scholarly journals Effects of Puerariae Radix Extract on Endotoxin Receptors and TNF-αExpression Induced by Gut-Derived Endotoxin in Chronic Alcoholic Liver Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Jing-Hua Peng ◽  
Tuan Cui ◽  
Zhao-Lin Sun ◽  
Fu Huang ◽  
Liang Chen ◽  
...  
Keyword(s):  
Liver Injury ◽  
Protein Expression ◽  
Alcohol Intake ◽  
Alcoholic Liver Injury ◽  
Chronic Alcohol ◽  
Gamma Glutamyl Transpeptidase ◽  
Chronic Alcoholic ◽  
Necrosis Factor Alpha ◽  
Puerariae Radix

Kudzu (Pueraria lobata) is one of the earliest medicinal plants used to treat alcohol abuse in traditional Chinese medicine for more than a millennium. However, little is known about its effects on chronic alcoholic liver injury. Therefore, the present study observed the effects of puerariae radix extract (RPE) on chronic alcoholic liver injury as well as Kupffer cells (KCs) activation to release tumor necrosis factor alpha (TNF-α) induced by gut-derived endotoxin in rats and macrophage cell line. RPE was observed to alleviate the pathological changes and lipids deposition in liver tissues as well as the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and hepatic gamma-glutamyl transpeptidase (GGT) activity. Meanwhile, RPE inhibited KCs activation and subsequent hepatic TNF-αexpression and downregulated the protein expression of endotoxin receptors, lipopolysaccharide binding protein (LBP), CD14, Toll-like receptor (TLR) 2, and TLR4 in chronic alcohol intake rats. Furthermore, anin vitrostudy showed that RPE inhibited the expression of TNF-αand endotoxin receptors, CD14 and TLR4, induced by LPS in RAW264.7 cells. In summary, this study demonstrated that RPE mitigated liver damage and lipid deposition induced by chronic alcohol intake in rats, as well as TNF-αrelease, protein expression of endotoxin receptorsin vivoorin vitro.

β-Sitosterol attenuates liver injury in a rat model of chronic alcohol intake

2020 ◽  
Vol 43 (11) ◽  
pp. 1197-1206
Author(s):  
Zhenjuan Chen ◽  
Ancheng Wu ◽  
Hongmei Jin ◽  
Fuhui Liu
Keyword(s):  
Liver Injury ◽  
Rat Model ◽  
Alcohol Intake ◽  
Chronic Alcohol

scholarly journals Mechanism of KLF4 Protection against Acute Liver Injury via Inhibition of Apelin Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Weitao Ji ◽  
Hongyun Shi ◽  
Hailin Shen ◽  
Jing Kong ◽  
Jiayi Song ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Acute Liver Injury ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Protein Levels ◽  
Klf4 Expression ◽  
Mrna And Protein Expression

Krüppel-like factor 4 (KLF4) is a key transcription factor that regulates genes involved in the proliferation or differentiation in different tissues. Apelin plays roles in cardiovascular functions, metabolic disease, and homeostatic disorder. However, the biological function of apelin in liver disease is still ongoing. In this study, we investigated the mechanism of KLF4-mediated protection against acute liver injury via the inhibition of the apelin signaling pathway. Mice were intraperitoneally injected with carbon tetrachloride (CCl4; 0.2 mL dissolved in 100 mL olive oil, 10 mL/kg) to establish an acute liver injury model. A KLF4 expression plasmid was injected through the tail vein 48 h before CCl4 treatment. In cultured LX-2 cells, pAd-KLF4 or siRNA KLF4 was overexpressed or knockdown, and the mRNA and protein levels of apelin were determined. The results showed that the apelin serum level in the CCl4-injected group was higher than that of control group, and the expression of apelin in the liver tissues was elevated while KLF4 expression was decreased in the CCl4-injected group compared to the KLF4-plasmid-injected group. HE staining revealed serious hepatocellular steatosis in the CCl4-injected mice, and KLF4 alleviated this steatosis in the mice injected with KLF4 plasmid. In vitro experiments showed that tumor necrosis factor-alpha (TNF-α) could downregulate the transcription and translation levels of apelin in LX-2 cells and also upregulate KLF4 mRNA and protein expression. RT-PCR and Western blotting showed that the overexpression of KLF4 markedly decreased basal apelin expression, but knockdown of KLF4 restored apelin expression in TNF-α-treated LX-2 cells. These in vivo and in vitro experiments suggest that KLF4 plays a key role in inhibiting hepatocellular steatosis in acute liver injury, and that its mechanism might be the inhibition of the apelin signaling pathway.

scholarly journals Metabolomics Study of Serum from a Chronic Alcohol-Fed Rat Model Following Administration of Defatted Tenebrio molitor Larva Fermentation Extract

Metabolites ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 436
Author(s):  
Ra-Yeong Choi ◽  
Moongi Ji ◽  
Mi-Kyung Lee ◽  
Man-Jeong Paik
Keyword(s):  
Liver Injury ◽  
Rat Model ◽  
Principal Component ◽  
Control Group ◽  
Alcoholic Liver Injury ◽  
Chronic Alcohol ◽  
Octadecanoic Acid ◽  
Oxidation Activity ◽  
Metabolomics Study ◽  
Etoh Group

We have previously showed that defatted mealworm fermentation extract (MWF) attenuates alcoholic liver injury by regulating lipid, inflammatory, and antioxidant metabolism in chronic alcohol-fed rats. The current metabolomics study was performed to monitor biochemical events following the administration of MWF (daily for eight weeks) to a rat model of alcoholic liver injury by gas chromatography-tandem mass spectrometry (GC-MS/MS). The levels of 15 amino acids (AAs), 17 organic acids (OAs), and 19 free fatty acids (FFAs) were measured in serum. Analysis of variance (ANOVA), principal component analysis (PCA), and partial least squares discriminant analysis (PLS-DA) were used to compare the levels of 51 metabolites in serum. In particular, 3-hydroxybutyric acid (3-HB), pyroglutamic acid (PG), octadecanoic acid, and docosahexaenoic acid (DHA) were evaluated as high variable importance point (VIP) scores and PCA loading scores as determined by PLS-DA and PCA, and these were significantly higher in the MWF and silymarin groups than in the EtOH group. MWF showed a protective effect from alcohol-induced liver damage by elevating hepatic β-oxidation activity, and serum 3-HB levels were significantly higher in the MWF group than in the EtOH control group. Glycine levels were higher in the MWF group than in the EtOH group, and PG levels (related to glutathione production) were also elevated, indicating a reduction in alcohol-related oxidative stress. In addition, MWF is protected from alcohol-induced inflammation and steatosis by increasing serum DHA, palmitic, and octadecanoic acid levels as compared with the EtOH group. These results suggest that MWF might attenuate alcoholic liver disease, due to its anti-inflammatory and antioxidant effects by up-regulating hepatic β-oxidation activity and down-regulating liver FFA uptake.

Salvianolic acid B protects against chronic alcoholic liver injury via SIRT1-mediated inhibition of CRP and ChREBP in rats

2017 ◽  
Vol 267 ◽  
pp. 1-10 ◽  
Author(s):  
Ning Zhang ◽  
Yan Hu ◽  
Chunchun Ding ◽  
Wenjing Zeng ◽  
Wen Shan ◽  
...  
Keyword(s):  
Liver Injury ◽  
Salvianolic Acid B ◽  
Alcoholic Liver Injury ◽  
Chronic Alcoholic ◽  
Salvianolic Acid

scholarly journals Inhibition of Poly(ADP-Ribose) Polymerase-1 Protects Chronic Alcoholic Liver Injury

2016 ◽  
Vol 186 (12) ◽  
pp. 3117-3130 ◽  
Author(s):  
Yanqing Zhang ◽  
Cheng Wang ◽  
Yunli Tian ◽  
Fengxiao Zhang ◽  
Wenjing Xu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Alcoholic Liver Injury ◽  
Chronic Alcoholic

scholarly journals Defatted Tenebrio molitor Larva Fermentation Extract Modifies Steatosis, Inflammation and Intestinal Microflora in Chronic Alcohol-Fed Rats

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1426
Author(s):  
Ra-Yeong Choi ◽  
Ju Ri Ham ◽  
Hyo-Seon Ryu ◽  
Sang Suk Lee ◽  
Michelle A. Miguel ◽  
...  
Keyword(s):  
Liver Injury ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Sequencing Analysis ◽  
Alcoholic Liver Injury ◽  
Chronic Alcohol ◽  
Defense System ◽  
Microbial Composition ◽  
Hepatocellular Damage ◽  
Etoh Group

This study examined the effects of defatted mealworm fermentation extract (MWF) on alcoholic liver injury in rats. The rats were fed either a Lieber-DeCarli control (Con) or alcohol liquid diet (EtOH). The alcohol-fed rats were administered MWF (50, 100, or 200 mg/kg/day) and silymarin (200 mg/kg/day) orally for eight weeks. MWF prevented alcohol-induced hepatocellular damage by decreasing their serum aspartate transaminase, alanine transaminase, and gamma-glutamyl transpeptidase levels significantly compared to the EtOH group. MWF effectively reduced the relative hepatic weight, lipid contents, and fat deposition, along with the down-regulation of transcriptional factors and genes involved in lipogenesis compared to the EtOH group. It also enhanced the antioxidant defense system by elevating the glutathione level and glutathione reductase activity. MWF attenuated the alcohol-induced inflammatory response by down-regulating hepatic inflammation-associated proteins expression, such as phosphorylated-inhibitor of nuclear factor-kappa B-alpha and tumor necrosis factor-alpha, in chronic alcohol-fed rats. Furthermore, sequencing analysis in the colonic microbiota showed that MWF tended to increase Lactobacillus johnsonii reduced by chronic alcohol consumption. These findings suggest that MWF can attenuate alcoholic liver injury by regulating the lipogenic and inflammatory pathway and antioxidant defense system, as well as by partially altering the microbial composition.

scholarly journals Omeprazole increases survival via different mechanisms in two rat models of liver injury

2021 ◽  
Author(s):  
Masaya Kotsuka ◽  
Yuki Hashimoto ◽  
Richi Nakatake ◽  
Tetsuya Okuyama ◽  
Masahiko Hatta ◽  
...  
Keyword(s):  
Liver Injury ◽  
Mrna Expression ◽  
Rat Hepatocytes ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Beneficial Effects ◽  
Factor Alpha ◽  
Oxide Synthase

Abstract Omeprazole (OMZ) is a proton pump inhibitor (PPI) that is used to reduce gastric acid secretion, but little is known about its possible liver protective effects. This study investigated whether OMZ has beneficial effects in rat septic models of lipopolysaccharide (LPS)-induced liver injury after D-galactosamine (GalN) treatment and 70% hepatectomy (PH), and to determine the mechanisms of OMZ in an in vitro model of liver injury. In the in vivo models, the effects of OMZ were examined 1 h before treatment. OMZ increased survival and decreased tumor necrosis factor-alpha, inducible nitric oxide synthase, cytokine-induced neutrophil chemoattractant 1, interleukin (IL)-6, and IL-1β mRNA expression, and increased IL-10 mRNA expression in the livers of both GaIN/LPS- and PH/LPS-treated rats. Necrosis and apoptosis were inhibited by OMZ in GaIN/LPS rats, but OMZ had no effects on necrosis in PH/LPS rats. Primary rat hepatocytes were treated with IL1-β in the presence or absence of OMZ (in vitro model). OMZ inhibited iNOS induction partially through suppression of NF-κB signaling in hepatocytes. Furthermore, OMZ inhibited the induction of several inflammatory mediators, resulting in the prevention of LPS-induced liver injury after GalN liver failure and PH, although OMZ showed different doses and mechanisms in the two models.

scholarly journals An in vitro method of alcoholic liver injury using precision-cut liver slices from rats

2008 ◽  
Vol 76 (3) ◽  
pp. 426-436 ◽  
Author(s):  
Lynell W. Klassen ◽  
Geoffrey M. Thiele ◽  
Michael J. Duryee ◽  
Courtney S. Schaffert ◽  
Amy L. DeVeney ◽  
...  
Keyword(s):  
Liver Injury ◽  
Alcoholic Liver Injury ◽  
In Vitro Method ◽  
Liver Slices
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