Suppression of inducible nitric oxide synthase by (−)-isoeleutherin from the bulbs of Eleutherine americana through the regulation of NF-κB activity

Song, Su-Hyun; Min, Hye‐Young; Han, Ah‐Reum; Nam, Joo‐Won; Seo, Eun‐Kyoung; Park, Seoung Woo; Lee, Sang Hyung; Lee, Sang Kook

doi:10.1016/j.intimp.2008.12.003

Cited by 27 publications

(18 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Similarly, in the present study, we observed an increased NF-κB p65 and iNOS expression induced by cytoplasmic irradiation only in ρ + SAE cells but not in ρ 0 SAE cells, indicating that NF-κB/iNOS pathways are associated with mitochondrial signaling events. Our finding is consistent with previous reports that NF-κB activation was partially lost in mtDNA-depleted ρ 0 HSF in response to α particle irradiation [43], and that iNOS activation is also dependent on transcription of NF-κB [44]. Therefore, it is not surprising that iNOS expression is not induced by cytoplasmic irradiation in ρ 0 SAE cells where NF-κB p65 expression is unchanged.…”

Section: Discussionsupporting

confidence: 93%

Mitochondria regulate DNA damage and genomic instability induced by high LET radiation

Zhang

Davidson

Hei

2014

Life Sciences in Space Research

View full text Add to dashboard Cite

High linear energy transfer (LET) radiation including α particles and heavy ions is the major type of radiation find in space and is considered a potential health risk for astronauts. Even though the chance that these high LET particles traversing through the cytoplasm of cells is higher than that through the nuclei, the contribution of targeted cytoplasmic irradiation, to the induction of genomic instability and other chromosomal damages induced by high LET radiation is not known. In the present study, we investigated whether mitochondria are the potential cytoplasmic target of high LET radiation in mediating cellular damage using a mitochondrial DNA (mtDNA) depleted (ρ0) human small airway epithelial (SAE) cell model and a precision charged particle microbeam with a beam width of merely one micron. Targeted cytoplasmic irradiation by high LET α particles induced DNA oxidative damage and double strand breaks in wild type ρ+ SAE cells. Furthermore, there was a significant increase in autophagy, micronuclei, which is an indication of genomic instability, together with the activation of nuclear factor kappa-B (NF-κB) and mitochondrial inducible nitric oxide synthase (iNOS) signaling pathways in ρ+ SAE cells. In contrast, ρ0 SAE cells exhibited a significantly lower response to these same endpoints examined after cytoplasmic irradiation with high LET α particles. The results indicate that mitochondria are essential in mediating cytoplasmic radiation induced genotoxic damage in mammalian cells. Furthermore, the findings may shed some light in the design of countermeasures for space radiation.

show abstract

Section: Discussionsupporting

confidence: 93%

Mitochondria regulate DNA damage and genomic instability induced by high LET radiation

Zhang

Davidson

Hei

2014

Life Sciences in Space Research

View full text Add to dashboard Cite

show abstract

“…Ahn et al showed that a furonaphthoquinone compound suppressed cyclooxygenase-2 expression in RAW 264.7 macrophages which may confer potential antiinflammatory activity to this compound [66]. Similarly, Song et al showed that isoeleutherin suppressed the expression of inducible NO synthase and various cytokines by inhibiting NF-κB activity [67]. The effectiveness of AgD on PGE 2- induced hyperalgesia suggests that it does not act by inhibiting NF-κB activity.…”

Section: Discussionmentioning

confidence: 99%

“…To further support this hypothesis, we found that treating macrophages with AgD did not change the LPS-induced NO production at any of the concentrations tested. Therefore, AgD did not appear to exert a similar effect as the one observed for isoeleutherin [67]. …”

Section: Discussionmentioning

confidence: 99%

Antinociceptive Activity of the Ethanolic Extract, Fractions, and Aggregatin D Isolated from Sinningia aggregata Tubers

et al. 2015

View full text Add to dashboard Cite

The present study investigated the effects of the ethanolic extract (ESa), fractions, and compounds isolated from Sinningia aggregata in male Swiss mice on carrageenan-induced paw edema, neutrophil migration, mechanical hyperalgesia, formalin-induced nociception, and lipopolysaccharide-induced fever. The ESa did not alter edema, neutrophil migration, or fever at any of the doses tested. However, the ESa reduced phase II of formalin-induced nociception and carrageenan-induced mechanical hyperalgesia. The petroleum ether (PE) and ethyl acetate (EA) fractions and aggregatin D (AgD; isolated from the EA fraction) reduced formalin-induced nociception. Anthraquinones from the PE fraction were ineffective. AgD also inhibited carrageenan-induced mechanical hyperalgesia. Neither the ESa nor AgD altered thermal nociception or motor performance. Local administration of AgD also reduced hyperalgesia induced by carrageenan, bradykinin, tumor necrosis factor-α, interleukin-1β, cytokine-induced neutrophil chemoattractant, prostaglandin E2, and dopamine but not hyperalgesia induced by forskolin or dibutyryl cyclic adenosine monophosphate. The positive control dipyrone reduced the response induced by all of the stimuli. Additionally, glibenclamide abolished the analgesic effect of dipyrone but not the one induced by AgD. AgD did not change lipopolysaccharide-induced nitric oxide production by macrophages or the nociception induced by capsaicin, cinnamaldehyde, acidified saline, or menthol. These results suggest that the ESa has important antinociceptive activity, and this activity results at least partially from the presence of AgD. AgD reduced mechanical hyperalgesia induced by several inflammatory mediators through mechanisms that are different from classic analgesic drugs.

show abstract

“…Therefore, the regulation of NF-kB is often considered a therapeutic target for inflammatory diseases and, in this regard, numerous phytochemicals that affect NF-kB activity have been identified. Anti-inflammatory effects of isoeleutherin, a phytochemical isolated from the flowering plant Eleutherine bulbosa, are mediated by inhibiting NF-kB in LPS-treated macrophages (Song et al, 2009). Capsaicin suppressed obesityinduced inflammation in adipose tissue macrophages, which was associated with inactivation of NF-kB and activation of peroxisome proliferator-activated receptor (PPAR)-g .…”

mentioning

confidence: 99%

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

et al. 2014

View full text Add to dashboard Cite

Suppression of inducible nitric oxide synthase by (−)-isoeleutherin from the bulbs of Eleutherine americana through the regulation of NF-κB activity

Cited by 27 publications

References 15 publications

Mitochondria regulate DNA damage and genomic instability induced by high LET radiation

Mitochondria regulate DNA damage and genomic instability induced by high LET radiation

Antinociceptive Activity of the Ethanolic Extract, Fractions, and Aggregatin D Isolated from Sinningia aggregata Tubers

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

Contact Info

Product

Resources

About