Beclin1/LC3II/P62 autophagy pathway activation is involved in the protective action of C-peptide against prostate injury in a rat model of type 1 diabetes.
Heba A Abdel-Hamid, Manar Fouli Gaber Ibrahim, Doaa Mohamed Elroby Ali, Elshymaa A Abdel-Hakeem
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引用次数: 0
Abstract
One of the undesirable complications of diabetes is sexual dysfunctions in males which may affect their fertility. This research aims to study the effect of C-peptide administration on the prostate of diabetic rats and focusing on exploring the role of the autophagy pathway in diabetic prostate and whether it is involved in C-peptide action. Forty adult male Wistar albino rats were separated into control group, diabetic group, diabetic + C-peptide and diabetic + C-peptide + 3-Methyladenine (autophagy inhibitor). Serum metabolic parameters and prostatic specific antigen (PSA) were measured. Markers of oxidative stress, inflammation, fibrosis, cell proliferation and cell autophagy were evaluated in prostate tissues using biochemical, western blotting and immunohistochemical techniques. C-peptide administration ameliorated the effects of diabetes on the prostate through its hypoglycaemic, antioxidant, anti-inflammatory, and antiproliferative effects which were reversed with autophagy inhibition. Thus, we concluded that C-peptide prevented the effects of diabetes on the prostate through stimulation of the autophagy pathway.
在 1 型糖尿病大鼠模型中,Beclin1/LC3II/P62 自噬途径的激活参与了 C 肽对前列腺损伤的保护作用。
糖尿病的不良并发症之一是男性性功能障碍,这可能会影响他们的生育能力。本研究旨在探讨服用 C 肽对糖尿病大鼠前列腺的影响,重点探索自噬途径在糖尿病前列腺中的作用,以及自噬途径是否参与 C 肽的作用。40 只成年雄性 Wistar 白化大鼠被分为对照组、糖尿病组、糖尿病 + C 肽组和糖尿病 + C 肽 + 3-甲基腺嘌呤(自噬抑制剂)组。测量了血清代谢参数和前列腺特异性抗原(PSA)。使用生化、Western 印迹和免疫组化技术评估了前列腺组织中氧化应激、炎症、纤维化、细胞增殖和细胞自噬的标志物。C肽通过降血糖、抗氧化、抗炎和抗增殖作用改善了糖尿病对前列腺的影响。因此,我们认为 C 肽通过刺激自噬途径防止了糖尿病对前列腺的影响。
期刊介绍:
Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders.
The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications.
Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics:
-Dysregulation of hormone receptors and signal transduction
-Contribution of gene variants and gene regulatory processes
-Impairment of intermediary metabolism at the cellular level
-Secretion and metabolism of peptides and other factors that mediate cellular crosstalk
-Therapeutic strategies for managing metabolic diseases
Special issues dedicated to topics in the field will be published regularly.