ABSTRACT
Mitochondrial autophagy is a process to clear dysfunctional mitochondria in the cytoplasm to maintain the integrity of mitochondrial function and cell homeostasis. Mitochondrial autophagy is a complex physiological process， which can maintain the balance of mitochondrial quality and quantity， cell survival under starvation and harsh conditions， and the stability of the intracellular environment. Its molecular mechanism involves a variety of proteins. Many factors can induce mitochondrial autophagy， such as starvation， oxidative stress， hypoxia， depolarization， and other stresses. The accumulation of unfolded proteins can also induce mitochondrial autophagy. In recent years， as a research hotspot， the abnormality of mitochondrial morphology and function is closely related to the occurrence of a variety of diseases. The research on mitochondrial autophagy and the pathogenesis of clinical diseases has attracted more attention， such as tumors， cardiovascular diseases， liver diseases， nervous system diseases， and glucose metabolism disorders. It has been found that regulating mitochondrial autophagy may inspire the treatment of some diseases. Meanwhile， clinical researchers have paid more attention to traditional Chinese medicine （TCM）. As revealed by in-depth research， Chinese medicine has a certain value in regulating mitochondrial autophagy. The research on the pathogenesis of mitochondrial autophagy in related diseases and the intervention of Chinese medicine has found that there are many reports on the regulation of mitochondrial autophagy by Chinese medicine in tumors， cardiovascular diseases， and nervous system diseases. However， the mechanism of mitochondrial autophagy， the balance of mitochondrial autophagy， and the difference in the activation or inhibition of mitochondrial autophagy by Chinese medicine remain unclear. The regulation of mitochondrial autophagy has become a new research target strategy of Chinese medicine in the prevention and treatment of diseases. This paper reviewed the available literature in recent years to provide reference materials for the regulation of mitochondrial autophagy by Chinese medicine and ideas for the follow-up research of Chinese medicine in mitochondrial autophagy.
ABSTRACT
Mitochondrial autophagy is a process to clear dysfunctional mitochondria in the cytoplasm to maintain the integrity of mitochondrial function and cell homeostasis. Mitochondrial autophagy is a complex physiological process， which can maintain the balance of mitochondrial quality and quantity， cell survival under starvation and harsh conditions， and the stability of the intracellular environment. Its molecular mechanism involves a variety of proteins. Many factors can induce mitochondrial autophagy， such as starvation， oxidative stress， hypoxia， depolarization， and other stresses. The accumulation of unfolded proteins can also induce mitochondrial autophagy. In recent years， as a research hotspot， the abnormality of mitochondrial morphology and function is closely related to the occurrence of a variety of diseases. The research on mitochondrial autophagy and the pathogenesis of clinical diseases has attracted more attention， such as tumors， cardiovascular diseases， liver diseases， nervous system diseases， and glucose metabolism disorders. It has been found that regulating mitochondrial autophagy may inspire the treatment of some diseases. Meanwhile， clinical researchers have paid more attention to traditional Chinese medicine （TCM）. As revealed by in-depth research， Chinese medicine has a certain value in regulating mitochondrial autophagy. The research on the pathogenesis of mitochondrial autophagy in related diseases and the intervention of Chinese medicine has found that there are many reports on the regulation of mitochondrial autophagy by Chinese medicine in tumors， cardiovascular diseases， and nervous system diseases. However， the mechanism of mitochondrial autophagy， the balance of mitochondrial autophagy， and the difference in the activation or inhibition of mitochondrial autophagy by Chinese medicine remain unclear. The regulation of mitochondrial autophagy has become a new research target strategy of Chinese medicine in the prevention and treatment of diseases. This paper reviewed the available literature in recent years to provide reference materials for the regulation of mitochondrial autophagy by Chinese medicine and ideas for the follow-up research of Chinese medicine in mitochondrial autophagy.
ABSTRACT
Objective To investigate the effect of schisandrin (SCH) treatment on learning and memory abilities and their mechanism in APP/PS1 dual transgenic dementia mice,and explore the effect of Chinese medicine on Alzheimer's disease (AD).Methods Thirty-five APP/PS1 dementia mouse models were randomly assigned into APP/PS1 model group (n=17) and APP/PS1+SCH group (n=18);another 10 male C57BL/6J mice were chosen as blank control group.The mice in the APP/PS1+SCH group were given intragastric administration of SCH at 2.6 mg/(kg· d) for 30 d;the mice in the APP/PS1 model group and blank control group were treated with distilled water for 30 d.The learning and memory abilities of these APP/PS1 mice (n=7) were detected by Morris water maze.Mice from the three groups were sacrificed;Nissl staining was used to observe Nissl bodies of neurons in brain tissues;real-time fluorescence quantitative PCR (qPCR) was used to detect the mRNA content of terminal glycosylationend products receptor (RAGE) in brain tissues;Western blotting was used to detect the expressions of RAGE and phosphorylated P38 mitogen-activated protein kinase (p-p38) in brain tissues.Results (1) The results of water maze space exploration experiment showed that the times of crossing the platform area in the three groups were statistically significant (P＜0.05);as compared with the APP/PS1 modelgroup,the times of crossing the platform area in the APP/PS1+SCH group were significantly increased (P＜0.05).(2) Nissl staining results showed that the contents of Nissl bodies in the hippocampal CA1 area and cortical neurons of the APP/PS 1 model group were significantly reduced,with light staining and cell body atrophy;the lesions in mice of the APP/PS1+SCH group were less severe than those of APP/PS1 model group,some neurons were atrophic,and the content of the neuronal nileite bodies in the hippocampal CA1 region was relatively abundant.(3) The qPCR results showed that there were statistically significant differences in RAGE mRNA expression levels in the cortex and hippocampus of the three groups (P＜0.05);as compared with the APP/PS1 model group,the APP/PS1+SCH group had significantly reduced RAGE mRNA expression in the hippocampal area (P＜0.05).(4) Western blotting results showed that RAGE and p-p38 protein expression levels in two parts of mice of APP/PS1+SCH group were significantly reduced as compared with those in the APP/PS1 model group (P＜0.05).Conclusion SCH may improve the functional status of hippocampal and cortical neurons and improve the spatial exploratory memory ability of APP/PS1 mice by down regulating the RAGE and P38 expressions.