کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5157051 | 1500595 | 2017 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inhibition of acrolein-induced autophagy and apoptosis by a glycosaminoglycan from Sepia esculenta ink in mouse Leydig cells
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کلمات کلیدی
Cyclophosphamide (PubChem CID: 2907)Acrolein - آکرولئین، آکرولینAutophagy - اتوفاژیApoptosis - خزان یاختهایLeydig cells - سلولهای Leydigmalondialdehyde (PubChem CID: 10964) - مالون دی آلدئید (PubChem CID: 10964)Propidium iodide (PubChem CID: 104981) - پرویدیم یود (PubChem CID: 104981)Glycosaminoglycan - گلیکوزآمینوگلیکان
موضوعات مرتبط
مهندسی و علوم پایه
شیمی
شیمی آلی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
In our recent reports, a squid ink polysaccharide (SIP) was found having preventive activity against cyclophosphamide induced damage in mouse testis and ovary. Here we further reveal the regulative mechanism of SIP against chemical toxicity on testis. Leydig cells exposed to acrolein (ACR) underwent apoptosis at 12Â h and 24Â h. Before apoptosis, cells occurred autophagy that was confirmed by high autophagic rate and Beclin-1 protein content at 3Â h. PI3K/Akt and p38 MAPK signal pathways involved in the regulatory mechanisms. These outcomes of ACR were recovered completely by SIP, which was demonstrated by attenuated disruption of redox equilibrium and increased testosterone production, through suppressing ACR-caused autophagy and apoptosis regulated by PI3K/Akt and p38 MAPK signal pathways in Leydig cells. Summarily, autophagy occurred before apoptosis caused by ACR-activated p38 MAPK and PI3K/Akt pathways were blocked by SIP, resulting in survival and functional maintenance of Leydig cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Carbohydrate Polymers - Volume 163, 1 May 2017, Pages 270-279
Journal: Carbohydrate Polymers - Volume 163, 1 May 2017, Pages 270-279
نویسندگان
Yi-Peng Gu, Xiao-Mei Yang, Ping Luo, Yan-Qun Li, Ye-Xing Tao, Zhen-Hua Duan, Wei Xiao, Da-Yan Zhang, Hua-Zhong Liu,