Muscone suppresses inflammatory responses and neuronal damage in a rat model of cervical spondylotic myelopathy by regulating Drp1‐dependent mitochondrial fission

Zhou, Long‐yun; Yao, Min; Tian, Z. Ryan; Liu, Shufen; Song, Yong-Jia; Ye, Jie; Gan, Li; Sun, Yue‐Li; Cui, Xue‐jun; Wang, Yongjun

doi:10.1111/jnc.15011

Cited by 37 publications

(26 citation statements)

References 63 publications

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“…These findings were also supported by those previously reported on muscone, the active ingredient of musk, which has been reported to exert antidementia (Liu et al, 2017), anticerebral ischemia (Surinkaew et al, 2018), and neuroprotective effects (Zhou et al, 2020). These activities and its underlying mechanisms are involved in promoting cell proliferation, ameliorating the loss of cell viability, preventing mitochondrial membrane potential collapse, lactate dehydrogenase, Ca 2+ overload, ROS generation, and reducing the release of inflammatory factors, such as IL-1β, TNF-α, prostaglandin E2, and myeloperoxidase (Liu et al, 2017;Surinkaew et al, 2018;Zhou et al, 2020). Wei et al (2012) and Zhang et al (2020) reported that muscone can inhibit apoptosis via inhibiting expression of caspase 8 and Fas in the cortex and stimulate neural stem cells proliferation transforming them into neurons in ischemia/reperfusion rats.…”

Section: Discussionsupporting

confidence: 90%

Musk (Moschus moschiferus) Attenuates Changes in Main Olfactory Bulb of Depressed Mice: Behavioral, Biochemical, and Histopathological Evidence

Almohaimeed

Batawi

Mohammedsaleh

et al. 2021

Front. Behav. Neurosci.

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BackgroundMusk (Moschus moschiferus) has been described to have a significant impact on the central nervous system, as well as anticonvulsion and antidepressant effects. This study was designed to evaluate the efficacy of musk in alleviating alterations induced in olfactory bulb of depressed mice exposed to chronic stress and identify the mechanism behind it.MethodsFifty male albino mice were divided into five groups (n = 10 each): control, musk, chronic unpredictable mild stress (CUMS), fluoxetine-treated, and musk-treated groups were included in this study. Behavioral changes and serum levels of corticosterone and proinflammatory cytokines included tumor necrosis factor α, interleukin 6, and oxidant/antioxidant profile were assessed at the end of the experiment. Main olfactory bulb (MOB) has been processed for histopathological examination. Gene expression of caspase-3, glial fibrillary acidic protein, and Ki67 were assessed in the MOB using quantitative real-time polymerase chain reaction.ResultsThe study showed that musk inhalation significantly reduced (p < 0.001) corticosterone level, immobility time, inflammatory cytokines, and oxidative stress markers in CUMS-exposed mice compared to the untreated CUMS group. Musk lessened CUMS-associated neuronal alterations in the MOB and significantly reduced apoptosis and enhanced neural cell proliferation (p < 0.001) comparable to fluoxetine. Musk significantly enhanced the level of antioxidants in the serum and significantly reduced inflammatory cytokines. The anti-inflammatory and antioxidant activity of musk and its constituents seemed to be behind its neuroprotective effect observed in this study.ConclusionMusk effectively ameliorated the chronic stress–induced behavioral, biochemical, and neuronal structural changes in MOB mostly through its antioxidant and anti-inflammatory effect.

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Section: Discussionsupporting

confidence: 90%

Musk (Moschus moschiferus) Attenuates Changes in Main Olfactory Bulb of Depressed Mice: Behavioral, Biochemical, and Histopathological Evidence

Almohaimeed

Batawi

Mohammedsaleh

et al. 2021

Front. Behav. Neurosci.

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“…The symptoms of CSM are changeable and the etiologies are complex, resulting in difficult to explain its natural course [2]. Although the development of CSM is relatively slow, it could lead to spinal cord dysfunction and seriously affect the quality of patients' life, even lead to disability [2,3]. At present, surgical decompression is the main treatment of CSM, which aims to remove compression of the spinal cord, so as to effectively restore the physiological curvature of the cervical spine and the corresponding spinal canal capacity and shape.…”

Section: Backgroundsmentioning

confidence: 99%

Cacna2d2 inhibits axonal regeneration following surgical decompression in a rat model of cervical spondylotic myelopathy

Liu

et al. 2022

BMC Neurosci

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Background Cervical spondylotic myelopathy (CSM) is a clinically symptomatic condition due to spinal cord compression, leading to spinal cord dysfunction. Surgical decompression is the main treatment of CSM, but the mechanisms of axonal regeneration after surgical decompression are still fragmentary. Methods In a rat model of CSM, the cacna2d2 (α2δ2) expression levels in anterior horn of spinal cord were observed following compression and decompression by western blot and immunofluorescence. The expression levels of 5 hydroxytryptamine (5HT) and GAP43 were also analyzed by immunofluorescence. Furthermore, gabapentin intervention was performed for 4 weeks after decompression to analyze the changes of behaviors and anterior horn of spinal cords. Results Following decompression, the expression levels of α2δ2 in the anterior horn of spinal cord were decreased, but the expression levels of 5HT andGAP43 were increased. Compared with the vehicle treated rats, gabapentin treatment for 4 weeks ameliorated the behaviors of rats and improved the damaged anterior horn of spinal cord. Besides, inhibition of α2δ2 through gabapentin intervention enhanced the axonal regeneration in the anterior horn of damaged spinal cord. Conclusions Inhibition of α2δ2 could enhance axonal recovery in anterior horn of damaged spinal cord induced by CSM after surgical decompression, providing a potential method for promoting axon regeneration following surgery.

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“…The dominant-negative mutant of Drp1, as well as siRNA-mediated silencing of Drp1, could reduce apoptosis in Q111/0 cells in Huntington’s disease ( Costa et al, 2010 ). By inhibiting Drp1 activation, mitochondrial debris and ROS can be reduced, and neuronal damage can be alleviated ( Zhou et al, 2020 ). Using propofol to treat oxidation-injured neurons could reduce the expression of Fis1 and increase the expression of Mfn1, maintaining normal levels of these two proteins, thus reducing the expression of apoptotic proteins in neurons and alleviating neuronal damage induced by hypoxia ( Zhang H. S. et al, 2020 ).…”

Section: The Role Of Mitochondrial Dynamics In Brain Injury After Ischemic Strokementioning

confidence: 99%

Mitochondrial Dynamics: A Potential Therapeutic Target for Ischemic Stroke

Zhou

Chen

Wang

et al. 2021

Front. Aging Neurosci.

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Stroke is one of the leading causes of death and disability worldwide. Brain injury after ischemic stroke involves multiple pathophysiological mechanisms, such as oxidative stress, mitochondrial dysfunction, excitotoxicity, calcium overload, neuroinflammation, neuronal apoptosis, and blood-brain barrier (BBB) disruption. All of these factors are associated with dysfunctional energy metabolism after stroke. Mitochondria are organelles that provide adenosine triphosphate (ATP) to the cell through oxidative phosphorylation. Mitochondrial dynamics means that the mitochondria are constantly changing and that they maintain the normal physiological functions of the cell through continuous division and fusion. Mitochondrial dynamics are closely associated with various pathophysiological mechanisms of post-stroke brain injury. In this review, we will discuss the role of the molecular mechanisms of mitochondrial dynamics in energy metabolism after ischemic stroke, as well as new strategies to restore energy homeostasis and neural function. Through this, we hope to uncover new therapeutic targets for the treatment of ischemic stroke.

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Muscone suppresses inflammatory responses and neuronal damage in a rat model of cervical spondylotic myelopathy by regulating Drp1‐dependent mitochondrial fission

Cited by 37 publications

References 63 publications

Musk (Moschus moschiferus) Attenuates Changes in Main Olfactory Bulb of Depressed Mice: Behavioral, Biochemical, and Histopathological Evidence

Musk (Moschus moschiferus) Attenuates Changes in Main Olfactory Bulb of Depressed Mice: Behavioral, Biochemical, and Histopathological Evidence

Cacna2d2 inhibits axonal regeneration following surgical decompression in a rat model of cervical spondylotic myelopathy

Mitochondrial Dynamics: A Potential Therapeutic Target for Ischemic Stroke

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