The protective role of Tongxinluo on blood–brain barrier after ischemia–reperfusion brain injury

Liu, Ye; Tang, Guang Hui; Sun, Yu; Lin, Xiao Jie; Yang, Guo‐Yuan; Liu, Jian Rong

doi:10.1016/j.jep.2013.05.018

Cited by 40 publications

(34 citation statements)

References 30 publications

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“…Cytotoxic edema is characterized by the intact blood-brain barrier (BBB), but a dysfunction of the sodium and potassium pump in the cell membrane, leading to a shift of water from the interstitial into the intracellular compartment and a net uptake of water from blood into brain parenchyma [12,13]. …”

Section: Brain Edemamentioning

confidence: 99%

“…In several pathological cerebral edemas, deprivation of nutrients and oxygen leads to the sodium-potassium pump failure on astrocytic cell membranes [12,14]. As a consequence, a massive accumulation of sodium ions occurs intracellularly.…”

Section: Brain Edemamentioning

confidence: 99%

“…Moreover, this type of edema has usually been seen in the late stages of cerebral ischemia, further inducing focal cerebral blood flow (CBF) reduction, cell necrosis and apoptosis [12]. Mechanisms contributing to vasogenic edema include physical crash by arterial hypertension or trauma and tumor-released vasoactive or endothelial destructive compounds (e.g., arachidonic acid, excitatory neurotransmitters, eicosanoids, bradykinin, histamine and free radicals) [3,23].…”

Section: Brain Edemamentioning

confidence: 99%

“…Neuroinflammation is a concomitant syndrome that has been demonstrated to significantly contribute to the progression of various brain injuries, including traumatic brain injury and ischemic or hemorrhagic stroke, among others [12,20,44]. Aquaporin-4 expression was found upregulated during the edema build-up and resolution phases in focal brain inflammation [16,45].…”

Section: Aquaporin-4 In Brain Edemamentioning

confidence: 99%

“…A CXCR4 antagonist drug called AMD3100 significantly suppressed inflammatory response and reduced BBB disruption in the context of ischemic stroke [20]. Besides, a renowned traditional Chinese medicine Tongxinluo was found to benefit BBB integrity by reducing the inflammatory cytokines’ expression, as well, in mice subjected to middle cerebral artery occlusion [12]. The beneficial effects on brain edema may at least partially be attributed to the block of the aquaporin-4 upregulation through the attenuated cytokines’ release.…”

Section: Aquaporin-4 As a Therapeutic Target In Cerebral Edemamentioning

confidence: 99%

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Aquaporin-4: A Potential Therapeutic Target for Cerebral Edema

Tang

Yang

2016

IJMS

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Aquaporin-4 (AQP4) is a family member of water-channel proteins and is dominantly expressed in the foot process of glial cells surrounding capillaries. The predominant expression at the boundaries between cerebral parenchyma and major fluid compartments suggests the function of aquaporin-4 in water transfer into and out of the brain parenchyma. Accumulating evidences have suggested that the dysregulation of aquaporin-4 relates to the brain edema resulting from a variety of neuro-disorders, such as ischemic or hemorrhagic stroke, trauma, etc. During edema formation in the brain, aquaporin-4 has been shown to contribute to the astrocytic swelling, while in the resolution phase, it has been seen to facilitate the reabsorption of extracellular fluid. In addition, aquaporin-4-deficient mice are protected from cytotoxic edema produced by water intoxication and brain ischemia. However, aquaporin-4 deletion exacerbates vasogenic edema in the brain of different pathological disorders. Recently, our published data showed that the upregulation of aquaporin-4 in astrocytes probably contributes to the transition from cytotoxic edema to vasogenic edema. In this review, apart from the traditional knowledge, we also introduce our latest findings about the effects of mesenchymal stem cells (MSCs) and microRNA-29b on aquaporin-4, which could provide powerful intervention tools targeting aquaporin-4.

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Section: Brain Edemamentioning

confidence: 99%

Section: Brain Edemamentioning

confidence: 99%

Section: Brain Edemamentioning

confidence: 99%

Section: Aquaporin-4 In Brain Edemamentioning

confidence: 99%

Section: Aquaporin-4 As a Therapeutic Target In Cerebral Edemamentioning

confidence: 99%

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Aquaporin-4: A Potential Therapeutic Target for Cerebral Edema

Tang

Yang

2016

IJMS

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Chinese medicine Tongxinluo increases tight junction protein levels by inducing KLF5 expression in microvascular endothelial cells

Liu

Zheng

Zhang

et al. 2015

Cell Biochemistry & Function

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Tongxinluo (TXL) is a compound prescription formulated according to the meridian theory of traditional Chinese medicine. It may play an important role in cardiovascular protection by improving endothelial cell function. The aim of present study was to investigate whether endothelial protection with TXL is related to its regulation of tight junction protein expression. Human cardiac microvascular endothelial cells (HCMECs) were cultured and treated with 10(-7) mol l(-1) angiotensin II (Ang II) and the different doses of TXL; the expression of tight junction proteins occludin, claudin, VE-cadherin and beta-catenin was determined by Western blotting and real-time PCR. Gain-of-function and loss-of-function of Krüppel-like factor 5 (KLF5) were carried out in HCMEC transfected with either KLF5 adenovirus pAd-KLF5 or siRNA specific for KLF5. Angiotensinogen transgenic mice were treated with TXL by oral administration of TXL of 0.75 g kg(-1) day(-1) , and immunohistochemical staining was performed with antioccludin, anticlaudin, anti-VE-cadherin, antibeta-catenin and anti-KLF5 antibodies. Ang II treatment significantly reduced the expression of tight junction proteins occludin, claudin, VE-cadherin and beta-catenin in cultured HCMECs. TXL pretreatment could abrogate the down-regulation of these tight junction proteins induced by Ang II. Ang II treatment also decreased KLF5 expression at the mRNA and protein levels; TXL pretreatment markedly reversed the inhibitory effect of Ang II on KLF5 expression. Gain-of-function and loss-of-function of KLF5 showed that KLF5 mediated the expression of tight junction proteins in HCMECs. TXL-enhanced expression of the tight junction proteins was mediated by KLF5. In angiotensinogen transgenic mice, TXL also increased the tight junction protein levels by inducing KLF5 expression. Chinese medicine TXL increases tight junction protein levels by inducing KLF5 expression in microvascular endothelial cells.

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Relationship between interleukin‐6 and brain ischemia

Hu¹,

2019

Ibrain

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Ischemic stroke is the most common disease of nervous system associated with high mortality worldwide. After the primary injury, secondary injury is caused by activation of the immune response due to an influx of neuro‐inflammatory cells increasing the production of inflammatory cytokines and edema. Inflammatory factors, such as interleukin‐6 (IL‐6), are suspected to play a role in arterial thrombogenesis. IL‐6 has a double role of pro‐inflammatory and anti‐inflammatory responding to the brain injury. Many of its effects are caused by trans‐signaling. However, the relationship between IL‐6 and brain ischemia remains unclear. Here we tried to review the role of IL‐6 in brain ischemia and summarized the underlying molecular mechanism.

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The protective role of Tongxinluo on blood–brain barrier after ischemia–reperfusion brain injury

Cited by 40 publications

References 30 publications

Aquaporin-4: A Potential Therapeutic Target for Cerebral Edema

Aquaporin-4: A Potential Therapeutic Target for Cerebral Edema

Chinese medicine Tongxinluo increases tight junction protein levels by inducing KLF5 expression in microvascular endothelial cells

Relationship between interleukin‐6 and brain ischemia

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