تشدید اپیگالوکتشین گالات ناشی ازفلوراید سمیت استرس اکسیداتیو واسطه بیضه در موش از طریق فعال سازی NRF2 مسیر سیگنالینگ
Epigallocatechin gallate exacerbates fluoride-induced oxidative stress mediated testicular toxicity in rats through the activation of Nrf2 signaling pathway
نویسندگان |
این بخش تنها برای اعضا قابل مشاهده است ورودعضویت |
اطلاعات مجله |
http://www.apjr.net/Asian Pacific Journal of Reproduction |
سال انتشار |
2015 |
فرمت فایل |
PDF |
کد مقاله |
12079 |
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چکیده (انگلیسی):
Objective: To explore the ameliorative potential of Epigallocatechin gallate (EGCG) by
evaluating markers of oxidative stress, apoptosis, and inflammation and antioxidant
competence in Fl intoxicated rats.
Methods: The animals were divided in to four groups that is control, EGCG alone, NaF,
and EGCG with NaF. Group III animal were exposed to Fl as sodium Fluoride (NaF)
(25 mg/kg BW) for 4 weeks. After the completion of the treatment, the testis tissues has
been removed and used for the experimental observations.
Results: Pre-administration of EGCG to Fl intoxicated rats showed a significant
normalization in the levels of steroidogenic enzymes, testosterone, sperm functions,
oxidative stress markers and antioxidant status. The altered levels of proinflammatory
cytokines and apoptotic markers were also relapsed in close proximity to control. In
addition, EGCG significantly improved antioxidant status and reduced the oxidative
stress and pathological changes in testes. The mRNA and protein analysis also substantiated
that EGCG pre-treatment markedly enhanced the expression of Nrf2 and its
target genes HO-1, NQO1 and gGCS and suppressed the expression of Keap1 in testis.
Conclusion: Altogether, our findings supports that EGCG attenuates Fl toxicity in testis
through Nrf2 activation.
کلمات کلیدی مقاله (فارسی):
فلورید- EGCG- بیضه- استرس اکسیداتیو -التهاب -آپوپتوز- NRF2
کلمات کلیدی مقاله (انگلیسی):
Fluoride- EGCG -Testes -Oxidative stress- Inflammation- Apoptosis- Nrf2
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