“…We have recently reported that SIRT-1 is an important player in the suppression of hypoxia-induced COX-2 by KRG in A549 cells [28]. We suggested that SIRT-1 activation by KRG has potential therapeutic value in the suppression of inflammation and in cancer therapies under hypoxic conditions.…”
Section: Discussionmentioning
confidence: 91%
“…The invasiveness was absent in the presence of PPARγ inhibitors, indicating that the anti-invasive properties of KRG under hypoxic microenvironments require PPARγ activation and occur via a COX-2/PGE2-dependent pathway. However, this migration and invasion were also inhibited by SIRT-1 inhibitors [28], suggesting that this cellular movement is a complicated phenomenon relying on multiple factors.Fig. 3Korean Red Ginseng (KRG) inhibits migration ability of A549 cells under hypoxia.…”
Section: Resultsmentioning
confidence: 97%
“…We have previously shown that KRG inhibits COX-2 expression under hypoxia in A549 lung cancer cells, where COX-2 is also strongly implicated in tumorigenesis [28]. In the course of studying the mechanism of KRG inhibition of COX-2 under hypoxia, the protein levels of PPARγ were examined.…”
Section: Resultsmentioning
confidence: 99%
“…Phytochemical characteristics of KRG with standard ginsenosides were identified by HPLC analysis as reported previously [29], [30]. HPLC analysis result of standard ginsenosides is provided by Korea Ginseng Cooperation [28]. The ginsenoside content in KRG is 7%, and it is composed of major ginsenosides (G-Rg1, 1.79 mg/g; G-Re, 1.86 mg/g; G-Rf, 1.24 mg/g; G-Rh1, 1.01 mg/g; G-Rg2s, 1.24 mg/g; G-Rb1, 7.44 mg/g; G-Rc, 3.04 mg/g; G-Rb2, 2.59 mg/g; and G-Rd, 0.91 mg/g), and other minor ginsenoside components [29], [30].…”
Section: Methodsmentioning
confidence: 99%
“…We previously showed that Korean Red Ginseng (KRG) efficiently blocks hypoxia-induced COX-2 mediated by sirtuin-1 (SIRT-1), the pathway of which differs from that of dexamethasone [28]. This provides scientific evidence of KRG being effective for the suppression of the inflammatory response and tumorigenesis under hypoxia through mechanisms other than those of steroids.…”
BackgroundKorean Red Ginseng (KRG) is a traditional herbal medicine made by steaming and drying fresh ginseng. It strengthens the endocrine and immune systems to ameliorate various inflammatory responses. The cyclooxygenase-2 (COX-2)/prostaglandin E2 pathway has important implications for inflammation responses and tumorigenesis. Peroxisome proliferator-activated receptor gamma (PPARγ) is a transcription factor that regulates not only adipogenesis and lipid homeostasis, but also angiogenesis and inflammatory responses.MethodsThe effects of the KRG on inhibition of hypoxia-induced COX-2 via PPARγ in A549 cells were determined by luciferase assay, Western blot, and/or quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The antimigration and invasive effects of KRG were evaluated on A549 cells using migration and matrigel invasion assays.Results and conclusionWe previously reported that hypoxia-induced COX-2 protein and mRNA levels were suppressed by KRG. This study examines the possibility of PPARγ as a cellular target of KRG for the suppression of hypoxia-induced COX-2. PPARγ protein levels and PPARγ-responsive element (PPRE)-driven reporter activities were increased by KRG. Reduction of hypoxia-induced COX-2 by KRG was abolished by the PPARγ inhibitor GW9662. In addition, the inhibition of PPARγ abolished the effect of KRG on hypoxia-induced cell migration and invasion.DiscussionOur results show that KRG inhibition of hypoxia-induced COX-2 expression and cell invasion is dependent on PPARγ activation, supporting the therapeutic potential for suppression of inflammation under hypoxia. Further studies are required to demonstrate whether KRG activates directly PPARγ and to identify the constituents responsible for this activity.
“…We have recently reported that SIRT-1 is an important player in the suppression of hypoxia-induced COX-2 by KRG in A549 cells [28]. We suggested that SIRT-1 activation by KRG has potential therapeutic value in the suppression of inflammation and in cancer therapies under hypoxic conditions.…”
Section: Discussionmentioning
confidence: 91%
“…The invasiveness was absent in the presence of PPARγ inhibitors, indicating that the anti-invasive properties of KRG under hypoxic microenvironments require PPARγ activation and occur via a COX-2/PGE2-dependent pathway. However, this migration and invasion were also inhibited by SIRT-1 inhibitors [28], suggesting that this cellular movement is a complicated phenomenon relying on multiple factors.Fig. 3Korean Red Ginseng (KRG) inhibits migration ability of A549 cells under hypoxia.…”
Section: Resultsmentioning
confidence: 97%
“…We have previously shown that KRG inhibits COX-2 expression under hypoxia in A549 lung cancer cells, where COX-2 is also strongly implicated in tumorigenesis [28]. In the course of studying the mechanism of KRG inhibition of COX-2 under hypoxia, the protein levels of PPARγ were examined.…”
Section: Resultsmentioning
confidence: 99%
“…Phytochemical characteristics of KRG with standard ginsenosides were identified by HPLC analysis as reported previously [29], [30]. HPLC analysis result of standard ginsenosides is provided by Korea Ginseng Cooperation [28]. The ginsenoside content in KRG is 7%, and it is composed of major ginsenosides (G-Rg1, 1.79 mg/g; G-Re, 1.86 mg/g; G-Rf, 1.24 mg/g; G-Rh1, 1.01 mg/g; G-Rg2s, 1.24 mg/g; G-Rb1, 7.44 mg/g; G-Rc, 3.04 mg/g; G-Rb2, 2.59 mg/g; and G-Rd, 0.91 mg/g), and other minor ginsenoside components [29], [30].…”
Section: Methodsmentioning
confidence: 99%
“…We previously showed that Korean Red Ginseng (KRG) efficiently blocks hypoxia-induced COX-2 mediated by sirtuin-1 (SIRT-1), the pathway of which differs from that of dexamethasone [28]. This provides scientific evidence of KRG being effective for the suppression of the inflammatory response and tumorigenesis under hypoxia through mechanisms other than those of steroids.…”
BackgroundKorean Red Ginseng (KRG) is a traditional herbal medicine made by steaming and drying fresh ginseng. It strengthens the endocrine and immune systems to ameliorate various inflammatory responses. The cyclooxygenase-2 (COX-2)/prostaglandin E2 pathway has important implications for inflammation responses and tumorigenesis. Peroxisome proliferator-activated receptor gamma (PPARγ) is a transcription factor that regulates not only adipogenesis and lipid homeostasis, but also angiogenesis and inflammatory responses.MethodsThe effects of the KRG on inhibition of hypoxia-induced COX-2 via PPARγ in A549 cells were determined by luciferase assay, Western blot, and/or quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The antimigration and invasive effects of KRG were evaluated on A549 cells using migration and matrigel invasion assays.Results and conclusionWe previously reported that hypoxia-induced COX-2 protein and mRNA levels were suppressed by KRG. This study examines the possibility of PPARγ as a cellular target of KRG for the suppression of hypoxia-induced COX-2. PPARγ protein levels and PPARγ-responsive element (PPRE)-driven reporter activities were increased by KRG. Reduction of hypoxia-induced COX-2 by KRG was abolished by the PPARγ inhibitor GW9662. In addition, the inhibition of PPARγ abolished the effect of KRG on hypoxia-induced cell migration and invasion.DiscussionOur results show that KRG inhibition of hypoxia-induced COX-2 expression and cell invasion is dependent on PPARγ activation, supporting the therapeutic potential for suppression of inflammation under hypoxia. Further studies are required to demonstrate whether KRG activates directly PPARγ and to identify the constituents responsible for this activity.
Avenanthramide C (AVC), found mainly in oats, mediates anti-inflammatory activities by reducing the anti-inflammatory cytokine levels. This study investigated the effects of AVC on hypoxiainduced cyclooxygenase-2 (COX-2) expression in A549 cells. AVC suppressed the hypoxiainduced increase in COX-2 protein levels and promoter activity. We also observed that the effects of AVC were reversed by a SIRT1 inhibitor, indicating that the inhibitory effects of AVC on hypoxia-induced COX-2 expression are mediated by SIRT1. Therefore, AVC inhibits the hypoxic induction of COX-2 expression via SIRT1 activation. Our results suggest that AVC could be beneficial for preventing lung inflammation under hypoxia.
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