The anti-apoptotic effects of nordihydroguaiaretic acid: Inhibition of cPLA2 activation during TNF-induced apoptosis arises from inhibition of calcium signaling

Culver, Carolyn A.; Michalowski, Susan; Maia, Rita C.; Laster, Scott M.

doi:10.1016/j.lfs.2005.03.023

Cited by 12 publications

(7 citation statements)

References 44 publications

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“…The inhibitory effect of NDGA on intracellular calcium level has been previously described. Culver et al 43 reported that NDGA inhibits TNF-induced apoptosis by preventing a rise in the intracellular calcium level in the 3T3-like murine fibroblast cell line. However, the effect of NDGA on Ca 2 þ oscillation associated with osteoclastogenesis has not been previously reported.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…43,45 NDGA regulates IFN-g-mediated inflammation through mechanisms unrelated to the inhibition of 5-LO. 43 In this work, we investigated the inhibitory mechanism of NDGA on osteoclastogenesis. Rev-5901, 30 another 5-LO inhibitor, showed no apparent inhibitory effect on osteoclast Figure 5 Effects of NDGA on the RANKL signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

“…17,46 Culver et al 43 and Eads et al 47 reported that NDGA and its methylated derivative, terameprocol, inhibit production of TNF-a and several other inflammatory cytokines induced by LPS. However, in this study, inflammatory parameters, such as paw swelling, and inflammatory scores in AA rats were not significantly reduced by NDGA treatment.…”

Section: Discussionmentioning

confidence: 99%

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Nordihydroguaiaretic acid inhibition of NFATc1 suppresses osteoclastogenesis and arthritis bone destruction in rats

Kukita

Watanabe

et al. 2012

Laboratory Investigation

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Nordihydroguaiaretic acid (NDGA) is known to have prominent anticancer activity against several cancers, and is also known to be an inhibitor of 5-lipoxygenase (5-LO). In this study, we investigated the regulatory function of NDGA on inflammatory bone destruction mediated by osteoclasts. NDGA markedly inhibited receptor activator of nuclear factor-kB (NF-kB) ligand (RANKL)-induced formation of osteoclasts in cultures of murine osteoclast precursor cell line RAW-D cells and primary bone marrow-derived macrophages culture systems. The inhibitory effect of NDGA on osteoclastogenesis did not arise from the inhibition of 5-LO activity. NDGA did not affect MAPKs, such as p38, JNK, and NF-kB, but significantly inhibited the induction of NFATc1, a key transcription factor for osteoclastogenesis. NDGA also suppressed activation of ERK in osteoclast precursors. RANKL-induced calcium oscillation observed in osteoclast precursors was completely diminished by the addition of NDGA. In mature osteoclasts, RANKL-induced nuclear translocation of NFATc1 was clearly inhibited by NDGA treatment. Finally, in vivo studies demonstrated that administration of NDGA significantly reduced severe bone destruction and osteoclast recruitment in the ankle joint of rats with adjuvant-induced arthritis. These results indicate the potential utility of NDGA as a therapeutic agent for ameliorating inflammatory bone destruction in rheumatoid arthritis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Nordihydroguaiaretic acid inhibition of NFATc1 suppresses osteoclastogenesis and arthritis bone destruction in rats

Kukita

Watanabe

et al. 2012

Laboratory Investigation

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“…1) [1]. NDGA possesses a number of interesting biological properties which are of potential use to humans such as enzyme inhibition [2], antimicrobial properties [3], protection from neurotoxicity and bladder toxicity [4,5], stimulation of the corpus luteum for the secretion of progesterone [6], potential vaso-and bronchodilation [7], and anti-apoptotic [8], estrogenic [9], antimutagenic [10] and anti-cancer [11] properties. NDGA has also been reported to possess both genotoxic [12] and anti-genotoxic potential [13] in vivo and in vitro.…”

Section: Introductionmentioning

confidence: 99%

Antigenotoxic effect of nordihydroguaiaretic acid against chlormadinone acetate-induced genotoxicity in mice bone-marrow cells

et al. 2007

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Nordihydroguaiaretic acid (NDGA), a phenolic lignan, was tested for its antigenotoxic potential against chlormadinone acetate (CMA)-induced genotoxic damage in mice bone-marrow cells. Doses of about 22.50 mg/kg body weight of CMA were given along with 1, 5 and 10 mg/kg body weight of NDGA intraperitoneally. The treatment resulted in the reduction of sister chromatid exchanges and chromosomal aberrations induced by CMA, suggesting an antigenotoxic potential of NDGA. Earlier studies show that CMA generates reactive oxygen species, responsible for genotoxic damage. The free radical-scavenging property of NDGA is responsible for the reduction of genotoxic damage induced by CMA in mice bone-marrow cells.

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A pinoresinol–lariciresinol reductase homologue from the creosote bush (Larrea tridentata) catalyzes the efficient in vitro conversion of p-coumaryl/coniferyl alcohol esters into the allylphenols chavicol/eugenol, but not the propenylphenols p-anol/isoeugenol

Vassão

Kim

Milhollan

et al. 2007

Archives of Biochemistry and Biophysics

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The anti-apoptotic effects of nordihydroguaiaretic acid: Inhibition of cPLA2 activation during TNF-induced apoptosis arises from inhibition of calcium signaling

Cited by 12 publications

References 44 publications

Nordihydroguaiaretic acid inhibition of NFATc1 suppresses osteoclastogenesis and arthritis bone destruction in rats

Nordihydroguaiaretic acid inhibition of NFATc1 suppresses osteoclastogenesis and arthritis bone destruction in rats

Antigenotoxic effect of nordihydroguaiaretic acid against chlormadinone acetate-induced genotoxicity in mice bone-marrow cells

A pinoresinol–lariciresinol reductase homologue from the creosote bush (Larrea tridentata) catalyzes the efficient in vitro conversion of p-coumaryl/coniferyl alcohol esters into the allylphenols chavicol/eugenol, but not the propenylphenols p-anol/isoeugenol

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