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Oxidative Stress Induces Chondrocyte Apoptosis through Caspase-Dependent and Caspase-Independent Mitochondrial Pathways and the Antioxidant Mechanism of Angelica Sinensis Polysaccharide
المؤلفون المشاركون
Zhuang, Chao
Ni, Su
Yang, Zhi-cheng
Liu, Rui-ping
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-12، 12ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-11-09
دولة النشر
مصر
عدد الصفحات
12
التخصصات الرئيسية
الملخص EN
Introduction.
Chondrocyte apoptosis is considered one of the pathogenic factors of osteoarthritis (OA), but its importance in the pathogenesis of OA remains unclear.
Recent research adds progress to the knowledge that the mitochondrial signaling pathway mediates chondrocyte apoptosis in OA.
Method.
Rat chondrocyte exposed to H2O2 was used as the experimental oxidative stress model.
Chondrocyte viability was tested by cell counting kit-8 (CCK-8) assay.
Cell apoptosis and ROS were tested by flow cytometry.
Contents of malondialdehyde (MDA), catalase (CAT), caspase-3, caspase-9, cytochrome C, superoxide dismutase (SOD)-2, and adenosine triphosphate (ATP) were evaluated by biochemical detection.
The expressions of related genes and proteins were assessed by quantitative polymerase chain reaction (qPCR) and western blot.
Results.
H2O2 provokes oxidative stress and decreases the viability of chondrocyte, which leads to the release of cytochrome C and inhibition of SOD-2 activity.
The damage of mitochondrion disturbs the energy metabolism of chondrocyte and eventually induces chondrocyte apoptosis through the mitochondrial pathway.
Furthermore, pretreated with anglicasinensis polysaccharide (ASP) or caspase inhibitors increase the expression of Bcl-2 and Bcl-xL but do not work for the expression of Bax and Bad.
Conclusion.
Oxidative stress induces chondrocyte apoptosis through caspase-dependent and caspase-independent mitochondrial pathways.
ASP protects chondrocyte from H2O2-induced oxidative stress and subsequent cell injury through its antioxidant effect by inhibiting the caspase pathway.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Zhuang, Chao& Ni, Su& Yang, Zhi-cheng& Liu, Rui-ping. 2020. Oxidative Stress Induces Chondrocyte Apoptosis through Caspase-Dependent and Caspase-Independent Mitochondrial Pathways and the Antioxidant Mechanism of Angelica Sinensis Polysaccharide. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1204225
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Zhuang, Chao…[et al.]. Oxidative Stress Induces Chondrocyte Apoptosis through Caspase-Dependent and Caspase-Independent Mitochondrial Pathways and the Antioxidant Mechanism of Angelica Sinensis Polysaccharide. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-12.
https://search.emarefa.net/detail/BIM-1204225
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Zhuang, Chao& Ni, Su& Yang, Zhi-cheng& Liu, Rui-ping. Oxidative Stress Induces Chondrocyte Apoptosis through Caspase-Dependent and Caspase-Independent Mitochondrial Pathways and the Antioxidant Mechanism of Angelica Sinensis Polysaccharide. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1204225
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1204225
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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