Erratum to “15-Deoxy-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi mathvariant="bold">γ</mml:mi></mml:mrow></mml:math>12,14-prostaglandin J2 Reduces Liver Impairment in a Model of ConA-Induced Acute Hepatic Inflammation by Activation of PPAR<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M2"><mml:mrow><mml:mi>γ</mml:mi></mml:mrow></mml:math> and Reduction in NF-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M3"><mml:mrow><mml:mi>κ</mml:mi></mm

Chen, Kan; Li, Jingjing; Wang, Junshan; Xia, Yujing; Dai, Weiqi; Wang, Fan; Miao, Song; Peng, Cheng; Zhang, Yan; Wang, Chengfen; Yang, Jing; Zhu, Rong; Zhang, Huawei; Zheng, Yuanyuan; Lu, Jie; Fan, Zhuoyi; Zhou, Yingqun; Guo, Chuanyong

doi:10.1155/2014/864839

Cited by 6 publications

(5 citation statements)

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“…Altogether, this data suggests that the reduction in myocardial infarct size afforded by these drugs is, at least in part, due to their ability to activate PPARγ. PPARγ also has inhibitory interactions with other transcription factors, such as NF-κB ( Arab et al, 2014 ; Chen et al, 2014 ). Specifically, we found that RosA treatment significantly decreased I/R induced NF-κB mRNA and protein expression in the absence of, but not in the presence of, GW9662 or T0070907.…”

Section: Discussionmentioning

confidence: 99%

Rosmarinic Acid Protects against Inflammation and Cardiomyocyte Apoptosis during Myocardial Ischemia/Reperfusion Injury by Activating Peroxisome Proliferator-Activated Receptor Gamma

Han

Wang

et al. 2017

Front. Pharmacol.

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The cardiac ischemia-reperfusion (I/R) injury greatly influences the therapeutic effect and remains an urgent challenge in clinical therapy. Polypharmacology opens a new therapeutic opportunity to design drugs with a specific target for improving the efficacy. In this study, we first forecasted that Rosmarinic acid (RosA) could be used for the treatment of cardiovascular disease using text mining, chemometric and chemogenomic methods. Consistent with the effect of the positive drug (pioglitazone, PIO), we subsequently validated that RosA pretreatment could restore the decreased cardiac hemodynamic parameters (LVDP, ± dp/dtmin, ± dp/dtmax and CF), decreased the infarct size and the cardiomyocyte apoptosis in a rat model of cardiac I/R injury. Furthermore, RosA pre-treatment inhibited the levels of inflammatory cytokines (IL-6, TNF-α and CRP), up-regulated PPARγ expression and down-regulated NF-κB expression in myocardial tissue isolated from the rat model of I/R-induced myocardial injury. In addition, the effects of RosA were reversed by co-treatment with PPAR-γ inhibitor GW9662 and T0070907, respectively. These data suggest that RosA attenuates cardiac injury through activating PPARγ and down-regulating NF-κB-mediated signaling pathway, which inhibiting inflammation and cardiomyocyte apoptosis in a rat model of cardiac I/R injury.

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Section: Discussionmentioning

confidence: 99%

Rosmarinic Acid Protects against Inflammation and Cardiomyocyte Apoptosis during Myocardial Ischemia/Reperfusion Injury by Activating Peroxisome Proliferator-Activated Receptor Gamma

Han

Wang

et al. 2017

Front. Pharmacol.

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“…Macrophage is one of the key mediators which regulate the progress of hepatic inflammation (Han et al, 2016). Furthermore, Increasing reports indicate that liver macrophages play an important role in modulating inflammation through phagocytosis cytokine production, and antigen presentation (Chen et al, 2014;Wijesundera et al, 2014). In response to microenvironmental signals, It has been reported that long-term pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β, are strongly associated with the development of acute and chronic inflammation (Murakami and Ohigashi, 2007).…”

Section: Discussionmentioning

confidence: 99%

Hesperetin derivative-14 alleviates inflammation by activating PPAR-γ in mice with CCl4-induced acute liver injury and LPS-treated RAW264.7 cells

Chen

Ding

et al. 2017

Toxicology Letters

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Hesperetin is a flavanone glycoside compound naturally occurring in the fruit peel of Citrusaurantium L. (Rutaceae). Previous studies revealed that hesperetin possesses various pharmacological effects, including anti-inflammation, anti-tumor, anti-oxidant and neuroprotective properties. Hesperetin derivative-14 (HD-14) is a derivative of hesperetin improved in water solubility and bioavailability. In this study, we indicated that HD-14 (2μM) significantly attenuated inflammation in LPS-treated RAW264.7 cells, besides, HD-14 (100mg/kg) exhibited hepato-protective effects and anti-inflammatory effects on C57BL/6J mice with CCl-induced acute liver injury. In addition, it was demonstrated that HD-14 dramatically up-regulated the expression of PPAR-γ in vivo and in vitro. Interestingly, over-expression of PPAR-γ had anti-inflammatory effects on the expressions of TNF-α, IL-6, and IL-1β, whereas, knockdown of PPAR-γ with small interfering RNA had pro-inflammatory effects in LPS-treated RAW264.7 cells. Thus, our findings demonstrated that HD-14 alleviated inflammation by activating PPAR-γ expression at least in part. Further studies founded that HD-14 remarkably inhibited the expression of p-JAK1 and p-STAT1 through up-regulating PPAR-γ. Together, these results suggested that HD-14 served as an activator of PPAR-γ and the JAK1/STAT1 signaling pathway may be involved in the progress of inflammation. Collectively, HD-14 may be utilized as a potential anti-inflammation monomeric compound in the treatment of acute liver injury.

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“…Altogether, this data suggests that the reduction in liver tissue injury afforded by these drugs is, at least in part, due to their ability to activate PPARγ. PPARγ also has inhibitory interactions with other transcription factors, such as NF-κB ( 25 , 26 ). Specifically, we found that LCE treatment significantly decreased CCl 4 -induced NF-κB mRNA and protein expression in the absence of, but not in the presence of GW9662.…”

Section: Discussionmentioning

confidence: 99%

Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma

Han

Wang

et al. 2017

Molecular Medicine Reports

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The present study aimed to investigate the hepatoprotective role of Licochalcone E (LCE) and its mechanism of action in a mouse model of carbon tetrachloride (CCl4)-induced liver toxicity. Hepatotoxicity was induced in Kunming mice via an intraperitoneal injection (IP) of CCl4, 10 ml/kg body weight, diluted with corn oil at a 1:500 ratio. LCE was administered once a day for 7 days (IP) as pretreatment at a dose of 5 mg/kg/day. The levels of C-reactive protein (CRP) and tumor necrosis factor (TNF)-α were analyzed to determine the inflammation status. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed using ELISA assays. Liver ultrastructure was observed via optical microscopy. The mRNA and protein expression levels of peroxisome proliferator-activated receptor (PPAR)γ, and nuclear factor (NF)-κB were assayed using quantitative polymerase chain reaction and western blot analysis, respectively. Pretreatment with LCE decreased levels of ALT, AST, CRP and TNF-α, and NF-κB expression in the experimental hepatotoxicity mice model induced by CCl4. In addition, LCE increased the expression of PPARγ and normalized the hepatic histoarchitecture. However, the effects of LCE were reversed by cotreatment with the PPARγ inhibitor GW9662. The present study suggests that LCE may be used for the treatment of hepatotoxicity, and primarily exhibits its protective role through a PPARγ/NF-κB-mediated pathway.

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Erratum to “15-Deoxy-γ12,14-prostaglandin J2 Reduces Liver Impairment in a Model of ConA-Induced Acute Hepatic Inflammation by Activation of PPARγ and Reduction in NF-κ

Abstract: In the paper titled "15-Deoxy-12,14-prostaglandin J2 reduces liver impairment in a model of ConA-induced acute hepatic inflammation by activation of PPAR and reduction in NF-B activity, " "15-Deoxy-12,14-prostaglandin" is corrected to be "15-Deoxy-Δ12,14-prostaglandin" in the main title.

Cited by 6 publications

References 0 publications

Rosmarinic Acid Protects against Inflammation and Cardiomyocyte Apoptosis during Myocardial Ischemia/Reperfusion Injury by Activating Peroxisome Proliferator-Activated Receptor Gamma

Rosmarinic Acid Protects against Inflammation and Cardiomyocyte Apoptosis during Myocardial Ischemia/Reperfusion Injury by Activating Peroxisome Proliferator-Activated Receptor Gamma

Hesperetin derivative-14 alleviates inflammation by activating PPAR-γ in mice with CCl4-induced acute liver injury and LPS-treated RAW264.7 cells

Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma

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