by HE staining of intestinal tissues．The gastrointestinal motility function of LSS gene heterozygous knockout mice did not show significant changes．The intestinal permeability of LSS gene het- erozygous knockout mice in the high-fat diet group decreased as detected by Evans blue ( P＜0. 05) ．The expres- sion levels of Claudin-5 protein in the intestinal tissue of LSS gene heterozygous knockout mice in the high-fat diet group increased ( P ＜0. 05 ) ，while the expression of LSS protein in the intestinal tissues of LSS heterozygous knockout mice decreased ( P ＜0. 05) ．
Conclusion:In the NAFLD model induced by a high-fat diet，LSS gene heterozygous knockout reduces liver fat deposition induced by a high-fat diet and improves intestinal barrier function by regulating cholesterol metabolism in intestinal tissues and up-regulating the expression of Claudin-5．
- Full text:2026032719302513422LSS功能缺失对NAFLD模型小鼠肠道功能的影响_白红枚.pdf
