[Retracted] Protective Effect of Luteolin on D‐Galactosamine (D‐Gal)/Lipopolysaccharide (LPS) Induced Hepatic Injury by in Mice

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.

Therapeutic Role of Crinum glaucum Bulb against Haematological and Hepatic Enzyme Alterations in a Rat Model

“…Current research supports several earlier reports that have shown that LPS induces hepatic damage, and therefore increases the concentrations of the aminotransferases (ALT, AST, ALP, and GGT) [11,[28][29][30][31][32][33]. The hepatic enzymes are cytoplasmic, and alteration in the membrane permeability will cause dysfunction and damaged structural integrity of hepatocytes and the aminotransferases to leak to the bloodstream, thereby resulting in an increase of the aminotransferases in the plasma of the male and female rat models, characterized by viral hepatitis, diabetes, heart failure, bile duct problems, haemorrhage, inflammation, cardiac, muscular, biliary, and injury, and microabscess formation, activation of the transcription factor nuclear factor-kappa B, and many inflammatory genes [11,27,28,30,33,[34][35][36][37].…”

Paeoniflorin ameliorates lipopolysaccharide‐induced acute liver injury by inhibiting oxidative stress and inflammation via SIRT1/FOXO1a/SOD2 signaling in rats

“…The liver prevents bacteria and endotoxins from entering the systemic circulation by removing them from the portal venous blood (Dhainaut et al, 2001; Srivastava & Gimson, 2013). During sepsis, the NLRP3 inflammasome is activated by LPS and mediates maturation of excess inflammatory cytokines, resulting in progression of ALI (Pu, Yang, & Mo, 2021; Wang et al, 2021). However, mice deficient in NLRP3 are completely resistant to LPS‐induced inflammation and liver injury (Wang et al, 2019).…”

Molecular mechanism of Ginkgo biloba in treating type 2 diabetes mellitus combined with non‐alcoholic fatty liver disease based on network pharmacology, molecular docking, and experimental evaluations

“…In addition to being involved in various stages of metabolic diseases, such as T2DM and NAFLD, inflammatory cytokines, such as IL6 and IL1B, contribute to IR by activating phosphatases that provide negative feedback to the insulin signaling cascade. Notably, significant inhibitory effects of luteolin on various inflammatory factors, including IL6 and IL‐1β, were reported in multiple disease models (Kou et al, 2022; Liu et al, 2022; Pu et al, 2021). The activation of VEGFA is strongly associated with the levels of oxidative stress, and VEGFA modulation can be effective in mitigating and preventing damage caused by oxidative stress (Hepp et al, 2021).…”