All-trans retinoic acid suppresses apoptosis in PC12 cells injured by oxygen and glucose deprivation via the retinoic acid receptor α signaling pathway.

نویسندگان

  • Xiaojian Zhang
  • Qin Yu
  • Wei Jiang
  • Yang Bi
  • Yun Zhang
  • Min Gong
  • Xiaoping Wei
  • Tingyu Li
  • Jie Chen
چکیده

Vitamin A (VA) has a number of important biological functions in human growth and development. Previous studies by our group demonstrated that the normal VA levels improved recovery of learning and memory function and decreased apoptosis in rats with hypoxic‑ischemic brain damage (HIBD). However, it has not been fully elucidated how VA regulates the apoptosis of neuronal cells. To investigate the anti‑apoptotic effect of VA, an in vitro oxygen glucose deprivation (OGD) model in PC12 cells was treated with four concentrations of all‑trans‑retinoic acid (ATRA), an active in vivo product of VA. Following in vitro OGD injury in PC12 cells, the percentage of apoptosis and the fluorescence intensity of the mitochondrial membrane potential (MMP) were increased in the cells, and the expression levels of B-cell lymphoma-associated X (Bax) were enhanced. ATRA treatment at 2‑4 µmol/l for 24 h decreased the percentage of apoptosis and the MMP of the PC12 cells injured by OGD. ATRA at 4 µmol/l also reduced the expression levels of Bax and enhanced the expression of B-cell lymphoma 2. Furthermore, RNA interference with retinoic acid receptor α (RARα) reversed the observed effect in PC12 cells following ATRA treatment at 4 µmol/l alone. In conclusion, the present study suggested that treatment with ATRA at 4 µmol/l suppressed apoptosis of PC12 cells following OGD injury, potentially through regulation of the RARα signaling pathway.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

افزایش اثرات درمانی سیس پلاتین و 5- فلورواوراسیل بر روی رده‌های سلولی AGS و KYSE-30 با استفاده از تیمار ترکیبی رتینوئیک اسید تمام ترانس

Backgrounds and Objectives: All-trans retinoic acid (ATRA) which is a derivative of vitamin A, exert fundamental effects on regulation of cell growth, differenation and apoptosis. Recently, resistance to cisplatin and 5-fluorouracil developed in gastric adenocarcinoma and squamous cell carcinoma. In this study, we investigated the combination treatment of ATRA with cisplatin and 5-fluorouracil ...

متن کامل

تاثیر رتینوئیک اسید تمام ترانس و ترکیب آن با سیس پلاتین بر روی بقاء رده سلولی سرطان معده(AGS)

Introduction & Objective: All-trans retinoic acid, a derivative of retinoids, is widely used to in-duce prolifferation, differentiation and apoptosis in normal, precancareous and cancerous cells. Cisplatin, an effective drug for cancer treatment, induces apoptosis via cross-linking to DNA. Previous studies on ovarian and melanoma cancer cells have showed synergistic ef-fects of cisplatin and ...

متن کامل

تاثیر غلظت‌های مختلف ال- ترانس رتینوئیک اسید بر رشد و بقای سلول‌های بنیادی فولیکول‌ موی موش سوری

Background and Objective: Hair follicle stem cells are multipotent, located in the bulge area, and are highly proliferating. Retinoids have an effect on epidermal differentiation and keratinization. Retinoic acid is used to treat some skin diseases such as Melasma, Acne and Ichthyosis. So, the study of all-trans retinoic acid effect on hair follicle stem cells and determination of the effective...

متن کامل

9-cis-Retinoic Acid and 1,25-dihydroxy Vitamin D3 Improve the Differentiation of Neural Stem Cells into Oligodendrocytes through the Inhibition of the Notch and Wnt Signaling Pathways

Background: Differentiating oligodendrocyte precursor cells (OPCs) into oligodendrocytes could be improved by inhibiting signaling pathways such as Wnt and Notch. 9-cis-retinoic acid (9-cis-RA) and 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) can ameliorate oligodendrogenesis. We investigated whether they could increase oligodendrogenesis by inhibiting the Wnt and Notch signaling pathways.Methods: Co...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Molecular medicine reports

دوره 10 5  شماره 

صفحات  -

تاریخ انتشار 2014