Department of Hepatobiliary Surgery, Xi-Jing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Department of Anatomy and K.K. Leung Brain Research Centre, Fourth Military Medical University, Xi'an, 710032, China.
Metab Brain Dis. 2018 Oct;33(5):1669-1678. doi: 10.1007/s11011-018-0275-6. Epub 2018 Jul 11.
Hepatic encephalopathy (HE) has been reported in more than 40% of patients with cirrhosis in clinical practice. HE changes mitochondrial dysfunction. Mitochondrial dynamics and autophagy are important for maintaining and removing damaged mitochondria. We used molecular biology and morphology methods to evaluate changes in mitochondrial dynamics and autophagy of the substantia nigra (SN) and prefrontal cortex (PFC) in HE. In this study, we observed that HE increased mitochondrial dynamics and autophagy in the SN, which was not seen in the PFC. HE stimulated dynamin-related protein 1 (DRP1) transformation from the cytosolic to the mitochondria within SN cells, which increased mitochondrial fission and the number of mitochondria. The fusion protein L-OPA1 (long isoforms of OPA1) was increased in the SN of HE mice. HE also increased the levels of autophagy proteins PINK1/PARKIN and P62/LC3-B in the SN, which can selectively remove damaged mitochondria and cell, respectively. Additionally, we used electron microscopy to directly observe changes in mitochondrial morphology in the SN of HE mice and found the number of mitochondria was increased. However, there were no significant changes in the fission, fusion or autophagy proteins in PFC-purified mitochondrial proteins in HE mice. The number of mitochondria also did not show alterations in the PFC of HE mice compared with that in a sham group. These results illustrate that mitochondria can protect themselves by changing the dynamics and autophagy in the SN of HE mice. Changes in the mitochondrial dynamics and autophagy related to HE can help repair damaged mitochondria and provide a further understanding of the mechanisms of hepatic encephalopathy.
肝性脑病(HE)在临床实践中已在超过 40%的肝硬化患者中报道。HE 改变线粒体功能。线粒体动力学和自噬对于维持和清除受损的线粒体非常重要。我们使用分子生物学和形态学方法来评估 HE 中线粒体动力学和自噬在黑质(SN)和前额叶皮层(PFC)中的变化。在这项研究中,我们观察到 HE 增加了 SN 中线粒体的动力学和自噬,而在 PFC 中则没有观察到。HE 刺激 SN 细胞中的动力相关蛋白 1(DRP1)从细胞质转化为线粒体,从而增加了线粒体分裂和线粒体数量。HE 还增加了 SN 中长型 OPA1(L-OPA1)的融合蛋白的水平。HE 还增加了 SN 中自噬蛋白 PINK1/PARKIN 和 P62/LC3-B 的水平,它们可以分别选择性地去除受损的线粒体和细胞。此外,我们使用电子显微镜直接观察 HE 小鼠 SN 中线粒体形态的变化,发现线粒体数量增加。然而,在 HE 小鼠 PFC 纯化的线粒体蛋白中,没有观察到 fission、fusion 或自噬蛋白的显著变化。与 sham 组相比,HE 小鼠 PFC 中的线粒体数量也没有改变。这些结果表明,线粒体可以通过改变 HE 小鼠 SN 中线粒体的动力学和自噬来保护自己。与 HE 相关的线粒体动力学和自噬的变化可以帮助修复受损的线粒体,并为肝性脑病的机制提供进一步的了解。