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| 1 | SCM-198 protects endometrial stromal cells from oxidative damage through Bax/Bcl-2 and ERK signaling pathways显示文摘In creasi ng amounts of evidence dem on strated that accumulative reactive oxyge n species (ROS) and apoptosis of human endometrial stromal cells (ESCs) are closely associated with endometrial dysfunction induced by oxidative stress, which plays an important role in the pathological process of multiple gyn ecological and reproduction-related diseases. SCM-198, an alkaloid active component of Leonurus japonicas Houtt, has been reported to have anti-oxidative activity. However, the specific mechanisms of SCM-198 in the prevention of endometrial damage remain unknown. In the present study, we assessed the effect of SCM-198 on hydrogen peroxide (H2O2Hnduced oxidative injury in ESCs. ESCs were pretreated with SCM-198 for 4 h and then challenged with H2O2.Morphology ch a nges, apoptosis rate, and intracellular ROS producti on were measured to assess the level of oxidative injury. Flow cytometry and western blot analysis were performed to detect the expression levels of Bax, Bcl-2, active-caspase-3, and mitogen-activated protein kinases pathways. Classic inflammation cytokines were measured by real-time polymerase chain reactions. Our results showed that SCM-198 attenuated apoptosis and ROS generation of ESCs induced by H2O2. H2O2 induced the apparent apoptotic characteristics, including fragmentation of DNA, upregulation of Bax/Bcl2, activation of caspase-3, and secretion of inflammation cytokines, which were all ameliorated by SCM-198. Furthermore, H2O2-induced apoptosis-related ERK1/2 pathway activation was restrained by SCM-198 pretreatme nt. These fin dings suggested that SCM-198 could protect ESCs from oxidative injury, mainly by inhibiting oxidative stress and reducing apoptosis. | Yunyun Li Yikong Lin Xixi Huang Chunfang Xu Xinhua Liu Li Wang Min Yu Dajin Li Yizhun Zhu Meirong Du | 2019 | Acta Biochimica et Biophysica Sinica2019，51，6： | 10 |
| 2 | 调节神经元CREB磷酸化水平对APP和γ分泌酶的影响显示文摘目的在人神经元样细胞SY5Y中激活和抑制环磷酸腺苷(cAMP)反应元件结合蛋白(CREB)的磷酸化,检测γ分泌酶复合体蛋白及β淀粉样蛋白前体(APP)水平的变化,分析通过调控CREB磷酸化防治阿尔茨海默病(AD)的可行性。方法培养空载体SY5Y细胞(Vector-SY5Y)、过表达Gαq(Gαq-SY5Y)细胞、过表达APP(APP-SY5Y)细胞,分别用cAMP激动剂Forskolin、蛋白激酶(PK)A受体抑制剂H 892HCL处理上述3种细胞,Western印迹检测APP及γ分泌酶复合体的蛋白成分早老素增强子(PEN2)及早老素C端(PS1-CTF)的水平变化。结果①在Vector-SY5Y细胞中,激动剂组APP的表达无明显变化,PEN2、PS1-CTF表达明显上调;抑制剂组APP的表达明显上调,PEN2、PS1-CTF变化不明显。②在Gαq-SY5Y细胞中,激动剂组APP明显下降,PEN2表达量明显上调,PS1-CTF明显下降;抑制剂组APP明显下降,PEN2明显下调,PS1-CTF无明显变化。③在APP-SY5Y细胞中,激动剂组APP变化不明显,PEN2表达明显上调,PS1-CTF表达明显下降;抑制剂组APP明显上升,PEN2表达明显下降,PS1-CTF明显上调。结论激活CREB的磷酸化可上调γ分泌酶复合体中PEN2水平,协同过表达Gαq可明显降低APP水平,可设计基于CREB和Gαq的AD防治策略。 | 邸畅 李国萍 罗浩丹 毕珊 孙欣 陈绍春 | 2021 | 中国老年学杂志2021，41，8： | 2 |
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