سامية محمود مناوي ابراهيم
أستاذ
Do Platelet Rich Plasma and Folic Acid Reverse Experimental Induced Ovarian Failure: Emphasis on Folliculogenesis, and Ovarian Steroidogenesis
• 2024
معلومات البحث
المؤلفون
Wardah Abdullah Alasmari1, Eman Mohamed Faruk1,2, Ola Elsayed Nafea3,4,
Hanan Fouad5,6, Dalia Ibrahim El-wafaey7 and Samia M. Manawy8
الكلمات المفتاحية
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المجلة العلمية
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الناشر
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المجلد
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العدد
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الصفحات
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publication.type
Local
رابط البحث
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المواد المرفقة
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الملخص
Background: Valproic acid (VPA) is a commonly prescribed antiepileptic drug. VPA could mediate endocrinal reproductive
dysfunction on a long-term use. This study was designed to evaluate the possible protective effects of platelet rich plasma
(PRP) alone and PRP in combination with folic acid (FA) in a rat model of VPA induced ovarian failure.
Materials and Methods: Thirty-five adult rats were randomly divided into five equal groups and 14 female rats were used
for PRP preparation as control, VPA, co-treated VPA with FA, co-treated VPA with PRP and co-treated VPA with FA and
PRP groups. All treatments were administered for 90 days. The effects of PRP and/or FA against VPA were evaluated through
assessment of ovarian oxidant/antioxidant biomarkers, hormonal assay of reproductive hormones, quantification of mRNA
gene expression for ovarian steroidogenesis pathway-encoding genes. Histopathological examination of the ovarian tissues
was implemented.
Results: Revealed that VPA exposure caused ovarian failure as documented by the decreased ovarian superoxide dismutase
and catalase activities, increased ovarian malondialdehyde levels, diminished serum reproductive hormones concentrations and
repressed the ovarian steroidogenesis pathway-encoding genes. In addition, VPA-induced marked ovarian histopathological
alterations and impaired folliculogenesis. PRP and/or FA treatment improved ovarian function after VPA exposure. Adding
FA to PRP produced more ovarian estrogen receptors immunoexpression than those produced by PRP alone. While other
protective effects against VPA induced ovarian failure are equal between the two agents.
Conclusion: PRP exhibited a protective role against VPA-induced ovarian failure in adult rats. A combined PRP and FA
therapy is superior to PRP alone to some extent.
dysfunction on a long-term use. This study was designed to evaluate the possible protective effects of platelet rich plasma
(PRP) alone and PRP in combination with folic acid (FA) in a rat model of VPA induced ovarian failure.
Materials and Methods: Thirty-five adult rats were randomly divided into five equal groups and 14 female rats were used
for PRP preparation as control, VPA, co-treated VPA with FA, co-treated VPA with PRP and co-treated VPA with FA and
PRP groups. All treatments were administered for 90 days. The effects of PRP and/or FA against VPA were evaluated through
assessment of ovarian oxidant/antioxidant biomarkers, hormonal assay of reproductive hormones, quantification of mRNA
gene expression for ovarian steroidogenesis pathway-encoding genes. Histopathological examination of the ovarian tissues
was implemented.
Results: Revealed that VPA exposure caused ovarian failure as documented by the decreased ovarian superoxide dismutase
and catalase activities, increased ovarian malondialdehyde levels, diminished serum reproductive hormones concentrations and
repressed the ovarian steroidogenesis pathway-encoding genes. In addition, VPA-induced marked ovarian histopathological
alterations and impaired folliculogenesis. PRP and/or FA treatment improved ovarian function after VPA exposure. Adding
FA to PRP produced more ovarian estrogen receptors immunoexpression than those produced by PRP alone. While other
protective effects against VPA induced ovarian failure are equal between the two agents.
Conclusion: PRP exhibited a protective role against VPA-induced ovarian failure in adult rats. A combined PRP and FA
therapy is superior to PRP alone to some extent.
