Protective effects of probiotic Lactobacillus casei Zhang against endotoxin- and d-galactosamine-induced liver injury in rats via anti-oxidative and anti-inflammatory capacities

2013 ◽  
Vol 15 (1) ◽  
pp. 30-37 ◽  
Author(s):  
Yuzhen Wang ◽  
Yunxu Li ◽  
Jiming Xie ◽  
Yong Zhang ◽  
Jinling Wang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Lactobacillus Casei ◽  
Protective Effects ◽  
Probiotic Lactobacillus ◽  
Lactobacillus Casei Zhang ◽  
Anti Inflammatory

scholarly journals Methane Alleviates Acetaminophen-Induced Liver Injury by Inhibiting Inflammation, Oxidative Stress, Endoplasmic Reticulum Stress, and Apoptosis through the Nrf2/HO-1/NQO1 Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Yang Feng ◽  
Ruixia Cui ◽  
Zeyu Li ◽  
Xia Zhang ◽  
Yifan Jia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Liver Injury ◽  
Endoplasmic Reticulum Stress ◽  
Signaling Pathway ◽  
Hepatic Injury ◽  
Protective Effects ◽  
Serum Aminotransferase ◽  
Anti Inflammatory

Acetaminophen- (APAP-) induced hepatic injury is an important clinical challenge. Oxidative stress, inflammation, apoptosis, and endoplasmic reticulum stress (ERS) contribute to the pathogenesis. Methane has potential anti-inflammatory, antioxidant, and antiapoptotic properties. This project was aimed at studying the protective effects and relative mechanisms of methane in APAP-induced liver injury. In the in vivo experiment, C57BL/6 mice were treated with APAP (400 mg/kg) to induce hepatic injury followed by methane-rich saline (MRS) 10 ml/kg i.p. after 12 and 24 h. We observed that MRS alleviated the histopathological lesions in the liver, decreased serum aminotransferase levels, reduced the levels of inflammatory cytokines, suppressed the nuclear factor-κB expression. Further, we found that MRS relieved oxidative stress by regulating the Nrf2/HO-1/NQO1 signaling pathway and their downstream products after APAP challenge. MRS also regulated proteins associated with ERS-induced apoptosis. In the in vitro experiment, the L-02 cell line was treated with APAP (10 mM) to induce hepatic injury. We found that a methane-rich medium decreased the levels of reactive oxygen species (DHE fluorescent staining), inhibited apoptosis (cell flow test), and regulated the Nrf2/HO-1/NQO1 signaling pathway. Our data indicated that MRS prevented APAP-induced hepatic injury via anti-inflammatory, antioxidant, anti-ERS, and antiapoptotic properties involving the Nrf2/HO-1/NQO1 signaling pathway.

Probiotic Lactobacillus casei Zhang improved the properties of stirred yogurt

2020 ◽  
Vol 37 ◽  
pp. 100718 ◽  
Author(s):  
Mei Bai ◽  
Tian Huang ◽  
Shuai Guo ◽  
Yuejiao Wang ◽  
Jicheng Wang ◽  
...  
Keyword(s):  
Lactobacillus Casei ◽  
Probiotic Lactobacillus ◽  
Lactobacillus Casei Zhang

Transcriptome analysis of probiotic Lactobacillus casei Zhang during fermentation in soymilk

2011 ◽  
Vol 39 (1) ◽  
pp. 191-206 ◽  
Author(s):  
Ji-Cheng Wang ◽  
Wen-Yi Zhang ◽  
Zhi Zhong ◽  
Ai-Bin Wei ◽  
Qiu-Hua Bao ◽  
...  
Keyword(s):  
Transcriptome Analysis ◽  
Lactobacillus Casei ◽  
Probiotic Lactobacillus ◽  
Lactobacillus Casei Zhang

scholarly journals Resveratrol and Montelukast Alleviate Paraquat-Induced Hepatic Injury in Mice: Modulation of Oxidative Stress, Inflammation, and Apoptosis

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Noha A. El-Boghdady ◽  
Nourtan F. Abdeltawab ◽  
Mohammed M. Nooh
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Antioxidant Properties ◽  
Protective Effects ◽  
Serum Total Protein ◽  
Stress Markers ◽  
Group I ◽  
Radical Generation ◽  
Anti Inflammatory ◽  
Induced Apoptosis

Paraquat (PQ) is one of the most used herbicide worldwide. Its cytotoxicity is attributed to reactive radical generation. Resveratrol (Res) and montelukast (MK) have anti-inflammatory and antioxidant properties. The protective effects of Res, MK, or their combination against PQ-induced acute liver injury have not been investigated before. Therefore, we explored the protective potential of Res and/or MK against PQ hepatic toxicity in a mouse model. Mice were randomly assigned to five groups: group I served as the normal control and group II received a single dose of PQ (50 mg/kg, i.p.). Groups III, IV, and V received PQ plus oral Res (5 mg/kg/day), MK (10 mg/kg/day), and Res/MK combination, respectively. Res and/or MK reduced PQ-induced liver injury, evidenced by normalization of serum total protein, ALT, and AST. Res and/or MK significantly reversed PQ-induced oxidative stress markers glutathione and malondialdehyde. Res and/or MK significantly reduced PQ-induced inflammation reflected in TNF-α levels. Furthermore, Res and/or MK reversed PQ-induced apoptosis assessed by differential expression of p53, Bax, and Bcl-2. Histopathologic examination supported the biochemical findings. Although Res and MK displayed antioxidative, anti-inflammatory, and antiapoptotic activities, their combination was not always synergistic.

scholarly journals Anti-Inflammatory Activity of Dehydroandrographolide by TLR4/NF-κB Signaling Pathway Inhibition in Bile Duct-Ligated Mice

2018 ◽  
Vol 49 (3) ◽  
pp. 1124-1137 ◽  
Author(s):  
Zhiyong Weng ◽  
Yue Chi ◽  
Jing Xie ◽  
Xuefeng Liu ◽  
Jiehua Hu ◽  
...  
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Kupffer Cells ◽  
Inflammatory Responses ◽  
Protective Effects ◽  
Bile Duct Proliferation ◽  
Duct Ligation ◽  
Anti Inflammatory ◽  
Cholestatic Liver Injury ◽  
Lps Binding

Background/Aims: Clinically, biliary obstruction is often accompanied by progressive inflammation. Dehydroandrographolide (DA) possesses anti-inflammatory properties. However, the anti-inflammatory activities of DA in cholestatic liver injury remain unclear. Methods: Mice were administered with DA by intraperitoneal injection after bile duct ligation (BDL) on day 1. Then mice were subjected to an ileocecal vein injection of lipopolysaccharide (LPS). Liver function markers, histology, pro-inflammatory cytokine levels, NF-κB activation and fibrosis formation were evaluated in BDL mice with LPS. LPS binding to primary Kupffer cells was examined by high-content cytometers. Results: DA was shown to greatly lower initially higher than normal levels of alanine aminotransferase (ALT) and total bilirubin (TBIL) in the serum and liver of BDL mice with LPS. DA exerted hepatic protective effects that were also confirmed by prolonged survival of BDL mice with LPS. Liver histopathology showed reduced inflammatory cellular infiltration, bile duct proliferation, and biliary necrosis with DA treatment. Furthermore, DA reduced the expression levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in liver tissue and plasma and showed decreased NF-κB activation in BDL mice with LPS. DA could prevent LPS binding to primary Kupffer cells in the normal liver and BDL mice liver. DA also suppressed LPS-stimulated inflammatory responses by blocking the interaction between LPS and TLR4 in primary Kupffer cells and human LX-2 cells, thereby inhibiting NF-κB activation. Conclusion: DA inhibition of inflammation against liver damage following BDL with LPS may be a promising agent for the treatment of cholestatic liver injury.

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