SC79 rescues osteoblasts from dexamethasone though activating Akt-Nrf2 signaling
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- 作者：Song-tao Lia ; 1 ; Nan-nan Chenb ; 1 ; Yin-biao Qiaoc ; 1 ; Wei-li Zhud ; Jian-wei Ruana ; e ; ray-tzmh@hotmail.com" class="auth_mail" title="E-mail the corresponding author ; Xiao-zhong Zhoua ; zhouxiaozhongorth@163.com" class="auth_mail" title="E-mail the corresponding author ; zhouxz@suda.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：Dexamethasone (Dex) ; SC79 ; Akt ; Oxidant stress ; Nrf2
- 刊名：Biochemical and Biophysical Research Communications
- 出版年：2016
- 出版时间：7 October 2016
- 年：2016
- 卷：479
- 期：1
- 页码：54-60
- 全文大小：652 K
文摘
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SC79 attenuates dexamethasone (Dex)-induced osteoblast cell death.
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SC79 attenuates Dex-induced both apoptosis and programmed necrosis in osteoblasts.
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Activation of Akt is required for SC79-mediated cytoprotection against Dex in osteoblasts.
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SC79 activates Akt downstream Nrf2 signaling to inhibit Dex-induced oxidative stress.