Diclofenac, a non-steroidal anti-inflammatory drug, suppresses apoptosis induced by endoplasmic reticulum stresses by inhibiting caspase signaling

Yamazaki, Takao; Muramoto, Masakazu; Oe, Tomoya; Morikawa, Noriyuki; Okitsu, Osamu; Nagashima, Takahiro; Nishimura, Shintaro; Katayama, Yoshiki; Kita, Yasuhiro

doi:10.1016/j.neuropharm.2005.10.016

Cited by 45 publications

(30 citation statements)

References 37 publications

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“…The data from this study indicated that blockade of either VGCC or TRP had significant effects on neutrophil [Ca 2+ ] i response to fMLP, although VGCC blockade produced the largest reduction. A previous study also reported that diclofenac, with or without nifedipine, inhibited VGCC in rat ventricular cardiomyocytes in a whole-cell voltage clamp technique study (Yarishkin et al, 2009). Yamazaki et al (2006 reported that the anti-apoptotic effects of diclofenac occurred independently of its effects on COX-2 activity, via modulation of endoplasmic reticulum stress.…”

Section: Discussionmentioning

confidence: 81%

“…Ca 2+ entry also plays an important role in the regulation of superoxide radical production by neutrophils (Ş ahin et al, 2011). Therefore, a change in intracellular Ca 2+ levels in neutrophils directly affects the neutrophil response (Yamazaki et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…Non-steroidal anti-inflammatory drugs (NSAIDs) such as diclofenac are frequently used for the treatment of inflammation and pain in a wide variety of disorders, including primary dysmenorrhea (Yamazaki et al, 2006;Harel, 2012). Diclofenac has been shown to be effective in the treatment of primary dysmenorrhea, and its use is widespread.…”

Section: Introductionmentioning

confidence: 99%

“…Diclofenac has been shown to be effective in the treatment of primary dysmenorrhea, and its use is widespread. Although the mechanisms of action of NSAIDs in patients with primary dysmenorrhea are not yet fully understood, they have been shown to have anti-inflammatory, antioxidant, and inhibitory effects on cardiac and neuronal cells (Yamazaki et al, 2006;Yarishkin et al, 2009), and diclofenac has been reported to inhibit voltage-gated calcium channels (VGCC) in neonatal rat ventricular cardiomyocytes (Yarishkin et al, 2009). …”

Section: Introductionmentioning

confidence: 99%

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Non-steroidal anti-inflammatory drug modulates oxidative stress and calcium ion levels in the neutrophils of patients with primary dysmenorrhea

Kaplan

Nazıroğlu

Güney

et al. 2013

Journal of Reproductive Immunology

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Section: Discussionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Non-steroidal anti-inflammatory drug modulates oxidative stress and calcium ion levels in the neutrophils of patients with primary dysmenorrhea

Kaplan

Nazıroğlu

Güney

et al. 2013

Journal of Reproductive Immunology

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“…Yamazaki et al [89] demonstrated that various NSAIDs (diclofenac, indomethacin, ibuprofen, aspirin, and ketoprofen) inhibit ER stress-induced cell death of human neuroblastoma SH-SY5Y cells. Cells were pretreated with each drug for 2 hours and then thapsigargin or tunicamycin was added to the culture medium for 24 hours.…”

Section: Neuroprotectionmentioning

confidence: 99%

Endoplasmic reticulum stress response in the roadway for the effects of non-steroidal anti-inflammatory drugs

Mügge

Silva

2015

Endoplasmic Reticulum Stress in Diseases

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Over the past decade, a handful of evidence has been provided that nonsteroidal anti-inflammatory drugs (NSAIDs) display effects on the homeostasis of the endoplasmic reticulum (ER). Their uptake into cells will eventually lead to activation or inhibition of key molecules that mediate ER stress responses, raising not only a growing interest for a pharmacological target in ER stress responses but also important questions how the ER-stress mediated effects induced by NSAIDs could be therapeutically advantageous or not. We review here the toxicity effects and therapeutic applications of NSAIDs involving the three majors ER stress arms namely PERK, IRE1, and ATF6. First, we provide brief introduction on the well-established and characterized downstream events mediated by these ER stress players, followed by presentation of the NSAIDs compounds and mode of action, and finally their effects on ER stress response. NSAIDs present promising drug agents targeting the components of ER stress in different aspects of cancer and other diseases, but a better comprehension of the mechanisms underlying their benefits and harms will certainly pave the road for several diseases’ therapy.

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In vivo response of GsdmA3^Dfl/+ mice to topically applied fish oil – effects on cellular markers and macrophages

2016

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Psoriasis is an incurable autoimmune disease characterized by patches of abnormal red, itchy and scaly skin. This work examined the modulation of inflammation, hyperproliferation and immune cell markers following topical application of fish oil ( FO ) in comparison to the antipsoriatic agents, betamethasone dipropionate ( BD ) and salicylic acid ( SA ), to GsdmA3 Dfl /+ mice, a hair loss mutant which also exhibits epidermal hyperproliferation akin to psoriasis. The mice were dosed with 100 mg of the test formulation and after 10 days, the mice were sacrificed, skin sections excised and subjected to immunohistochemical determination of COX ‐2, K17 and MAC ‐1; and immunofluorescence of Ki‐67. Unchanged expression of the proinflammatory enzyme COX ‐2 was observed in all treatments, suggesting the noninvolvement of COX ‐2 in the aetiology of cutaneous aberration seen in GsdmA3 Dfl /+ mice. Intense staining of K17 and MAC ‐1 in the FO ‐treated group mirrored the epidermal thickening seen observed in live mice by optical coherence tomography ( OCT ). The ratio of Ki‐67‐positive nuclei per 100 basal cells indicated that hyperproliferation of keratinocytes occurred in FO ‐treated mice and the opposite was true for BD ‐treated mice. There was a positive correlation ( R 2 0.995) between Ki‐67 and the epidermal thickness data observed previously. In all immunochemical procedures, the combined BD , SA and FO formulation did not show any significant difference with the control group, reflecting observations seen previously. In conclusion, the epidermal changes observed following topical FO treatment on GsdmA3 Dfl /+ mice involves an increase in cellular proliferation and macrophages, although COX ‐2 does not appear to play an important role.

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Diclofenac, a non-steroidal anti-inflammatory drug, suppresses apoptosis induced by endoplasmic reticulum stresses by inhibiting caspase signaling

Cited by 45 publications

References 37 publications

Non-steroidal anti-inflammatory drug modulates oxidative stress and calcium ion levels in the neutrophils of patients with primary dysmenorrhea

Non-steroidal anti-inflammatory drug modulates oxidative stress and calcium ion levels in the neutrophils of patients with primary dysmenorrhea

Endoplasmic reticulum stress response in the roadway for the effects of non-steroidal anti-inflammatory drugs

In vivo response of GsdmA3^Dfl/+ mice to topically applied fish oil – effects on cellular markers and macrophages

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Diclofenac, a non-steroidal anti-inflammatory drug, suppresses apoptosis induced by endoplasmic reticulum stresses by inhibiting caspase signaling

Cited by 45 publications

References 37 publications

Non-steroidal anti-inflammatory drug modulates oxidative stress and calcium ion levels in the neutrophils of patients with primary dysmenorrhea

Non-steroidal anti-inflammatory drug modulates oxidative stress and calcium ion levels in the neutrophils of patients with primary dysmenorrhea

Endoplasmic reticulum stress response in the roadway for the effects of non-steroidal anti-inflammatory drugs

In vivo response of GsdmA3Dfl/+ mice to topically applied fish oil – effects on cellular markers and macrophages

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In vivo response of GsdmA3^Dfl/+ mice to topically applied fish oil – effects on cellular markers and macrophages