Anti-inflammatory mechanism of PPARγ on LPS-induced pulp cells: Role of the ROS removal activity

Kim, Jae-Cheol; Lee, Younghee; Yu, Mi-Kyung; Lee, Nan-Hee; Park, Jong-Duk; Bhattarai, Govinda; Yi, Ho-Keun

doi:10.1016/j.archoralbio.2011.09.009

Cited by 54 publications

(37 citation statements)

References 33 publications

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“…A role for PPAR␥ in regulating reactive oxygen species (ROS) levels in the hypothalamus in high fat-fed mice was previously reported (9). The anti-inflammatory effect of PPAR␥ on LPS-induced pulpal inflammation is also due to decreasing ROS levels (28). Our data indicating that the sEH deficiency downregulates oxidative stress in UUO kidneys are consistent with these reports.…”

Section: Discussionsupporting

confidence: 91%

Inhibition of soluble epoxide hydrolase prevents renal interstitial fibrosis and inflammation

Kim

Imig

Yang

et al. 2014

American Journal of Physiology-Renal Physiology

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Section: Discussionsupporting

confidence: 91%

Inhibition of soluble epoxide hydrolase prevents renal interstitial fibrosis and inflammation

Kim

Imig

Yang

et al. 2014

American Journal of Physiology-Renal Physiology

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“…14 This molecule plays an important role in LPS-mediated pulp inflammation, by removing ROS from cells and tissues. 37,38 PPARg overexpressed HDPCs increased their viability after exposure to toxic concentrations of H 2 O 2 , associated with increased activity of the anti-oxidant enzymes Cu/ZnSOD and MnSOD, and up-regulation of DSPP and DMP-1 proteins. 14 Therefore, both OH-1 and PPARg plays a protective role in the induction of dentinogenesis under oxidative stress in human pulp cells.…”

Section: Discussionmentioning

confidence: 98%

Responses of human dental pulp cells after application of a low-concentration bleaching gel to enamel

Soares

Basso

Scheffel

et al. 2015

Archives of Oral Biology

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“…PPARγ acted as a molecular switch in moderating myocardial injury via blocking the MAPK pathway in isoproterenol-induced myocardial injury in rats [43]. PPARγ agonist suppressed ERK MAPK signal activation to inhibit activity of cellular NO and reactive oxygen species formation, counteracting LPS-induced inflammatory response in pulp cells [44]. These data suggested that the activation of MAPK pathways is regulated by PPARγ.…”

Section: Discussionmentioning

confidence: 99%

Activation of PPARγ suppresses proliferation and induces apoptosis of esophageal cancer cells by inhibiting TLR4-dependent MAPK pathway

Yang

Liu

et al. 2016

Oncotarget

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Although substantial studies on peroxisome proliferator-activated receptor γ (PPARγ) have focused on the mechanisms by which PPARγ regulates glucose and lipid metabolism, recent reports have suggested that PPARγ shows tumorigenic or antitumorigenic effects. The roles and mechanisms of PPARγ activation in esophageal cancer remain unclarified. EC109 and TE10 esophageal cancer cells were treated with 0, 10, 20 and 40 mM of PPARγ agonist rosiglitazone (RGZ) for 24, 48, and 72 h, and the cell viability and apoptosis were detected using methyl thiazolyl tetrazolium (MTT) assay and Flow cytometric (FCM) analysis, respectively. Moreover, the effects of inhibition of PPARγ by antagonist or specific RNA interference on cell viability, apoptosis, the Toll-like receptor 4 (TLR4) and mitogen-activated protein kinase (MAPK) pathways were evaluated. Additionally, the effect of TLR4 signaling on the MAPK pathway, cell viability and apoptosis was assessed. The results showed that RGZ suppressed proliferation and induced apoptosis of esophageal cancer cells, which could be partly restored by inactivation of PPARγ. RGZ suppressed the MAPK and TLR4 pathways, and the inhibitory effect could be counteracted by PPARγ antagonist or specific RNA interference. We also suggested that MAPK activation was regulated by the TLR4 pathway and that blocking the TLR4 and MAPK pathways significantly suppressed proliferation and induced apoptosis of esophageal cancer cells. In conclusion, our data suggested that activation of PPARγ suppressed proliferation and induced apoptosis of esophageal cancer cells by inhibiting TLR4-dependent MAPK pathway.

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Anti-inflammatory mechanism of PPARγ on LPS-induced pulp cells: Role of the ROS removal activity

Cited by 54 publications

References 33 publications

Inhibition of soluble epoxide hydrolase prevents renal interstitial fibrosis and inflammation

Inhibition of soluble epoxide hydrolase prevents renal interstitial fibrosis and inflammation

Responses of human dental pulp cells after application of a low-concentration bleaching gel to enamel

Activation of PPARγ suppresses proliferation and induces apoptosis of esophageal cancer cells by inhibiting TLR4-dependent MAPK pathway

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