Effect of baicalin on oxygen–glucose deprivation-induced endothelial cell damage

Luo, Si; Li, Shi; Zhu, Lei; Fang, Shuhuan; Chen, Junli; Xu, Qingqing; Li, Hongying; Luo, Nachuan; Yang, Cong; Luo, Dan; Li, Lin; Ma, Xing-Hong; Zhang, Rong; Wang, Hong; Chen, Yunbo; Wang, Qi

doi:10.1097/wnr.0000000000000749

Cited by 16 publications

(10 citation statements)

References 22 publications

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“…Many other studies reported that blood-brain barrier (BBB) disruption occurs under brain injury conditions such as ischemia, traumatic brain injury, and seizure [55,56,57]. In severe hypoglycemia, BBB is destroyed as early critical events, because glucose deprivation destroys endothelial cells that make up BBB [58,59,60]. To determine disruption of the BBB, we conducted IgG staining by detecting the degree of extravasation of serum immunoglobulin G (IgG) with a previously described method [43] and myeloperoxidase (MPO) staining to look for an influx of neutrophils after hypoglycemia.…”

Section: Resultsmentioning

confidence: 99%

The Effects of Sodium Dichloroacetate on Mitochondrial Dysfunction and Neuronal Death Following Hypoglycemia-Induced Injury

Kho

Choi

Lee

et al. 2019

Cells

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Our previous studies demonstrated that some degree of neuronal death is caused by hypoglycemia, but a subsequent and more severe wave of neuronal cell death occurs due to glucose reperfusion, which results from the rapid restoration of low blood glucose levels. Mitochondrial dysfunction caused by hypoglycemia leads to increased levels of pyruvate dehydrogenase kinase (PDK) and suppresses the formation of ATP by inhibiting pyruvate dehydrogenase (PDH) activation, which can convert pyruvate into acetyl-coenzyme A (acetyl-CoA). Sodium dichloroacetate (DCA) is a PDK inhibitor and activates PDH, the gatekeeper of glucose oxidation. However, no studies about the effect of DCA on hypoglycemia have been published. In the present study, we hypothesized that DCA treatment could reduce neuronal death through improvement of glycolysis and prevention of reactive oxygen species production after hypoglycemia. To test this, we used an animal model of insulin-induced hypoglycemia and injected DCA (100 mg/kg, i.v., two days) following hypoglycemic insult. Histological evaluation was performed one week after hypoglycemia. DCA treatment reduced hypoglycemia-induced oxidative stress, microglial activation, blood–brain barrier disruption, and neuronal death compared to the vehicle-treated hypoglycemia group. Therefore, our findings suggest that DCA may have the therapeutic potential to reduce hippocampal neuronal death after hypoglycemia.

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Section: Resultsmentioning

confidence: 99%

The Effects of Sodium Dichloroacetate on Mitochondrial Dysfunction and Neuronal Death Following Hypoglycemia-Induced Injury

Kho

Choi

Lee

et al. 2019

Cells

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“…Baicalin reduced brain infarction volume, brain edema, BBB damage and brain inflammation in rodent ischemic stroke models 138 , 141 , 142 , 143 , 144 , 145 . Baicalin decreased BBB permeability and protected brain microvascular endothelial cells (BMVECs) in vivo and in vitro 46 , 145 , 146 and reduced neurotoxicity under an OGD condition 147 , 148 , 149 . The neurovascular protective effects of baicalin may be attributed to its antioxidant effects 138 , 150 , 151 .…”

Section: Natural Active Compounds Targeting Onoo − mentioning

confidence: 99%

Targeting RNS/caveolin-1/MMP signaling cascades to protect against cerebral ischemia-reperfusion injuries: potential application for drug discovery

Chen

et al. 2018

Acta Pharmacol Sin

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Reactive nitrogen species (RNS) play important roles in mediating cerebral ischemia-reperfusion injury. RNS activate multiple signaling pathways and participate in different cellular events in cerebral ischemia-reperfusion injury. Recent studies have indicated that caveolin-1 and matrix metalloproteinase (MMP) are important signaling molecules in the pathological process of ischemic brain injury. During cerebral ischemia-reperfusion, the production of nitric oxide (NO) and peroxynitrite (ONOO−), two representative RNS, down-regulates the expression of caveolin-1 (Cav-1) and, in turn, further activates nitric oxide synthase (NOS) to promote RNS generation. The increased RNS further induce MMP activation and mediate disruption of the blood-brain barrier (BBB), aggravating the brain damage in cerebral ischemia-reperfusion injury. Therefore, the feedback interaction among RNS/Cav-1/MMPs provides an amplified mechanism for aggravating ischemic brain damage during cerebral ischemia-reperfusion injury. Targeting the RNS/Cav-1/MMP pathway could be a promising therapeutic strategy for protecting against cerebral ischemia-reperfusion injury. In this mini-review article, we highlight the important role of the RNS/Cav-1/MMP signaling cascades in ischemic stroke injury and review the current progress of studies seeking therapeutic compounds targeting the RNS/Cav-1/MMP signaling cascades to attenuate cerebral ischemia-reperfusion injury. Several representative natural compounds, including calycosin-7-O-β-D-glucoside, baicalin, Momordica charantia polysaccharide (MCP), chlorogenic acid, lutein and lycopene, have shown potential for targeting the RNS/Cav-1/MMP signaling pathway to protect the brain in ischemic stroke. Therefore, the RNS/Cav-1/MMP pathway is an important therapeutic target in ischemic stroke treatment.

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“…In addition, baicalin attenuated cell apoptosis and increased mitophagy [ 13 ]. Luo et al [ 48 ] evaluated the protective effect of baicalin against OGD-induced ischemic injury in endothelial cells. The authors found that baicalin effectively inhibited cell death, decreased cell membrane damage, and maintained the integrity of the nucleus.…”

Section: Neuroprotective Effects Of Baicalinmentioning

confidence: 99%

Neuroprotective and Cognitive Enhancement Potentials of Baicalin: A Review

et al. 2018

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Neurodegenerative diseases are a heterogeneous group of disorders that are characterized by the gradual loss of neurons. The development of effective neuroprotective agents to prevent and control neurodegenerative diseases is specifically important. Recently, there has been an increasing interest in selecting flavonoid compounds as potential neuroprotective agents, owing to their high effectiveness with low side effects. Baicalin is one of the important flavonoid compounds, which is mainly isolated from the root of Scutellaria baicalensis Georgi (an important Chinese medicinal herb). In recent years, a number of studies have shown that baicalin has a potent neuroprotective effect in various in vitro and in vivo models of neuronal injury. In particular, baicalin effectively prevents neurodegenerative diseases through various pharmacological mechanisms, including antioxidative stress, anti-excitotoxicity, anti-apoptotic, anti-inflammatory, stimulating neurogenesis, promoting the expression of neuronal protective factors, etc. This review mainly focuses on the neuroprotective and cognitive enhancement effects of baicalin. The aim of the present review is to compile all information in relation to the neuroprotective and cognitive enhancement effects of baicalin and its molecular mechanisms of action in various in vitro and in vivo experimental models.

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Effect of baicalin on oxygen–glucose deprivation-induced endothelial cell damage

Cited by 16 publications

References 22 publications

The Effects of Sodium Dichloroacetate on Mitochondrial Dysfunction and Neuronal Death Following Hypoglycemia-Induced Injury

The Effects of Sodium Dichloroacetate on Mitochondrial Dysfunction and Neuronal Death Following Hypoglycemia-Induced Injury

Targeting RNS/caveolin-1/MMP signaling cascades to protect against cerebral ischemia-reperfusion injuries: potential application for drug discovery

Neuroprotective and Cognitive Enhancement Potentials of Baicalin: A Review

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