کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2580290 1561614 2015 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Nitric oxide-releasing indomethacin enhances susceptibility to Trypanosoma cruzi infection acting in the cell invasion and oxidative stress associated with anemia
ترجمه فارسی عنوان
اندومتاسین آزاد کننده اکسید نیتروژن باعث افزایش حساسیت به عفونت تریپانوزومای کریزی می شود که در حمله سلولی و استرس اکسیداتیو همراه با آنمی
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی


• NO-indomethacin acts on cell invasion and oxidative stress in Chagas disease.
• NO-indomethacin alters macrophages to exert anti-T. cruzi activity.
• Nitric oxide-releasing indomethacin enhances susceptibility to T. cruzi infection.
• NO-NSAIDs and T. cruzi infection.

Trypanosoma cruzi is the causative agent of Chagas disease. Approximately 8 million people are thought to be affected with this disease worldwide. T. cruzi infection causes an intense inflammatory response, which is critical for the control of parasite proliferation and disease development. Nitric oxide-donating nonsteroidal anti-inflammatory drugs (NO-NSAIDs) are an emergent class of pharmaceutical derivatives with promising utility as chemopreventive agents. In this study, we investigated the effect of NO-indomethacin on parasite burden, cell invasion, and oxidative stress in erythrocytes during the acute phase of infection. NO-indomethacin was dissolved in dimethyl formamide followed by i.p. administration of 50 ppm into mice 30 min after infection with 5 × 103 blood trypomastigote forms (Y strain). The drug was administered every day until the animals died. Control animals received 100 μL of drug vehicle via the same route. Within the NO-indomethacin-treatment group, parasitemia and mortality (100%) were higher and oxidative stress in erythrocytes, anemia, and entry of parasites into macrophages were significantly greater than that seen in controls. Increase in the entry and survival of intracellular T. cruzi was associated with inhibition of nitric oxide production by macrophages treated with NO-indomethacin (2.5 μM). The results of this study provide strong evidence that NO-NSAIDs potently inhibit nitric oxide production, suggesting that NO-NSAID-based therapies against infections would be difficult to design and would require caution.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chemico-Biological Interactions - Volume 227, 5 February 2015, Pages 104–111
نویسندگان
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