The protective role of sesame oil against bisphenol A-induced cardiotoxicity: a histological and immunohistochemical study
• 2019
معلومات البحث
المؤلفون
Eman El Banaa
, Kamal M. Kamala
, Nehal Shaheena
, Sahar Abowafa
الكلمات المفتاحية
Not Available
المجلة العلمية
Not Available
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
Introduction
Bisphenol-A (BPA), an estrogenic compound, is used in the manufacture of
polycarbonate plastics and epoxy resins. Sesame oil (SO) is a potent
antioxidant dietary source for human health.
Aim
The present study was conducted to estimate the protective effects of SO against
BPA-induced cardiotoxicity.
Materials and methods
Thirty two adult rats were divided into 4 equal groups eight rat for each; Control
group, 2 Treated group, one group received BPA (25 mg/kg b wt) orally 5 times/
weak for 4 weeks and other group rats received (50 mg/kg b. wt) orally 5 times /weak
for 4 weeks. Protected group received sesame oil orally at a dose 10 mL/kg b wt
orally daily for 4 weeks to the rat group which received the high dose of BPA. After
the end of treatments, the heart of each killed animal was subjected to
histopathological examination by hematoxylin and eosin, Masson’s, and NOS
stain. In addition, blood was collected for biochemical assessment of the enzymes.
Results
Administration of high-dose BPA (50 mg/kg b. wt) significantly increased the weight
of rats. Several histopathological alterations in cardiac tissue and elevation in
malondialdehyde, creatine phosphokinase-MB, and glutathione-S-transferase
activity and reduction of glutathione and catalase occurred when compared with
the control. Low-dose BPA (25 mg/kg b. wt) produced mild histopathological effect
on the heart. On the contrary, oral gavages of SO with BPA was effective in the
reduction of weight, amelioration of histopathological alterations, and in the
reduction of the malondialdehyde, creatine phosphokinase-MB, and glutathioneS-transferase activity levels and elevation of glutathione and catalase activity when
compared with high-dose BPA-treated rats.
Conclusion
The present study provided clear evidence that SO possesses a promising
protective activity against the cardiotoxic effects of BPA
Bisphenol-A (BPA), an estrogenic compound, is used in the manufacture of
polycarbonate plastics and epoxy resins. Sesame oil (SO) is a potent
antioxidant dietary source for human health.
Aim
The present study was conducted to estimate the protective effects of SO against
BPA-induced cardiotoxicity.
Materials and methods
Thirty two adult rats were divided into 4 equal groups eight rat for each; Control
group, 2 Treated group, one group received BPA (25 mg/kg b wt) orally 5 times/
weak for 4 weeks and other group rats received (50 mg/kg b. wt) orally 5 times /weak
for 4 weeks. Protected group received sesame oil orally at a dose 10 mL/kg b wt
orally daily for 4 weeks to the rat group which received the high dose of BPA. After
the end of treatments, the heart of each killed animal was subjected to
histopathological examination by hematoxylin and eosin, Masson’s, and NOS
stain. In addition, blood was collected for biochemical assessment of the enzymes.
Results
Administration of high-dose BPA (50 mg/kg b. wt) significantly increased the weight
of rats. Several histopathological alterations in cardiac tissue and elevation in
malondialdehyde, creatine phosphokinase-MB, and glutathione-S-transferase
activity and reduction of glutathione and catalase occurred when compared with
the control. Low-dose BPA (25 mg/kg b. wt) produced mild histopathological effect
on the heart. On the contrary, oral gavages of SO with BPA was effective in the
reduction of weight, amelioration of histopathological alterations, and in the
reduction of the malondialdehyde, creatine phosphokinase-MB, and glutathioneS-transferase activity levels and elevation of glutathione and catalase activity when
compared with high-dose BPA-treated rats.
Conclusion
The present study provided clear evidence that SO possesses a promising
protective activity against the cardiotoxic effects of BPA
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