Baicalin attenuates in vivo and in vitro hyperglycemia-exacerbated ischemia/reperfusion injury by regulating mitochondrial function in a manner dependent on AMPK

Li, Shanshan; Sun, Xiaoxu; Xu, Long; Sun, Ruoxi; Ma, Zhigui; Deng, Xiaozhao; Liu, Baolin; Fu, Qiang; Qu, Rong

doi:10.1016/j.ejphar.2017.07.041

Cited by 91 publications

(57 citation statements)

References 62 publications

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“…The main pathological features of AD are progressive loss of memory and deterioration of cognitive function. BAI, the major flavonoid glycoside responsible for the biological activity of S. baicalensis, has been hypothesized to possess neuroprotective effects . A previous study reported that BAI effectively improved memory deficits and reduced AD‐like pathological changes in Aβ‐injected ICR mice .…”

Section: Discussionmentioning

confidence: 99%

Baicalin mitigates cognitive impairment and protects neurons from microglia‐mediated neuroinflammation via suppressing NLRP3 inflammasomes and TLR4/NF‐κB signaling pathway

et al. 2019

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Summary Aims Baicalin (BAI), a flavonoid compound isolated from the root of Scutellaria baicalensis Georgi, has been established to have potent anti‐inflammation and neuroprotective properties; however, its effects during Alzheimer's disease ( AD ) treatment have not been well studied. This study aimed to investigate the effects of BAI pretreatment on cognitive impairment and neuronal protection against microglia‐induced neuroinflammation and to explore the mechanisms underlying its anti‐inflammation effects. Methods To determine whether BAI plays a positive role in ameliorating the memory and cognition deficits in APP (amyloid beta precursor protein)/PS1 (presenilin‐1) mice, behavioral experiments were conducted. We assessed the effects of BAI on microglial activation, the production of proinflammatory cytokines, and neuroinflammation‐mediated neuron apoptosis in vivo and in vitro using Western blot, RT ‐ PCR , ELISA , immunohistochemistry, and immunofluorescence. Finally, to elucidate the anti‐inflammation mechanisms underlying the effects of BAI , the protein expression of NLRP 3 inflammasomes and the expression of proteins involved in the TLR 4/ NF ‐κB signaling pathway were measured using Western blot and immunofluorescence. Results The results indicated that BAI treatment attenuated spatial memory dysfunction in APP / PS 1 mice, as assessed by the passive avoidance test and the Morris water maze test. Additionally, BAI administration effectively decreased the number of activated microglia and proinflammatory cytokines, as well as neuroinflammation‐mediated neuron apoptosis, in APP / PS 1 mice and LPS (lipopolysaccharides)/Aβ‐stimulated BV 2 microglial cells. Lastly, the molecular mechanistic study revealed that BAI inhibited microglia‐induced neuroinflammation via suppression of the activation of NLRP 3 inflammasomes and the TLR 4/ NF ‐κB signaling pathway. Conclusion Overall, the results of the present study indicated that BAI is a promising neuroprotective compound for use in the prevention and treatment of microglia‐mediated neuroinflammation during AD progression.

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Section: Discussionmentioning

confidence: 99%

Baicalin mitigates cognitive impairment and protects neurons from microglia‐mediated neuroinflammation via suppressing NLRP3 inflammasomes and TLR4/NF‐κB signaling pathway

et al. 2019

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“…Second, the exact mechanism that controls how oxidative stress suppresses DRP-1 expression and phosphorylation remains unknown. Research has implied that the phosphorylation of DRP-1 may affect the ROS-AMPK pathway (Li et al, 2017), which is one of the critical pathways in oxidative regulation and may be an essential target in the study of senescence and AHL. Third, our study would be more convincing if it were to show whether DRP-1 delays the development of AHL in transgenic mice.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of DRP-1-Dependent Mitophagy Promotes Cochlea Hair Cell Senescence and Exacerbates Age-Related Hearing Loss

Lin

Xiong

et al. 2019

Front. Cell. Neurosci.

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Background: Mitochondrial dysfunction is considered to contribute to the development of age-related hearing loss (AHL). The regulation of mitochondrial function requires mitochondrial quality control, which includes mitophagy and dynamics. Dynamin-related Protein 1 (DRP-1) is believed to play a central role in this regulation. However, the underlying mechanism of DRP-1 in AHL remains unclear. Here, we examined whether the decline of DRP-1-dependent mitophagy contributes to the development of AHL. Methods: We induced cellular and cochlear senescence using hydrogen peroxide (H 2 O 2) and evaluated the level of senescence through senescence-associated β-galactosidase staining. We evaluated mitophagy levels via fluorescence imaging and Western Blotting of LC3II and P62. Mitochondrial function was assessed by ATP assay, mtDNA assay, and JC-1. Results: We found that both the expression of DRP-1 and the mitophagy level decreased in senescent cells and aged mice. DRP-1 overexpression in HEI-OC1 cells initiated mitophagy and preserved mitochondrial function when exposed to H 2 O 2 , while cells with DRP-1 silencing displayed otherwise. Moreover, inhibition of DRP-1 by Mdivi-1 blocked mitophagy and exacerbated hearing loss in aged C57BL/6 mice. Conclusion: These results indicated that DRP-1 initiated mitophagy, eliminated mitochondrial dysfunction, and may protect against oxidative stress-induced senescence. These results provide a potential therapeutic target for AHL.

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“…Defects in the mitochondrial fusion process may lead to neurodegenerative disorders such as Charcot-Marie-Tooth neuropathy [186] , [187] . Mitochondrial fusion proteins including Mfn1, Mfn2, and Opa1 are less studied in cerebral ischemia [188] , [189] , [190] , [191] . It was revealed that in vivo and in vitro hypoxic models decreased Mfn2 expression, and Mfn2 may exert anti-apoptotic effect via restoration of mitochondrial function [188] , [189] .…”

Section: Mitochondrial Dynamics In Cell Death and Survival During Cermentioning

confidence: 99%

Diverse roles of mitochondria in ischemic stroke

2018

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Stroke is the leading cause of adult disability and mortality in most developing and developed countries. The current best practices for patients with acute ischemic stroke include intravenous tissue plasminogen activator and endovascular thrombectomy for large-vessel occlusion to improve clinical outcomes. However, only a limited portion of patients receive thrombolytic therapy or endovascular treatment because the therapeutic time window after ischemic stroke is narrow. To address the current shortage of stroke management approaches, it is critical to identify new potential therapeutic targets. The mitochondrion is an often overlooked target for the clinical treatment of stroke. Early studies of mitochondria focused on their bioenergetic role; however, these organelles are now known to be important in a wide range of cellular functions and signaling events. This review aims to summarize the current knowledge on the mitochondrial molecular mechanisms underlying cerebral ischemia and involved in reactive oxygen species generation and scavenging, electron transport chain dysfunction, apoptosis, mitochondrial dynamics and biogenesis, and inflammation. A better understanding of the roles of mitochondria in ischemia-related neuronal death and protection may provide a rationale for the development of innovative therapeutic regimens for ischemic stroke and other stroke syndromes.

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Baicalin attenuates in vivo and in vitro hyperglycemia-exacerbated ischemia/reperfusion injury by regulating mitochondrial function in a manner dependent on AMPK

Cited by 91 publications

References 62 publications

Baicalin mitigates cognitive impairment and protects neurons from microglia‐mediated neuroinflammation via suppressing NLRP3 inflammasomes and TLR4/NF‐κB signaling pathway

Baicalin mitigates cognitive impairment and protects neurons from microglia‐mediated neuroinflammation via suppressing NLRP3 inflammasomes and TLR4/NF‐κB signaling pathway

Inhibition of DRP-1-Dependent Mitophagy Promotes Cochlea Hair Cell Senescence and Exacerbates Age-Related Hearing Loss

Diverse roles of mitochondria in ischemic stroke

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