Effect of Curcumol on the Fenestrae of Liver Sinusoidal Endothelial Cells Based on NF-κB Signaling Pathway.

Yang Zheng,Haiyuan Xie,Jiahui Wang,Jiaru Wang,Tiejian Zhao

doi:10.1155/2020/8590638

Abstract

Objective To study the effect of curcumol on liver sinusoidal endothelial cells (LSECs) and to analyze the mechanism of antihepatic fibrosis. Methods The effects of drug intervention on cell proliferation rates were detected by MTT assay. The expression of NF-κB was detected by RT-PCR and WB. The NF-κB expression and entry into the nucleus were detected by immunofluorescence; scanning electron microscopy was used to observe the changes of LSECs fenestrae. Results MTT results showed that the interference of cell proliferation in each group was small. RT-PCR showed that the expression of NF-κB in the curcumol intervention group was significantly lower than that in the positive control group (P < 0.05). The WB detection found that, in the curcumol intervention group, the expression of pNF-κB in the NF-κB signaling pathway was significantly lower than that in the positive control group (P < 0.05). Scanning electron microscopy showed that the LSEC fenestrae were significantly improved compared with the positive control group. Conclusion Curcumol may be one of the mechanisms of antihepatic fibrosis by inhibiting the activity of the NF-κB signaling pathway and increasing the fenestrae of LSECs.

Highlights

Hepatic fibrosis is a common result of chronic liver disease and is mainly characterized by extensive deposition of extracellular matrix (ECM) [1]
In the early stage of liver fibrosis, Liver sinusoidal endothelial cells (LSECs) show loss of fenestrae and subendothelial basement membrane formation. is phenomenon is named the capillarization of hepatic sinusoidal, which is an essential pathological change in the formation of liver fibrosis [4,5,6]
Percoll Density Gradient Centrifugation. e hepatocyte suspension is divided into density gradients of 4 different regions. e upper layer mainly contains debris, damaged cells, and a small amount of nonparenchymal cells. e boundary layer between 25% Percoll and 50% Percoll is rich in LSEC, with a small amount of unknown small white and red blood cells. e third layer (50% Percoll gradient zone) contains Kupffer cells (KC) and red blood cells

Summary

Introduction

Hepatic fibrosis is a common result of chronic liver disease and is mainly characterized by extensive deposition of extracellular matrix (ECM) [1]. Liver injury leads to the loss of function of hepatic sinusoidal fenestrae, and hepatic sinusoidal thrombosis may promote liver fibrosis [2]. Liver sinusoidal endothelial cells (LSECs) play an essential role in the development of liver fibrosis [3]. LSECs are the primary boundary component of the hepatic sinusoidal wall, which are with fenestrae and the loose connection between cells, but without the basement membrane under endothelium. LSECs have an active endocytic function and play an important role in regulating liver microcirculation and secreting extracellular matrix. In the early stage of liver fibrosis, LSECs show loss of fenestrae and subendothelial basement membrane formation. Is phenomenon is named the capillarization of hepatic sinusoidal, which is an essential pathological change in the formation of liver fibrosis [4,5,6] In the early stage of liver fibrosis, LSECs show loss of fenestrae and subendothelial basement membrane formation. is phenomenon is named the capillarization of hepatic sinusoidal, which is an essential pathological change in the formation of liver fibrosis [4,5,6]

Methods

Results

Conclusion