Prototheca zopfii isolated from bovine mastitis induced oxidative stress and apoptosis in bovine mammary epithelial cells.
Prototheca zopfii isolated from bovine mastitis induced oxidative stress and apoptosis in bovine mammary epithelial cells.
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从牛乳腺炎中分离的 Prototheca zopfii 诱导牛乳腺上皮细胞氧化应激和凋亡
DOI：
10.18632/oncotarget.16653
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发表时间：
2017-05-09
期刊：
影响因子：
--
通讯作者：
Han B
中科院分区：
文献类型：
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作者：
Shahid M;Gao J;Zhou Y;Liu G;Ali T;Deng Y;Sabir N;Su J;Han B
牛原鞘型乳腺炎在世界范围内造成了巨大的经济损失。然而，Prototheca zopfii诱导的形态学改变和氧化应激在牛乳腺上皮细胞（bMEC）尚未得到全面的研究。因此，本研究的目的是研究佐氏疟原虫诱导bMEC的病理形态学变化、氧化应激和凋亡。通过检测过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）、丙二醛（MDA）含量和乳酸脱氢酶（LDH）活性来评估氧化应激，同时通过共聚焦激光扫描显微镜来测量ROS产生和细胞凋亡。结果显示，与对照组相比，感染Ⅱ型（GTII）猪疟原虫后12 h和24 h，bMEC的形态发生明显改变，细胞凋亡率和MDA含量显著增加（p < 0.05和p < 0.01），并呈时间依赖性。12 h和24 h LDH活性和ROS生成量也明显增加（p < 0.01）。GTII感染bMEC后12 h SOD和CAT含量显著降低（p < 0.05），24 h GPx、SOD和CAT含量显著降低（p < 0.01）。在GTI的情况下，只有CAT和GPx活性显着下降时，延长到24小时，但小于GTII。这表明GTII在bMEC中具有更具破坏性的致病作用，并且本研究的结果得出结论，GTII通过氧化剂和抗氧化剂防御的不平衡以及细胞内ROS的产生诱导bMEC中的凋亡和氧化应激。
Bovine protothecal mastitis results in considerable economic losses worldwide. However, Prototheca zopfii induced morphological alterations and oxidative stress in bovine mammary epithelial cells (bMECs) is not comprehensively studied yet. Therefore, the aim of this current study was to investigate the P. zopfii induced pathomorphological changes, oxidative stress and apoptosis in bMECs. Oxidative stress was assessed by evaluating catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), malondialdehyde (MDA) contents and lactate dehydrogenase (LDH) activity, while ROS generation and apoptosis was measured by confocal laser scanning microscopy. The results revealed that infection of P. zopfii genotype II (GTII) significantly changed bMECs morphology, increased apoptotic rate and MDA contents at 12 h (p < 0.05) and 24 h (p < 0.01) in comparison with control group, in time-dependent manner. LDH activity and ROS generation was also increased (p < 0.01) at 12 h and 24 h. However, SOD and CAT contents in bMECs infected with GTII were decreased (p < 0.05) at 12 h, while GPx (p < 0.01), SOD (p < 0.05) and CAT (p < 0.01) levels were reduced at 24 h. In case of GTI, only CAT and GPx activities were significantly decreased when the duration prolonged to 24 h but lesser than GTII. This suggested that GTII has more devastating pathogenic effects in bMECs, and the findings of this study concluded that GTII induced apoptosis and oxidative stress in bMECs via the imbalance of oxidant and antioxidant defenses as well as the production of intracellular ROS.