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耗尽 CD147 可使人类恶性黑素瘤细胞对过氧化氢诱导的氧化应激敏感。

Depletion of CD147 sensitizes human malignant melanoma cells to hydrogen peroxide-induced oxidative stress.

机构信息

Department of Dermatology, XiangYa Hospital, Central South University, Changsha, Hunan, China.

出版信息

J Dermatol Sci. 2010 Jun;58(3):204-10. doi: 10.1016/j.jdermsci.2010.03.022. Epub 2010 Apr 9.

DOI:10.1016/j.jdermsci.2010.03.022
PMID:20451353
Abstract

BACKGROUND

Increased sensitivity to reactive oxygen species (ROS) contributes to the effectiveness of therapeutic strategies in patients with malignant melanoma (MM). CD147, a cell surface receptor for cyclophilin A (CypA), is thought to exert antioxidant activities.

OBJECTIVE

To understand the influences and mechanisms of CD147 on proliferation, apoptosis and redox state of A375 cells under H(2)O(2)-induced oxidative stress.

METHODS

The effect of CD147 silencing on cell viability, apoptosis, the generation of ROS, superoxide dismutase (SOD) activity, and the malondialdehyde (MDA) level that reflects oxidative damage, was measured in human malignant melanoma cell line A375 treated or untreated with hydrogen peroxide (H(2)O(2)).

RESULTS

In A375 cells, CD147 silencing increased the H(2)O(2)-induced inhibition of cell viability, H(2)O(2)-induced apoptosis, H(2)O(2)-mediated ROS- and MDA generation, and the H(2)O(2)-triggered decrease in SOD activity.

CONCLUSIONS

Our results demonstrated that CD147 silencing increased cellular ROS and destroyed the intrinsic antioxidant defenses in A375, indicating that CD147 exerts a cytoprotective effect against H(2)O(2)-induced oxidative damage.

摘要

背景

对活性氧(ROS)的敏感性增加有助于恶性黑色素瘤(MM)患者治疗策略的有效性。CD147 是环孢素 A(CypA)的细胞表面受体,被认为具有抗氧化活性。

目的

了解 CD147 在 H2O2 诱导的氧化应激下对 A375 细胞增殖、凋亡和氧化还原状态的影响及其机制。

方法

在人恶性黑色素瘤细胞系 A375 中,用或不用过氧化氢(H2O2)处理,测定 CD147 沉默对细胞活力、凋亡、ROS 生成、超氧化物歧化酶(SOD)活性以及反映氧化损伤的丙二醛(MDA)水平的影响。

结果

在 A375 细胞中,CD147 沉默增加了 H2O2 诱导的细胞活力抑制、H2O2 诱导的凋亡、H2O2 介导的 ROS 和 MDA 生成,以及 H2O2 触发的 SOD 活性降低。

结论

我们的结果表明,CD147 沉默增加了细胞内的 ROS,并破坏了 A375 中的内在抗氧化防御系统,表明 CD147 对 H2O2 诱导的氧化损伤具有细胞保护作用。

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