Arachidonic acid alleviates the detrimental effects of acetylsalicylic acid on human granulosa cells performance in Vitro

Arachidonic acid alleviates the detrimental effects of acetylsalicylic acid on human granulosa cells performance in Vitro


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دانشگاه علوم پزشکی تبریز
دانشگاه علوم پزشکی تبریز

نویسندگان: معصومه خواجه , محمد نوری , عالیه قاسم زاده , امیر مهدی زاده حقیقی , داریوش شانه بندی , سودابه یوسفی , مسعود دارابی امین , رضا رهبرقاضی

کلمات کلیدی: acetylsalicylic acid; arachidonic acid; fatty acid profile; human granulosa cells; steroid hormones

نشریه: 24452 , 5 , 87 , 2020

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نویسنده ثبت کننده مقاله مسعود دارابی امین
مرحله جاری مقاله تایید نهایی
دانشکده/مرکز مربوطه دانشکده پزشکی
کد مقاله 72391
عنوان فارسی مقاله Arachidonic acid alleviates the detrimental effects of acetylsalicylic acid on human granulosa cells performance in Vitro
عنوان لاتین مقاله Arachidonic acid alleviates the detrimental effects of acetylsalicylic acid on human granulosa cells performance in Vitro
ناشر 8
آیا مقاله از طرح تحقیقاتی و یا منتورشیپ استخراج شده است؟ بلی
عنوان نشریه (خارج از لیست فوق)
نوع مقاله Original Article
نحوه ایندکس شدن مقاله ایندکس شده سطح یک – ISI - Web of Science
آدرس لینک مقاله/ همایش در شبکه اینترنت

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Here, we investigated the biological effects of arachidonic acid (AA) in human cumulus granulosa cells (CGCs) after exposure to ASA. Cells were isolated from the follicular fluid and incubated with 0.5 mM acetylsalicylic acid (ASA) and 50 µM AA. Cell viability was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. E2 and P4 levels were measured by chemiluminescence assay. Expression of genes including CYP19A1, FACN, and SCD1 was measured by real-time polymerase chain reaction assay. Oxidative status was analyzed by monitoring glutathione peroxidase activity. The fatty acid profile was analyzed by the gas chromatography technique. Enzyme-linked immunosorbent assay was used to measure prostaglandin E2 (PGE2 ) in CGCs after exposure to ASA and AA. Protein levels of the estrogen receptor were studied by immunofluorescence staining. Ultrastructural changes were evaluated by transmission electron microscopy imaging. ASA treatment reduced E2 production, Cyp19a1 expression, glutathione peroxidase (GPx) activity, and estradiol receptor expression in CGCs. The addition of AA prevented the ASA-induced E2 reduction (p < .05) and expression of Cyp19a1. Moreover, AA increased the antioxidant capacity of CGCs exposed to ASA by promoting GPx activity (p < .05). AA increased monounsaturated fatty acid/saturated fatty acid ratio compared with the ASA group (p < .05). AA supplementation triggered the synthesis and secretion of PGE2 in ASA-treated CGCS (p < .05). Cytoplasmic vacuolation observed in the ASA group and treatment with AA intensified vacuolation rate. The expression of the estrogen receptor was increased after AA supplementation. Data demonstrated that AA decreased the detrimental effects of ASA on human CGCs after 72 hr.

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نویسنده نفر چندم مقاله
معصومه خواجهاول
محمد نوریدوم
عالیه قاسم زادهسوم
امیر مهدی زاده حقیقیچهارم
داریوش شانه بندیپنجم
سودابه یوسفیششم
مسعود دارابی امینهفتم
رضا رهبرقاضیهشتم

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