Ursolic acid protects mouse liver against CCl4-induced oxidative stress and inflammation by the MAPK/NF-κB pathway

Ma, Jie-Qiong; Ding, Jie; Zhang, Li; Liu, Chan-Min

doi:10.1016/j.etap.2014.03.011

Cited by 107 publications

(77 citation statements)

References 30 publications

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“…The present study quantified the serum levels of MDA and SOD, and these were significantly suppressed by treatment with ursolic acid in the I/R-IAKI rat. Ma et al (22) suggested that ursolic acid protects against CCl 4 -induced oxidative stress and inflammation of the liver in mice. Ramachandran et al (23) concluded that ursolic acid protects against exposure to ultraviolet B-induced reactive oxygen species through modulation of antioxidants (23).…”

Section: Discussionmentioning

confidence: 99%

Renoprotective effects of ursolic acid on ischemia/reperfusion-induced acute kidney injury through oxidative stress, inflammation and the inhibition of STAT3 and NF-κB activities

Peng

Ren

Lan

et al. 2016

Molecular Medicine Reports

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Abstract. Ursolic acid, a pentacyclic triterpene compound with low toxicity and easy availability, has a variety of biological activities, including antitumor, antioxidant, antihepatitis, anti-inflammatory and antibacterial effects. The present study aimed to investigate the renoprotective effects of ursolic acid on ischemia/reperfusion-induced acute kidney injury (I/R-IAKI) in rats associated with its antioxidant and anti-inflammatory effects, as well as interference with the signal transducer and activator of transcription (STAT)3/nuclear factor (NF)-κB signaling pathway. The present study demonstrated that pre-treatment with ursolic acid significantly increased renal functioning and attenuated increases of serum angiotensin II levels in rats subjected to I/R-IAKI. In addition, I/R-IAKI-induced inflammation and oxidative stress were significantly reduced by pre-treatment with ursolic acid. Furthermore, ursolic acid significantly suppressed the upregulation of STAT3, NF-κB and caspase-3 activities in rats following I/R-IAKI. These results indicated that ursolic acid may be a potential drug for reducing I/R-IAKI through suppression of inflammation and oxidative stress damage, as well as modulation of STAT3 and NF-κB activities.

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Section: Discussionmentioning

confidence: 99%

Renoprotective effects of ursolic acid on ischemia/reperfusion-induced acute kidney injury through oxidative stress, inflammation and the inhibition of STAT3 and NF-κB activities

Peng

Ren

Lan

et al. 2016

Molecular Medicine Reports

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“…On the other hand, excessive (chronic) inflammation has been linked with various chronic diseases such as obesity, diabetes, cardiovascular disorders and some cancers 23. A previous study reported that UA can protect mouse liver from CCl 4 ‐induced inflammatory response by decreasing the activation of JNK, p38 MAPK and ERK in the MAPK signaling pathway and by regulating the NF‐κB signaling pathway 24. Moreover, UA was able to inhibit mitogen‐induced phosphorylation of ERK and JNK as well as their upstream kinases, MEK and c‐Raf, in lymphocytes 25.…”

Section: Discussionmentioning

confidence: 99%

Ursolic Acid, a Natural Nutraceutical Agent, Targets Caspase3 and Alleviates Inflammation‐Associated Downstream Signal Transduction

Yuan

Wang

et al. 2017

Molecular Nutrition Food Res

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ScopeUrsolic acid (UA) is a pentacyclicterpenoid carboxylic acid that is present in a wide variety of plant foods. There are many beneficial health effects that are attributed to the properties of UA. However, the specific cellular targets of UA and the mechanism underlying downstream signal transduction processes linked to the anti‐inflammation pathway have not been thoroughly elucidated to date.Methods and resultsChemical biology strategies such as target fishing, click reaction synthesis of a UA probe and molecular imaging were used to identify potential target proteins of UA. Cysteinyl aspartate specific proteinase 3 (CASP3) and its downstream signaling pathway were verified as potential targets by molecular docking, intracellular enzyme activity evaluation and accurate pathway analysis. The results indicated that UA acted on CASP3, ERK1 and JNK2 targets, alleviated inflammation‐associated downstream multiple signal transduction factors, including ERK1, NF‐κB and STAT3, and exhibited anti‐inflammation activities.ConclusionAs a natural dietary supplement, UA demonstrated anti‐inflammation activity via inhibition of CASP3 and shows the potential to improve the therapy effect of several inflammation‐associated diseases.

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“…Various cellular pathways are activated during a prolonged inflammation process in the liver, such as NF-B (Assenat, Grebal-Chaloin, Maurel, Vilarem, & Pascussi, 2006) and JAK/STAT3 (Park et al, 2010), as well as MAPK signalings (Ma, Ding, Zhang, & Liu, 2014). EMCDO alleviated the inflammation mediator production and ear inflammation, possibly through the activation of NF-B in the RAW264.7 system, but no effects on MAPK were observed.…”

Section: Discussionmentioning

confidence: 99%

Suppression of Hepatitis B Virus Production and Inflammatory Response in vitro and in vivo by Mormodica charantia Compound EMCDO

Chang¹,

Chen²,

Chen³

et al. 2015

JAS

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Eight compounds were purified from Mormodica charanti, and their chemical structures were determined in this study. Their anti-HBV and anti-inflammation activities were investigated. Compound EMCDO exhibited the most efficient effect in terms of reducing HBV surface antigen, e antigen and viral DNA levels in HBV particles or surface antigen-producing cells 2.2.15 and PLC/PRF/5, respectively. Tumor suppressor p53 played a significant role in EMCDO-mediated anti-HBV effects. Pretreatment with EMCDO prevented 2.2.15 cells-induced tumor formation in a nude mice subcutaneous model. The anti-HBV and anti-tumor activities of EMCDO were better than those of oltipraz, an inhibitor of HBV transcription. EMCDO reduced the proinflammatory cytokines and mediators in LPS-treated RAW264.7 cells in a dose-dependent manner. The LPS-upregulated phosphorylation level of I was reduced in the presence of EMCDO. The transcription activity of NF-B was increased in cells treated with EMCDO. Utilization of a mouse ear edema model further confirmed the activity of EMCDO against TPA-elicited inflammation.

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Ursolic acid protects mouse liver against CCl4-induced oxidative stress and inflammation by the MAPK/NF-κB pathway

Cited by 107 publications

References 30 publications

Renoprotective effects of ursolic acid on ischemia/reperfusion-induced acute kidney injury through oxidative stress, inflammation and the inhibition of STAT3 and NF-κB activities

Renoprotective effects of ursolic acid on ischemia/reperfusion-induced acute kidney injury through oxidative stress, inflammation and the inhibition of STAT3 and NF-κB activities

Ursolic Acid, a Natural Nutraceutical Agent, Targets Caspase3 and Alleviates Inflammation‐Associated Downstream Signal Transduction

Suppression of Hepatitis B Virus Production and Inflammatory Response in vitro and in vivo by Mormodica charantia Compound EMCDO

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