Rac2 deficiency attenuates CCl4-induced liver injury through suppressing inflammation and oxidative stress

Zou, Yan; Xiong, Ji-bin; Ma, Ke; Wang, Aizhong; Qian, Kun

doi:10.1016/j.biopha.2017.07.074

Cited by 30 publications

(20 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As previously mentioned, the pathological basis of acute liver injury induced by triptolide was oxidative stress, and the study of oxidative stress had become a potential target for the treatment of acute liver injury. The generation of H 2 O 2 and MDA could reflect the severity of oxidative stress in vivo (Zou et al 2017). SOD, as the first antioxidant line of body defense, could eliminate the superoxide anion radical (O 2 − ) and reflecte the anti-oxidative ability to protect cells from damage.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Vitamin C on Triptolide-induced Acute Hepatotoxicity in Mice through mitigation of oxidative stress

et al. 2019

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

Triptolide, a purified diterpenoid from the herb Tripterygium wilfordii Hook.f., was widely used to treat many diseases. However, the hepatotoxicity of triptolide limited its clinical use. Research showed oxidative stress played an important role in triptolide-induced liver injury. To investigate the effect of vitamin C, which was one of the most effective antioxidants, on triptolide-induced hepatotoxicity and its potential mechanism in mice. In the present study, acute liver injury was induced by intraperitoneal injection of triptolide and vitamin C was orally administered. The results showed treatment with vitamin C prevented the triptolide-induced liver injury by reducing the levels of aspartate transaminase from 286.86 to 192.48 U/mL and alanine aminotransferase from 746.75 to 203.36 U/mL. Histopathological changes of liver corresponded to the same trend. Furthermore, vitamin C also protected the liver against triptolideinduced oxidative stress by inhibiting the generation of malondialdehyde (2.22 to 1.49 nmol/mgprot) and hydrogen peroxide (14.74 to 7.19 mmol/gprot) and restoring the level of total superoxide dismutase (24.32 to 42.55 U/mgprot) and glutathione (7.69 to 13.03 μg/mgprot). These results indicated that vitamin C could protect against triptolide-induced liver injury via reducing oxidative stress, and vitamin C may pose a significant health protection in the clinical use of triptolide.

show abstract

Section: Discussionmentioning

confidence: 99%

Protective Effect of Vitamin C on Triptolide-induced Acute Hepatotoxicity in Mice through mitigation of oxidative stress

et al. 2019

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

show abstract

“…RAC2 is a key signal transduction factor in inflammatory cells and plays a key role in the activation of the various NADPH oxidases (NOXes) family members, which play important role in the production of ROS through response to receptor agonists such as growth factors or inflammatory cytokines [41]. Moreover, a previous study suggested that RAC2 deficiency inhibits the action of pro-inflammatory cytokines and chemokines [42]. In chickens, RAC2 is involved in the production of ROS in phagosomes of chicken heterophils to kill pathogens [43].…”

Section: Integration Of Ppi Network and Module Analysismentioning

confidence: 99%

Identification of key genes and pathways associated with feed efficiency of native chickens based on transcriptome data via bioinformatics analysis

Yang

Xiong

et al. 2020

BMC Genomics

View full text Add to dashboard Cite

Background: Improving feed efficiency is one of the important breeding targets for poultry industry. The aim of current study was to investigate the breast muscle transcriptome data of native chickens divergent for feed efficiency. Residual feed intake (RFI) value was calculated for 1008 closely related chickens. The 5 most efficient (LRFI) and 5 least efficient (HRFI) birds were selected for further analysis. Transcriptomic data were generated from breast muscle collected post-slaughter. Results: The differently expressed genes (DEGs) analysis showed that 24 and 325 known genes were significantly up-and down-regulated in LRFI birds. An enrichment analysis of DEGs showed that the genes and pathways related to inflammatory response and immune response were up-regulated in HRFI chickens. Moreover, Gene Set Enrichment Analysis (GSEA) was also employed, which indicated that LRFI chickens increased expression of genes related to mitochondrial function. Furthermore, protein network interaction and function analyses revealed ND2, ND4, CYTB, RAC2, VCAM1, CTSS and TLR4 were key genes for feed efficiency. And the 'phagosome', 'cell adhesion molecules (CAMs)', 'citrate cycle (TCA cycle)' and 'oxidative phosphorylation' were key pathways contributing to the difference in feed efficiency. Conclusions: In summary, a series of key genes and pathways were identified via bioinformatics analysis. These key genes may influence feed efficiency through deep involvement in ROS production and inflammatory response. Our results suggested that LRFI chickens may synthesize ATP more efficiently and control reactive oxygen species (ROS) production more strictly by enhancing the mitochondrial function in skeletal muscle compared with HRFI chickens. These findings provide some clues for understanding the molecular mechanism of feed efficiency in birds and will be a useful reference data for native chicken breeding.

show abstract

“…The inflammation response is also an important event for CCl 4 -induced acute liver injury [ 9 ]. Previous studies have demonstrated that CCl 4 exposure could trigger the production of some inflammatory mediators, including tumor necrosis factor-alpha (TNF-α), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (Cox-2), through nuclear factor-kappaB ( NF-κB ) activation in the liver of rats or mice [ 9 , 10 , 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Attenuates on Carbon Tetrachloride-Induced Acute Liver Injury in Mice via Modulation of the Nrf2/HO-1 and TGF-β1/Smad3 Pathway

et al. 2018

View full text Add to dashboard Cite

This study aimed to investigate the protective effect of curcumin against carbon tetrachloride (CCl4)-induced acute liver injury in a mouse model, and to explain the underlying mechanism. Curcumin at doses of 50, 100 and 200 mg/kg/day were administered orally once daily for seven days prior to CCl4 exposure. At 24 h, curcumin-attenuated CCl4 induced elevated serum transaminase activities and histopathological damage in the mouse’s liver. Curcumin pre-treatment at 50, 100 and 200 mg/kg significantly ameliorated CCl4-induced oxidative stress, characterized by decreased malondialdehyde (MDA) formations, and increased superoxide dismutase (SOD), catalase (CAT) activities and glutathione (GSH) content, followed by a decrease in caspase-9 and -3 activities. Curcumin pre-treatment significantly decreased CCl4-induced inflammation. Furthermore, curcumin pre-treatment significantly down-regulated the expression of TGF-β1 and Smad3 mRNAs (both p < 0.01), and up-regulated the expression of nuclear-factor erythroid 2-related factor 2 (Nrf2) and HO-1 mRNA (both p < 0.01) in the liver. Inhibition of HO-1 attenuated the protective effect of curcumin on CCl4-induced acute liver injury. Given these outcomes, curcumin could protect against CCl4-induced acute liver injury by inhibiting oxidative stress and inflammation, which may partly involve the activation of Nrf2/HO-1 and inhibition of TGF-β1/Smad3 pathways.

show abstract

Rac2 deficiency attenuates CCl4-induced liver injury through suppressing inflammation and oxidative stress

Cited by 30 publications

References 39 publications

Protective Effect of Vitamin C on Triptolide-induced Acute Hepatotoxicity in Mice through mitigation of oxidative stress

Protective Effect of Vitamin C on Triptolide-induced Acute Hepatotoxicity in Mice through mitigation of oxidative stress

Identification of key genes and pathways associated with feed efficiency of native chickens based on transcriptome data via bioinformatics analysis

Curcumin Attenuates on Carbon Tetrachloride-Induced Acute Liver Injury in Mice via Modulation of the Nrf2/HO-1 and TGF-β1/Smad3 Pathway

Contact Info

Product

Resources

About