Mechanisms and therapeutic targets of mitophagy after intracerebral hemorrhage

Huang, Qinghua; Yu, Xiaoqin; Fu, Peijie; Wu, Moxin; Yin, Xiaoping; Chen, Zhiying; Zhang, Manqing

doi:10.1016/j.heliyon.2023.e23941

Heliyon

2024

DOI: 10.1016/j.heliyon.2023.e23941

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Mechanisms and therapeutic targets of mitophagy after intracerebral hemorrhage

Qinghua Huang,

Xiaoqin Yu,

Peijie Fu

et al.

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2024

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Cited by 3 publications

References 66 publications

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Activation of PARP in secondary brain injury following intracerebral haemorrhage

Zhang,

Su,

et al. 2024

Brain Hemorrhages

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Activation of PARP in secondary brain injury following intracerebral haemorrhage

Zhang,

Su,

et al. 2024

Brain Hemorrhages

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Rhopaloic acid A triggers mitochondria damage-induced apoptosis in oral cancer by JNK/BNIP3/Nix-mediated mitophagy

Chen,

Tsai,

Zhang

et al. 2024

Phytomedicine

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Ginsenoside Rb1 ameliorates hippocampal neuroinflammation in rats after intracerebral hemorrhage by inactivating the TLR4/NF-kB pathway

Liu,

Wang,

Han

et al. 2024

Journal of Pharmacy and Pharmacology

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Purpose This work elucidated the therapeutic effect and mechanism of ginsenoside Rb1 on intracerebral hemorrhage (ICH). Methods ICH rat models were treated by ginsenoside Rb1. Modified neurological deficit score, and Y-maze and Morris water-maze tests were performed on rats. Hippocampal neuronal damage was observed by Nissl staining. Rat primary astrocytes were exposed to ginsenoside Rb1, Hemin, and lipopolysaccharide (LPS). TNF-α, IL-1β, and IL-6 levels were assessed via enzyme-linked immunosorbent assay. TLR4/NF-kB pathway activity was appraised by Western blot. Immunofluorescence staining was for hippocampal glial fibrillary acidic protein (GFAP) expression and P65 protein location in hippocampus and astrocytes. Results In rats after ICH, ginsenoside Rb1 ameliorated neurological impairment and hippocampal neuronal damage; improved learning and memory ability; reduced brain water content; decreasedhippocampal TNF-α, IL-1β, and IL-6; inactivated TLR4/NF-kB pathway; and declined hippocampal GFAP expression. In rat primary astrocytes exposed to Hemin, ginsenoside Rb1 declined TNF-α, IL-1β, and IL-6; inactivated TLR4/NF-kB pathway; and hindered P65 protein entry into nucleus. However, these functions of ginsenoside Rb1 on the Hemin-induced astrocytes were abolished by LPS. Conclusion Ginsenoside Rb1 has promising future for clinical ICH treatment, which exerts therapeutic effect on ICH by ameliorating hippocampal neuroinflammation via inactivating the TLR4/NF-kB pathway.

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Mechanisms and therapeutic targets of mitophagy after intracerebral hemorrhage

Cited by 3 publications

References 66 publications

Activation of PARP in secondary brain injury following intracerebral haemorrhage

Activation of PARP in secondary brain injury following intracerebral haemorrhage

Rhopaloic acid A triggers mitochondria damage-induced apoptosis in oral cancer by JNK/BNIP3/Nix-mediated mitophagy

Ginsenoside Rb1 ameliorates hippocampal neuroinflammation in rats after intracerebral hemorrhage by inactivating the TLR4/NF-kB pathway

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