姜黄素
MFN2型
线粒体分裂
细胞生物学
氧化应激
线粒体融合
线粒体
基因敲除
化学
粒体自噬
细胞凋亡
生物
生物化学
线粒体DNA
基因
自噬
作者
Dan Xu,Kun Zhang,Xin-Hui Qu,Tao Wang,Ping Yang,Yun Yang,Liping Jiang,Yuying Wan,Fangfang Tou,Zhiping Chen,Xiao‐Jian Han
标识
DOI:10.1016/j.exer.2022.109239
摘要
Oxidative stress plays a crucial role in the damage of retinal neuronal cells. Curcumin, the phytocompound, has anti-inflammatory and antioxidative properties. It was shown that curcumin exerted a beneficial effect on retinal neuronal cell survival. However, the role of mitochondrial dynamics in curcumin-mediated protective effect on retinal neuronal cells remains to be elucidated. Here, H2O2 was used to mimic the oxidative stress in retinal neuronal R28 cells. Drp1 and Mfn2 are key regulators of mitochondrial fission and fusion. 100 μM of H2O2 significantly increased the cleavage of caspase-3 and Drp1 expression, but downregulated the expression of Mfn2. Pretreatment with 5 μM curcumin effectively alleviated H2O2-induced alterations in the expression of Drp1 and Mfn2 and mitochondrial fission in R28 cells. In addition, curcumin and Drp1 knockdown prevented H2O2-induced intracellular ROS increment and mitochondrial membrane potential disruption. On the contrary, knockdown of Mfn2 diminished curcumin-mediated protection against ROS increment and mitochondrial membrane potential disruption after H2O2. Moreover, curcumin protected R28 cells against H2O2-induced PINK1 expression, mitophagy, caspase-3 cleavage and apoptosis. Knockdown of Mfn2 significantly alleviated the protective effect of curcumin on R28 cells after H2O2. Taken together, our data indicate that curcumin protects against oxidative stress-induced injury in retinal neuronal cells by promoting mitochondrial fusion.
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