Effect of Dl-3-n-butylphthalide on mitochondrial Cox7c in models of cerebral ischemia/reperfusion injury

Abstract

Several studies have demonstrated the protective effect of dl-3-n-Butylphthalide (NBP) against cerebral ischemia, which may be related to the attenuation of mitochondrial dysfunction. However, the specific mechanism and targets of NBP in cerebral ischemia/reperfusion remains unclear. In this study, we used a chemical proteomics approach to search for targets of NBP and identified cytochrome C oxidase 7c (Cox7c) as a key interacting target of NBP. Our findings indicated that NBP inhibits mitochondrial apoptosis and reactive oxygen species (ROS) release and increases ATP production through upregulation of Cox7c. Subsequently, mitochondrial respiratory capacity was improved and the HIF-1α/VEGF pathway was upregulated, which contributed to the maintenance of mitochondrial membrane potential and blood brain barrier integrity and promoting angiogenesis. Therefore, our findings provided a novel insight into the mechanisms underlying the neuroprotective effects of NBP, and also proposed for the first time that Cox7c exerts a critical role by protecting mitochondrial function.

Identification of Key Modules and Hub Genes Involved in Regulating the Color of Chicken Breast Meat Using WGCNA

“…UQCR10, a functional protein in mitochondrial complex III [41], is a member of the multi-subunit phanquinone-cytochrome c reductase complex [42] and is crucial for respiratory electron transport [43], which is used by ATP synthase during oxidative phosphorylation to produce the majority of the cellular ATP [44]. COX7C is a member of the cytochrome c oxidase complex, which plays a critical role in maintaining mitochondrial membrane potential and promoting ATP generation during oxidative phosphorylation [45]. Knockdown of COX7C reduced the mitochondrial membrane potential, whereas upregulation of COX7C promoted ATP synthesis and improved mitochondrial respiratory capacity [45].…”

“…COX7C is a member of the cytochrome c oxidase complex, which plays a critical role in maintaining mitochondrial membrane potential and promoting ATP generation during oxidative phosphorylation [45]. Knockdown of COX7C reduced the mitochondrial membrane potential, whereas upregulation of COX7C promoted ATP synthesis and improved mitochondrial respiratory capacity [45]. The identification of these hub genes suggests that affecting mitochondrial activity may be an important way in which the blue module contributes to L* and b* values.…”

Multi-omics profiling identifies microglial Annexin A2 as a key mediator of NF-κB pro-inflammatory signaling in ischemic reperfusion injury

“…Cerebral stroke is a devastating and debilitating cerebrovascular disease, that causes high disability and mortality, and has emerged as one of the major public health issues around the world ( 1 , 2 , 3 ). More than 80% of cerebral strokes are ischemic stroke ( 4 , 5 , 6 ).…”