Abstract
The compound, 2,3,5,4′-tetrahydroxystilbene-2-O-β-d-glucoside (TSG), a primary bioactive polyphenolic component of Polygonum multiflorum exerts numerous pharmacological activities. However, its protective effect against non-alcoholic steatohepatitis (NASH), in the context of metabolic syndrome, remains poorly understood. The aim of the present study is to evaluate the effects of TSG treatment on middle-aged (12-mo-old) male LDLr−/− mice, which were fed a high fat diet for 12 weeks to induce metabolic syndrome and NASH. At the end of the experiment, the blood samples of mice were collected for determination of metabolic parameters. Liver and aorta tissues were collected for analysis, such as histology, immunofluorescence, hepatic lipid content, real-time PCR, and western blot. Our data show that TSG treatment improved the different aspects of NASH (steatosis, inflammation, and fibrosis) and atherosclerosis, as well as some of the metabolic basal characteristics. These modulatory effects of TSG are mediated, at least in part, through regulating key regulators of lipid metabolism (SREBP1c, PPARα and their target genes, ABCG5 and CYP7A1), inflammation (CD68, TNF-α, IL-6 and ICAM), fibrosis (α-SMA and TNFβ) and oxidative stress (NADPH-oxidase 2/4, CYP2E1 and antioxidant enzymes). These results suggest that TSG may be a promising candidate for preventing and treating the progression of NASH.
Highlights
With the global increase in obesity and metabolic syndrome, the associated complications, such as non-alcoholic steatohepatitis (NASH), atherosclerosis, and diabetes are presenting significant public health burdens in developed countries
NASH is the progressive form of non-alcoholic fatty liver disease (NAFLD) and is defined as hepatosteatosis in concert with inflammation, hepatocyte injury, and fibrosis [1]
The first hit involves excessive hepatic steatosis associated with metabolic syndrome, which causes the liver to be vulnerable to any hit that may follow, including inflammation and oxidative stress, thereby
Summary
With the global increase in obesity and metabolic syndrome, the associated complications, such as non-alcoholic steatohepatitis (NASH), atherosclerosis, and diabetes are presenting significant public health burdens in developed countries. NASH is the progressive form of non-alcoholic fatty liver disease (NAFLD) and is defined as hepatosteatosis in concert with inflammation, hepatocyte injury (ballooning), and fibrosis [1]. NASH is a serious liver disease that can further progress to cirrhosis, hepatocellular cancer, and liver failure and is projected to become the leading cause of liver transplantation in the several years, since, currently, there are no approved therapeutic strategies for NAFLD/NASH [3]. The first hit involves excessive hepatic steatosis associated with metabolic syndrome, which causes the liver to be vulnerable to any hit that may follow, including inflammation and oxidative stress, thereby
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