کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6189006 | 1256707 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Targeted anti-apoptosis activity for ovarian protection against chemotherapy-induced ovarian gonadotoxicity
ترجمه فارسی عنوان
فعالیت ضد آپوپتوز هدفمند برای محافظت از تخمدان در برابر سم زدایی تخمدان ناشی از شیمیدرمانی
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کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
زنان، زایمان و بهداشت زنان
چکیده انگلیسی
Chemotherapy damages the reproductive system by enhancing apoptosis, and evidence suggests that targeted anti-apoptotic therapy may preserve fertility in patients receiving chemotherapy. To investigate the protective effect of sphingosine-1-phosphate (S1P) on chemotherapeutic agent-induced ovarian gonadotoxicity, busulfan-treated female mice were pre-treated with low (0.5âmM) and high (2.0âmM) doses of S1P or vehicle 1âh before busulfan injection. In the S1P groups, each mouse was injected with low-dose S1P in one ovary and high-dose S1P in the contralateral ovary. Four weeks later, the ovaries were removed for histological and biochemical examinations. Caspase 3 immunoreactivity was greater in mice treated with busulfan compared with mice pre-treated with S1P, in which more primordial follicles were observed (P < 0.05). The mRNA level of anti-Müllerian hormone was higher in mice pre-treated with S1P than those that received busulfan only, indicating a better ovarian function in mice pre-treated with S1P. No difference was observed in the levels of growth differentiation factor-9 among all groups. In conclusion, S1P protects primordial follicles from chemotherapy-induced gonadotoxicity, and may partially preserve ovarian function.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Reproductive BioMedicine Online - Volume 29, Issue 5, November 2014, Pages 612-620
Journal: Reproductive BioMedicine Online - Volume 29, Issue 5, November 2014, Pages 612-620
نویسندگان
Shun-Jen Tan, Li-Jen Lee, Chii-Ruey Tzeng, Chia-Woei Wang, Ming-I Hsu, Chi-Huang Chen,