Abstract
Liver fibrosis represents a serious global health-care problem and is the outcome of many chronic liver diseases, cirrhosis, hepatitis, and toxin accumulation. The present study aimed to evaluate the antifibrotic curative effect of Dunaliella salina (D. salina) on thioacetamide- (TAA-) induced liver fibrosis in rats. Liver fibrosis was induced by TAA (200mg/kg; i.p.) twice per week for 6 weeks. D. salina was given orally (100 and 200 mg/kg) and silymarin was given orally (100 mg/kg) daily, for 4 weeks after TAA. Serum transaminase activities, liver inflammatory cytokines, fibrotic biomarkers, and liver histopathology were assessed. TAA significantly (p<0.05) elevated serum activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and serum levels of total bilirubin, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and transforming growth factor-beta (TGF-β) with a reduction in albumin. In addition, TAA increased hepatic contents of collagen I, a-smooth muscle actin (α-SMA), and tissue inhibitors of metalloproteinase (TIMP-1), reduced matrix metalloproteinase 9 (MMP9), and finally produced marked degeneration and fibrosis of hepatocytes. Treatment with D. salina or silymarin improved the histological feature of hepatocytes and ameliorated the deleterious effects of TAA in a dose-dependent manner. Based on these results, it could be concluded that the use of D. salina could be assigned for liver fibrosis treatment via its anti-inflammatory and antifibrotic properties.
Highlights
Liver fibrosis is a health problem that leads to morbidity and mortality and is usually insidious [1]
Liver fibrosis results from chronic damage to the liver in conjunction with accumulation of extracellular matrix (ECM) proteins, which is a characteristic of most types of chronic liver diseases. e accumulation of ECM proteins distorts the hepatic architecture by forming a fibrous scar, and the subsequent development of nodules of regenerating hepatocytes defines cirrhosis as provoking hepatic failure or hepatocellular carcinoma [2]
Injection of TAA, for 6 weeks, produced hepatic fibrosis evidenced by significant increases in serum aspartate transaminase (AST), alanine transaminase (ALT) activities, and bilirubin level and decreased albumin level as compared to normal control values
Summary
Liver fibrosis is a health problem that leads to morbidity and mortality and is usually insidious [1]. Liver fibrosis results from chronic damage to the liver in conjunction with accumulation of extracellular matrix (ECM) proteins, which is a characteristic of most types of chronic liver diseases. E accumulation of ECM proteins distorts the hepatic architecture by forming a fibrous scar, and the subsequent development of nodules of regenerating hepatocytes defines cirrhosis as provoking hepatic failure or hepatocellular carcinoma [2]. Liver fibrosis is thought to be a process of hepatic parenchyma and collagen collapse, and it may happen as a result of some etiological factors such as alcohol consumption, obesity, metabolic disorders, cholestasis, steatosis, viral infection, and toxin accumulation [3]. ECM controls cellular functions and its dysregulation linked with liver disease development [4]. Matrix metalloproteinases (MMPs), endopeptidases, destroy ECM components and degrade proteins [5].
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