Kynurenine pathway as a possible pharmacological target in interferon-induced depression in rats / by Mohanad Zaki Abdelsalam Zaki ; Supervision Dr. Nesrine Salah Eldin El-Sayed, Dr. Gouda Kamel Helal, Dr. Reham Mohamed Essam.
نوع المادة :
نصاللغة: الإنجليزية لغة الملخص: الإنجليزية المنتج: 2025الوصف: 134 pages : illustrations ; 25 cm. + CDنوع المحتوى: - text
- Unmediated
- volume
- المسار الكينوريني كهدف دوائي محتمل في الاكتئاب المستحث بالإنترفيرون في الجرذان [عنوان مضاف عنوان الصفحة]
- 615.32
- Issues also as CD.
| نوع المادة | المكتبة الحالية | المكتبة الرئيسية | رقم الاستدعاء | حالة | الباركود | |
|---|---|---|---|---|---|---|
Thesis
|
قاعة الرسائل الجامعية - الدور الاول | المكتبة المركزبة الجديدة - جامعة القاهرة | Cai01.08.09.M.Sc.2025.Mo.K (استعراض الرف(يفتح أدناه)) | Not for loan | 01010110093789000 |
Thesis (M.Sc)-Cairo University, 2025.
Bibliography: pages 99-133.
Depression is a highly prevalent and disabling disorder that is
frequently linked to neuroinflammation and dysregulation of the kynurenine
pathway, a major branch of tryptophan metabolism. The present study
investigated the potential therapeutic effects of epigallocatechin gallate
(EGCG), a polyphenolic constituent of green tea, on depressive-like behaviors
and kynurenine pathway modulation in a rat model of interferon (IFN)-
induced depression. Rats received IFN at a dose of 6 × 10⁴ IU/kg/day,
subcutaneously (s.c.), while EGCG was administered at 20 mg/kg/day for
seven consecutive days. Behavioral testing, biochemical measurements, and
histopathological analyses were performed to assess the impact of EGCG on
depressive-like behavior, tryptophan and serotonin metabolism, kynurenine
pathway intermediates, oxidative stress parameters, neuroinflammatory
cytokines, and glial activation. The results demonstrated that EGCG
significantly improved depression-like behaviors, normalized serotonin
levels, and decreased neurotoxic kynurenine derivatives, including quinolinic
acid. In addition, EGCG attenuated oxidative stress, as indicated by lower
malondialdehyde levels, reduced pro-inflammatory cytokines such as TNF-α,
enhanced antioxidant defenses including glutathione, and upregulated anti-
inflammatory cytokines such as IL-4. Histological evaluation further revealed
that EGCG preserved hippocampal neuronal architecture and reduced glial
activation, as reflected by diminished glial fibrillary acidic protein expression.
Collectively, these findings suggest that EGCG exerts antidepressant-like
effects by regulating the kynurenine pathway, mitigating neuroinflammation,
and protecting neuronal integrity, underscoring its potential as a therapeutic
agent in depression management.
Issues also as CD.
Text in English and abstract in Arabic & English.
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