Understanding the Potential Role of Nanotechnology in Liver Fibrosis: A Paradigm in Therapeutics

Abstract

The liver is a vital organ that plays a crucial role in the physiological operation of the human body. The liver controls the body's detoxification processes as well as the storage and breakdown of red blood cells, plasma protein and hormone production, and red blood cell destruction; therefore, it is vulnerable to their harmful effects, making it more prone to illness. The most frequent complications of chronic liver conditions include cirrhosis, fatty liver, liver fibrosis, hepatitis, and illnesses brought on by alcohol and drugs. Hepatic fibrosis involves the activation of hepatic stellate cells to cause persistent liver damage through the accumulation of cytosolic matrix proteins. The purpose of this review is to educate a concise discussion of the epidemiology of chronic liver disease, the pathogenesis and pathophysiology of liver fibrosis, the symptoms of liver fibrosis progression and regression, the clinical evaluation of liver fibrosis and the research into nanotechnology-based synthetic and herbal treatments for the liver fibrosis is summarized in this article. The herbal remedies summarized in this review article include epigallocathechin-3-gallate, silymarin, oxymatrine, curcumin, tetrandrine, glycyrrhetinic acid, salvianolic acid, plumbagin, Scutellaria baicalnsis Georgi, astragalosides, hawthorn extract, and andrographolides.

Keywords: antifibrotic activity; chronic liver disease; hepatic stellate cells; liver fibrosis; nanotechnology; phytoconstituents.

Figure 1

Schematic depiction of pathogenesis and pathophysiology during liver fibrosis progression. Chronic hepatic inflammation causes activation of quiescent hepatic stellate cells, which obtains transdifferentiate into MFB-like cells, which have contractile, proinflammatory, and fibrogenic properties. MFB: myofibroblast, HSC: hepatic stellate cell, ROS: reactive oxygen species, TGF-β1: transforming growth factor-β1, PDGF: platelet-derived growth factor, and CCL2: chemokine.

Figure 2

Illustrative representation indicating the interaction between hepatic stellate cells and macrophages during liver fibrosis progression and regression. HSC: hepatic stellate cell, PDGF: platelet-derived growth factor, TGF-β1: transforming growth factor-β, TNF-ɑ: tumor necrosis factor-ɑ, TRAIL: tumor necrosis (TNF)-related apoptosis-inducing ligand; TIMP: tissue inhibitors of metalloproteinases.