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Tsutsumi, Shinji; Haruna, Reiko; Tomisato, Wataru; Takano, Tatsunori; Hoshino, Tatsuya; Tsuchiya, Tomofusa; Mizushima, Tohru

doi:10.1023/a:1013267504584

Cited by 11 publications

(4 citation statements)

References 19 publications

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“…Prostaglandins (PGs), signaling compounds derived from arachidonic acid (C20:4n-6), also act in apoptosis. In their work on cytoprotective effects of PGs in gastric mucosa, Tsutsumi et al (2002) found that PGE 1 and PGE 2 inhibited maturation-related spontaneous apoptosis in a dose-related way. PGs can also be proapoptotic.…”

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confidence: 99%

Prostaglandin A₂ induces apoptosis in three cell lines derived from the fall armyworm, Spodoptera frugiperda

Wang

Goodman

Ringbauer

et al. 2021

Arch Insect Biochem Physiol

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Animals maintain homeostasis of cell numbers, constantly creating new cells and eliminating others. Programmed cell death, apoptosis, is a mechanism of cell elimination and it acts in many aspects of animal biology. Drawing on the biomedical background, several signals launch the apoptosis mechanisms, including prostaglandins (PGs). Based on this information, we posed the hypothesis that PGs similarly induce apoptosis in insect cell lines. We used three Spodoptera frugiperda cell lines, including two newly established, BCIRL-SfNS-0518B-YL derived from the central nervous system and BCIRL-Sf4FB-0614-SGS derived from fat body, and the commercially available Sf9 cells. Using a kinetic apoptosis kit, we found treating SfNS cells for 18 h with 15 or 20 μM PGA 2 led to decreases in cell numbers, coupled with increased numbers of apoptotic and dead cells. Similar exposures to 10 μM PGA 2 (24 h) led to substantial increases in apoptotic cells, confirmed by a terminal deoxynucleotidyl transferase dUTP nick end labeling assay on a flow cytometer. The influence of PGA 2 treatments increased with dosage, as we recorded about 20% apoptosis at 24 h post-PGA 2 treatments (10 μM) and about 34% apoptosis at 24 h post-30 μM treatments. PGA 2 treatments led to 10-to 30-fold increases in messenger RNAs (mRNAs) encoding apoptosis-specific caspases-1, −2, −3, and −5 at 12 h and 40-to 60-fold increases in mRNAs encoding

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confidence: 99%

Prostaglandin A₂ induces apoptosis in three cell lines derived from the fall armyworm, Spodoptera frugiperda

Wang

Goodman

Ringbauer

et al. 2021

Arch Insect Biochem Physiol

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“…[1][2][3][4] PGE2 enhances interleukin 10 (IL-10) synthesis and modulates the intestinal immune response to dietary antigen. 5,6) The breakdown of systemic tolerance to luminal antigen is reportedly involved in the development of indomethacin-induced enteropathy.…”

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An Herbal Medicine Orengedokuto Prevents Indomethacin-Induced Enteropathy

Miura

Fukutake

Yamamoto

et al. 2007

Biological & Pharmaceutical Bulletin

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Prostaglandin E2 (PGE2) is a key regulator of gastrointestinal, immunological, and mucosal homeostasis. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the prostaglandin-producing enzyme cyclooxygenases (COXs), and can induce serious complications, such as gastrointestinal damage, with long-term treatment. Orengedokuto (OGT), a Japanese traditional herbal medicine (Kampo medicine), is effective in various animal models of enteropathy. In the present study we examined whether OGT prevents enteropathy induced by NSAIDs in mice. Ulceration in the small intestine was induced with 2 subcutaneous injections of indomethacin (20 mg/kg body weight). Orally administered OGT prevented or reduced lethality, intestinal lesions, bleeding, increased serum nitrate/nitrite levels, and reduction of mucosal PGE2 induced by indomethacin. These beneficial effects of OGT were accompanied by increased production of PGE2 and interleukin 10 by isolated lamina propria mononuclear cells; COX-2 in these cells may be a major source of PGE2 in normal intestines. These findings suggest that OGT could be an effective therapeutic agent for the treatment of inflammatory bowel disease and adverse reactions to NSAIDs.Key words nonsteroidal anti-inflammatory drug; interleukin 10; herbal medicine; inflammatory bowel disease; prostaglandin E2

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“…42 , 43 EPA gives rise to a different family of eicosanoid mediators, including the 3-series prostaglandin and leucotriene B 5 , which are considered to be less inflammatory than AA-derived eicosanoids. 44 , 45 In addition, AA-derived eicosanoids themselves promote cancer cell growth and progression via several biological processes, including carcinogenic activity, 46 inhibition of apoptosis, 47 promotion of angiogenesis, 25 and cancer cell adhesion, 48 whereas EPA exerts other anticarcinogenic effects through a reduction in the production of free radicals and reactive oxygen species, 49 an increment of insulin sensitivity, 50 and an alteration of estrogen metabolism. 19 These findings support the hypothesis that the balance between EPA and AA is important for regulating the production of mediators and subsequent carcinogenesis and cancer proliferation.…”

Section: Discussionmentioning

confidence: 99%

The ratio of serum eicosapentaenoic acid to arachidonic acid and risk of cancer death in a Japanese community: The Hisayama Study

Nagata¹,

Hata²,

Hirakawa³

et al. 2017

Journal of Epidemiology

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BackgroundWhether the intake of eicosapentaenoic acid (EPA) or arachidonic acid (AA) affects the risk of cancer remains unclear, and the association between the serum EPA:AA ratio and cancer risk has not been fully evaluated in general populations.MethodsA total of 3098 community-dwelling subjects aged ≥40 years were followed up for 9.6 years (2002–2012). The levels of the serum EPA:AA ratio were categorized into quartiles (<0.29, 0.29–0.41, 0.42–0.60, and >0.60). The risk estimates were computed using a Cox proportional hazards model. The same analyses were conducted for the serum docosahexaenoic acid to arachidonic acid (DHA:AA) ratio and individual fatty acid concentrations.ResultsDuring the follow-up period, 121 subjects died of cancer. Age- and sex-adjusted cancer mortality increased with lower serum EPA:AA ratio levels (P trend<0.05). In the multivariable-adjusted analysis, the subjects in the first quartile of the serum EPA:AA ratio had a 1.93-fold (95% confidence interval, 1.15–3.22) greater risk of cancer death than those in the fourth quartile. Lower serum EPA concentrations were marginally associated with higher cancer mortality (P trend<0.11), but the serum DHA or AA concentrations and the serum DHA:AA ratio were not (all P trend>0.37). With regard to site-specific cancers, lower serum EPA:AA ratio was associated with a higher risk of death from liver cancer. However, no such associations were detected for deaths from other cancers.ConclusionsThese findings suggest that decreased level of the serum EPA:AA ratio is a significant risk factor for cancer death in the general Japanese population.

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Cited by 11 publications

References 19 publications

Prostaglandin A₂ induces apoptosis in three cell lines derived from the fall armyworm, Spodoptera frugiperda

Prostaglandin A₂ induces apoptosis in three cell lines derived from the fall armyworm, Spodoptera frugiperda

An Herbal Medicine Orengedokuto Prevents Indomethacin-Induced Enteropathy

The ratio of serum eicosapentaenoic acid to arachidonic acid and risk of cancer death in a Japanese community: The Hisayama Study

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Cited by 11 publications

References 19 publications

Prostaglandin A2 induces apoptosis in three cell lines derived from the fall armyworm, Spodoptera frugiperda

Prostaglandin A2 induces apoptosis in three cell lines derived from the fall armyworm, Spodoptera frugiperda

An Herbal Medicine Orengedokuto Prevents Indomethacin-Induced Enteropathy

The ratio of serum eicosapentaenoic acid to arachidonic acid and risk of cancer death in a Japanese community: The Hisayama Study

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Prostaglandin A₂ induces apoptosis in three cell lines derived from the fall armyworm, Spodoptera frugiperda

Prostaglandin A₂ induces apoptosis in three cell lines derived from the fall armyworm, Spodoptera frugiperda