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Sodium Selenate Ameliorates Cardiac Injury Developed from High-Fat Diet in Mice through Regulation of Autophagy Activity.
Scientific Reports ( IF 3.8 ) Pub Date : 2019-12-10 , DOI: 10.1038/s41598-019-54985-3 Shuqiang Zhang 1 , Jialiang Xu 2 , Zhisong He 2 , Feng Xue 2 , Tingbo Jiang 2 , Mingzhu Xu 2
Scientific Reports ( IF 3.8 ) Pub Date : 2019-12-10 , DOI: 10.1038/s41598-019-54985-3 Shuqiang Zhang 1 , Jialiang Xu 2 , Zhisong He 2 , Feng Xue 2 , Tingbo Jiang 2 , Mingzhu Xu 2
Affiliation
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Obesity is often accompanied by dyslipidemia, high blood glucose, hypertension, atherosclerosis, and myocardial dysfunction. Selenate is a vital antioxidant in the cardiovascular system. The beneficial effects of selenate on obesity-associated cardiac dysfunction and potential molecular mechanism were identified in both H9C2 cells and C57BL/6J mice hearts. The cardiac histological preformation in C57BL/6J mice were evaluated by cross-sectional area (CSA) of cardiomyocytes and percent area of fibrosis in the left ventricles. The cardiac autophagy flux in H9C2 cells and C57BL/6J mice hearts was analyzed by Western blots and the number of autophagosomes and autolysosome in H9C2 cells. In the present study, we found that lipid overload caused increases in serum lipid, CSA, and percent area of fibrosis. We further found that lipid-induced accumulation of autophagosomes was due to depressed autophagy degradation, which was not restored in the pretreatment with 3-methyladenine and chloroquine, whereas, it was improved by rapamycin. Moreover, we demonstrated that increased levels of serum lipid, CSA, percent area of fibrosis and mRNA expression related to cardiomyocytes hypertrophy and fibrosis were significantly reduced after selenate treatments of mice. We also found selenate treatment significantly down-regulated activity of the Akt pathway, which was activated in response to lipid-overload. Furthermore, selenate dramatically improved cardiac autophagic degradation which was suppressed after exposure to lipid-overload in both H9C2 cells and C57BL/6J mice hearts. Taken together, selenate offers therapeutic intervention in lipid-related metabolic disorders, and protection against cardiac remodeling, likely through regulation of the activity of autophagic degradation and Akt pathway.
中文翻译：
高脂饮食通过自噬活性的调节而引起的小鼠硒酸钠对心脏的伤害。
肥胖症通常伴有血脂异常，高血糖，高血压，动脉粥样硬化和心肌功能障碍。硒酸盐是心血管系统中至关重要的抗氧化剂。在H9C2细胞和C57BL / 6J小鼠心脏中均发现了硒酸对肥胖相关心脏功能障碍的有益作用和潜在的分子机制。通过心肌细胞的横截面积（CSA）和左心室纤维化的百分比来评估C57BL / 6J小鼠的心脏组织学形成情况。通过Western印迹分析H9C2细胞和C57BL / 6J小鼠心脏中的心脏自噬通量，以及H9C2细胞中自噬体和自溶酶体的数量。在本研究中，我们发现脂质超负荷导致血清脂质，CSA和纤维化百分比的增加。我们进一步发现脂质诱导的自噬体积累是由于抑制的自噬降解引起的，在用3-甲基腺嘌呤和氯喹进行的预处理中不能恢复这种降解，而雷帕霉素可以改善这种情况。此外，我们证明硒化处理小鼠后，血清脂质，CSA，纤维化百分比面积和与心肌肥大和纤维化相关的mRNA表达水平显着降低。我们还发现硒酸盐处理显着下调了Akt通路的活性，该活性在响应脂质超载时被激活。此外，硒酸盐显着改善了心脏自噬降解，这在暴露于H9C2细胞和C57BL / 6J小鼠心脏脂质超负荷后均得到抑制。在一起
更新日期：2019-12-11
中文翻译：
高脂饮食通过自噬活性的调节而引起的小鼠硒酸钠对心脏的伤害。
肥胖症通常伴有血脂异常，高血糖，高血压，动脉粥样硬化和心肌功能障碍。硒酸盐是心血管系统中至关重要的抗氧化剂。在H9C2细胞和C57BL / 6J小鼠心脏中均发现了硒酸对肥胖相关心脏功能障碍的有益作用和潜在的分子机制。通过心肌细胞的横截面积（CSA）和左心室纤维化的百分比来评估C57BL / 6J小鼠的心脏组织学形成情况。通过Western印迹分析H9C2细胞和C57BL / 6J小鼠心脏中的心脏自噬通量，以及H9C2细胞中自噬体和自溶酶体的数量。在本研究中，我们发现脂质超负荷导致血清脂质，CSA和纤维化百分比的增加。我们进一步发现脂质诱导的自噬体积累是由于抑制的自噬降解引起的，在用3-甲基腺嘌呤和氯喹进行的预处理中不能恢复这种降解，而雷帕霉素可以改善这种情况。此外，我们证明硒化处理小鼠后，血清脂质，CSA，纤维化百分比面积和与心肌肥大和纤维化相关的mRNA表达水平显着降低。我们还发现硒酸盐处理显着下调了Akt通路的活性，该活性在响应脂质超载时被激活。此外，硒酸盐显着改善了心脏自噬降解，这在暴露于H9C2细胞和C57BL / 6J小鼠心脏脂质超负荷后均得到抑制。在一起
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