journal of Histology & Histopathology

Journal of Histology & Histopathology

ISSN 2055-091X
Original Research

A new perspective in liver fibrosis: Etiology removal does not cause regression of liver fibrosis

Suzan Bakr Abdu

*Correspondence: Suzan Bakr Abdu suzanabdu3@gmail.com

Associate Professor of Cell Biology and Histology, Faculty of Science, King Abdulaziz University, P.O. Box 80200, Jeddah, Saudi Arabia.

Abstract

Liver fibrosis is a wound healing process involves inflammation, extracellular matrix deposition, and vascularization. It results from chronic injuries and often progresses to cirrhosis. However, many studies proposed that fibrosis regression occurred when the underlying etiology is removed. Thus, this study aimed to investigate the histological events of hepatic fibrosis regression after removing the causative agent. Three groups of rats were assigned, control, dimethylnitrosamine (DMN) to induce fibrosis (10 mg/kg/day, 3 days/week for 3 weeks), and DMN cessation group to monitor fibrosis regression(at the fourth week). Statistical analysis was performed by one-way analysis of variance (ANOVA). DMN administration demonstrated a significant decrease of body weight, as well as a marked increase of inflammatory infiltrate, collagen fibers deposition, bile ducts proliferation, new blood vessels formation, and necrosis. However, cessation of DMN caused a marked alleviation of the histopathological findings including, body weight, inflammatory infiltrates, bile ducts proliferation as well as necrosis. On the other hand, vascular remodeling continued through collagen fibers deposition and branching to the adjacent blood vessels, substituting the parenchyma with scar tissue. Subsequently resorbed, and displayed large luminal vascular structures which called angiogenesis. In conclusion, removal of the etiology clearly declined the necro-inflammatory level along with ducts proliferation. However, fibrosis had progressed to cirrhosis which may correlate to angiogenesis.

Keywords: Liver fibrosis, early cirrhosis, angiogenesis, vascular endothelial cells

ISSN 2055-091X
Volume 5
Abstract Download