Pseudoginsenoside-F11 improves long-term neurological function and promotes neurogenesis after transient cerebral ischemia in mice

Yuan, Linlin; Sun, Shibo; Pan, Xiaohan; Zheng, Liqin; Li, Yuting; Yang, Jingyu; Wu, Chunfu

doi:10.1016/j.neuint.2019.104586

Cited by 16 publications

(10 citation statements)

References 55 publications

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“…Autophagy regulates tissue homeostasis ( Takagi et al, 2007 ), and previously showed that activation of autophagy improved the survival of random-pattern skin flaps ( Yuan et al, 2019 ). PF11 exerted neuroprotective effects during stroke by augmenting autophagy and restoring autophagy flux ( Yuan et al, 2020 ). However, there is no study has investigated the effect of PF11 on autophagy in skin flaps.…”

Section: Discussionmentioning

confidence: 99%

Pseudoginsenoside F11 Enhances the Viability of Random-Pattern Skin Flaps by Promoting TFEB Nuclear Translocation Through AMPK-mTOR Signal Pathway

et al. 2021

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Random-pattern skin flap is widely used in tissue reconstruction. However, necrosis occurring in the distal part of the flap limits its clinical application to some extent. Activation of autophagy has been considered as an effective approach to enhance the survival of skin flaps. Pseudoginsenoside F11 (PF11), an ocotillol-type saponin, is an important component of Panax quinquefolium which has been shown to confer protection against cerebral ischemia and alleviate oxidative stress. However, it is currently unknown whether PF11 induces autophagy to improve the survival of skin flaps. In this study, we investigated the effects of PF11 on blood flow and tissue edema. The results of histological examination and western blotting showed that PF11 enhanced angiogenesis, alleviated apoptosis and oxidative stress, thereby improving the survival of the flap. Further experiments showed that PF11 promoted nuclear translocation of TFEB and by regulating the phosphorylation of AMPK. In summary, this study demonstrates that PF11 activates autophagy through the AMPK-TFEB signal pathway in skin flaps and it could be a promising strategy for enhancing flap viability.

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Section: Discussionmentioning

confidence: 99%

Pseudoginsenoside F11 Enhances the Viability of Random-Pattern Skin Flaps by Promoting TFEB Nuclear Translocation Through AMPK-mTOR Signal Pathway

et al. 2021

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“…Interestingly, patients without apparent improvement still exhibited complex changes over time due to motor network connectivity [ 91 ]. Investigated mechanisms of motor functional recovery include axonal sprouting [ 92 , 93 ], white matter repair [ 94 ], neurogenesis [ 95 ], and ipsilesional/contralesional network reorganization [ 96 ]. Just as consequences of stroke disability maladaptively alter cortical mapping and hinder recovery [ 97 ], interventions targeting beneficial neuroplastic reorganization can strengthen tracts and improve recovery [ 98 , 99 ].…”

Section: Motor Pathway Disruptionmentioning

confidence: 99%

Beyond the Brain: The Systemic Pathophysiological Response to Acute Ischemic Stroke

et al. 2020

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Stroke research has traditionally focused on the cerebral processes following ischemic brain injury, where oxygen and glucose deprivation incite prolonged activation of excitatory neurotransmitter receptors, intracellular calcium accumulation, inflammation, reactive oxygen species proliferation, and ultimately neuronal death. A recent growing body of evidence, however, points to far-reaching pathophysiological consequences of acute ischemic stroke. Shortly after stroke onset, peripheral immunodepression in conjunction with hyperstimulation of autonomic and neuroendocrine pathways and motor pathway impairment result in dysfunction of the respiratory, urinary, cardiovascular, gastrointestinal, musculoskeletal, and endocrine systems. These end organ abnormalities play a major role in the morbidity and mortality of acute ischemic stroke. Using a pathophysiology-based approach, this current review discusses the pathophysiological mechanisms following ischemic brain insult that result in end organ dysfunction. By characterizing stroke as a systemic disease, future research must consider bidirectional interactions between the brain and peripheral organs to inform treatment paradigms and develop effective, comprehensive therapeutics for acute ischemic stroke.

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“…Another ginsenoside with effects on neurogenesis in ischemia reperfusion models is the ocotillol-type saponin pseudoginsenoside F11 (pF11). Repeated doses of pF11 before and after the onset of tMCAO in mice, improved the long-term behavioral outcome regarding cognitive and sensorimotor dysfunction, and also promoted neurogenesis by increasing the number of cortical NeuN + cells and BDNF expression levels ( Yuan et al., 2020 ). Concerning immunomodulation, pF11 was shown to shift neutrophils and macrophages in vitro from an OGD-induced M1-like phenotype towards a CD206 + immunoregulatory functional state ( Hou et al., 2020 ).…”

Section: Saponins As Immunomodulators and Regulators Of Cell Death In Strokementioning

confidence: 99%

Emerging immune and cell death mechanisms in stroke: Saponins as therapeutic candidates

García-Pupo

San

Hernández

et al. 2020

Brain, Behavior, & Immunity - Health

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The complexity of the ischemic cascade is based on the integrated crosstalk of every cell type in the neurovascular unit. Depending on the features of the ischemic insult, several cell death mechanisms are triggered, such as apoptosis, necroptosis, ferroptosis/oxytosis, ETosis or pyroptosis, leading to reactive astrogliosis. However, emerging evidence demonstrates a dual role for the immune system in stroke pathophysiology, where it exerts both detrimental and also beneficial functions. In this review, we discuss the relevance of several cell death modalities and the dual role of the immune system in stroke pathophysiology. We also provide an overview of some emerging immunomodulatory therapeutic strategies, amongst which saponins, which are promising candidates that exert multiple pharmacological effects.

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Pseudoginsenoside-F11 improves long-term neurological function and promotes neurogenesis after transient cerebral ischemia in mice

Cited by 16 publications

References 55 publications

Pseudoginsenoside F11 Enhances the Viability of Random-Pattern Skin Flaps by Promoting TFEB Nuclear Translocation Through AMPK-mTOR Signal Pathway

Pseudoginsenoside F11 Enhances the Viability of Random-Pattern Skin Flaps by Promoting TFEB Nuclear Translocation Through AMPK-mTOR Signal Pathway

Beyond the Brain: The Systemic Pathophysiological Response to Acute Ischemic Stroke

Emerging immune and cell death mechanisms in stroke: Saponins as therapeutic candidates

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