Mdivi-1 ameliorates early brain injury after subarachnoid hemorrhage via the suppression of inflammation-related blood–brain barrier disruption and endoplasmic reticulum stress-based apoptosis

Fan, Linfeng; He, Pingyou; Peng, Yucong; Du, Quan; Ma, Yi-jun; Jin, Jianxiang; Xu, Hangzhe; Li, Jianru; Wang, Zhijiang; Cao, Shenglong; Li, Tao; Yan, Feng; Gu, Chi; Wang, Lin; Chen, Gao

doi:10.1016/j.freeradbiomed.2017.08.003

Cited by 95 publications

(65 citation statements)

References 62 publications

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“…Park et al demonstrated in murine microglial cells that inhibition of LPS‐induced mitochondrial fission and ROS generation by Mdivi‐1 attenuated production of proinflammatory mediators via reduced nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) and MAPK signaling (Park et al, ). In a recent study, Fan et al elegantly showed that Mdivi‐1 attenuated early brain injury after experimental subarachnoid hemorrhage, probably via suppression of inflammation‐related blood–brain barrier disruption (Fan et al, ). In line with these findings, an association between inflammation and an impaired mitochondrial fission and fusion has been described for inflammation‐induced bone destruction (Zhang et al, ), inflammasome activation (Zhou et al, ), and efferocytosis (Wang et al, ).…”

Section: Discussionmentioning

confidence: 99%

Resolvin E1 Improves Mitochondrial Function in Human Alveolar Epithelial Cells during Severe Inflammation

Mayer

Sommer

Hache

et al. 2019

Lipids

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Severe inflammatory disorders such as sepsis are a major cause of morbidity and mortality worldwide. Mitochondrial dysfunction is regarded as a key feature involved in inflammation pathogenesis. In the present study, we investigated the impact of the omega‐3 fatty acid‐derived lipid mediator Resolvin E1 (RvE1) on mitochondrial function in experimental pulmonary inflammation. RvE1 was found to exert anti‐inflammatory properties in human alveolar epithelial cells during severe inflammation. RvE1 is capable of restoring inflammation‐induced mitochondrial dysfunction and the impaired imbalance of mitochondrial fission and fusion. Experimental inhibition of mitochondrial fission with Mdivi‐1 in our model is associated with a significantly reduced inflammatory response and improved mitochondrial function. These findings suggest a novel functional mechanism for the beneficial effects of RvE1 in experimental pulmonary inflammatory reactions.

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Section: Discussionmentioning

confidence: 99%

Resolvin E1 Improves Mitochondrial Function in Human Alveolar Epithelial Cells during Severe Inflammation

Mayer

Sommer

Hache

et al. 2019

Lipids

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“…Mitochondrial fragmentation is closely associated with increased ROS production, which leads to neural cell death and neuroinflammatory responses (Fan, He, et al, 2017, Panchal & Tiwari 2019, Park et al, 2013. As shown in Figure 7a, the elongated tubular (Figure 7c), which was partly ameliorated in musconetreated rats.…”

Section: Muscone Regulated Mitochondrial Morphology and Intracellulmentioning

confidence: 94%

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

Zhou

Yao

Tian

et al. 2020

Journal of Neurochemistry

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“…BBB permeability. The permeability of the BBB was assessed using Evans blue extravasation as previously reported (22,23). Briefly, rats were anesthetized with 40 mg/kg pentobarbital (intraperitoneal) at 71 h after SAH and 2% Evans Blue dye (5 ml/kg) was injected into the right femoral vein.…”

Section: Methodsmentioning

confidence: 99%

Calpastatin peptide attenuates early brain injury following experimental subarachnoid hemorrhage

et al. 2020

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Calpain activation may have an important role in early brain injury (EBI) following subarachnoid hemorrhage (SAH). The present study investigated the effects of the calpastatin peptide, a cell-permeable peptide that functions as a potent inhibitor of calpain, on EBI in a rat SAH model. It was revealed that calpastatin peptide treatment significantly reduced SAH-induced body weight loss and neurological deficit at 72 h when compared with untreated SAH controls. Furthermore, the quantification of brain water content and the extravasation of Evans blue dye revealed a significant reduction in SAH-induced brain edema and blood-brain barrier permeability at 72 h due to treatment with the calpastatin peptide when compared with untreated SAH controls. Finally, calpastatin peptide treatment significantly attenuated the protein levels of Bax, cytochrome c, cleaved caspase-9 and cleaved caspase-3, and reduced the number of terminal deoxynucleotidyl transferase dUTP nick end labelling-positive cells in the basal cortex at 72 h after SAH when compared with untreated SAH controls. These results indicated that the calpastatin peptide may ameliorate EBI following SAH in rat models.

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Mdivi-1 ameliorates early brain injury after subarachnoid hemorrhage via the suppression of inflammation-related blood–brain barrier disruption and endoplasmic reticulum stress-based apoptosis

Cited by 95 publications

References 62 publications

Resolvin E1 Improves Mitochondrial Function in Human Alveolar Epithelial Cells during Severe Inflammation

Resolvin E1 Improves Mitochondrial Function in Human Alveolar Epithelial Cells during Severe Inflammation

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

Calpastatin peptide attenuates early brain injury following experimental subarachnoid hemorrhage

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