Abstract
To observe the effects of luteolin on galactosamine (D-Gal)/lipopolysaccharide (LPS) induced liver injury in mice. Male C57BL/6 mice were randomly divided into 4 groups: normal control group, D-GaI/LPS group, D-GaI/LPS + luteolin (Lu, 20 mg/kg), and D-GaI/LPS + luteolin (Lu, 40 mg/kg). Mice in the normal control group and D-GaI/LPS group were given distilled water while other groups were given drugs in 7 days by gavage. 4 hours after the continuous administration, Gal (700 mg/kg) and LPS (10 mg/kg) were injected intraperitoneally. Mice in the normal control group were given the same volume of vegetable oil solution. 24 h after the establishment of the mice model, blood and liver samples were collected. Hematoxylin (HE) staining was used to observe the changes of hepatic histopathology. Alanine aminotransferase (ALT) and glutamic oxalacetic transaminase (AST) in serum, interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor (TNF-α) were measured by related kits. Western blotting was used to demonstrate the expression levels of related inflammation proteins. Lu significantly reduced levels of proinflammatory cytokines including interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in serum and liver. Lu restored the pathological changes after galactosamine (D-Gal)/lipopolysaccharide (LPS) treatment. In addition, Lu regulated proteins levels of the NLRP3/NF-κB pathway in liver. Lu exhibited therapeutical effects on D-GaI/LPS induced liver injury in mice which might be related to the regulation of the NLRP3/NF-κB pathway.
Highlights
Acute hepatic failure (AFT) is a serious clinical syndrome, which is the result of a large number of hepatocyte deaths [1]
Interleukin- (IL-) 6, IL-1β, and tumor necrosis factor(TNF-) α enzyme-linked immunosorbent assay (ELISA) kits were obtained from Elabscience (Wuhan, China)
It was found that Lu could significantly reduce ALT and AST activities and reduce the content of proinflammatory cytokines such as IL-1β, IL-6, and tumor necrosis factor-α (TNF-α) in serum and liver induced by D-GaI/LPS
Summary
Acute hepatic failure (AFT) is a serious clinical syndrome, which is the result of a large number of hepatocyte deaths [1]. The prognosis of acute liver failure is very poor, and there is no effective treatment unless liver transplantation. Druginduced liver injury (DILI) is a major cause of AFT which is one of the leading causes for liver transplantation [2]. The liver injury caused by simultaneous injection of d-galactosamine (d-gal) and lipopolysaccharide (LPS) has been widely used to study the pathogenesis of AFT [3,4,5]. The mechanism of liver injury induced by d-gal/LPS is not completely clear [6]. It is urgent to study the mechanism of AFT and the drug treatment
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