Protective Effect and Mechanism of Total Flavones from <i>Rhododendron simsii</i> Planch on Endothelium‐Dependent Dilatation and Hyperpolarization in Cerebral Ischemia‐Reperfusion and Correlation to Hydrogen Sulphide Release in Rats

Han, Jun Hyun; He, Guo‐Wei; Chen, Zhiwu

doi:10.1155/2014/904019

Cited by 9 publications

(13 citation statements)

References 45 publications

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“…Ischemic cerebrovascular disease is one of the most common disorders that greatly threaten human health with high morbidity, disability, and mortality [ 51 ]. Cerebral I/R injury is mainly characterized by a deterioration of ischemic but potentially salvageable brain tissue of an ischemic injury after reperfusion [ 52 , 53 ].…”

Section: H 2 S and I/r Injurymentioning

confidence: 99%

Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury

Wang

et al. 2015

Oxidative Medicine and Cellular Longevity

122

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Ischemia-reperfusion (I/R) injury is one of the major causes of high morbidity, disability, and mortality in the world. I/R injury remains a complicated and unresolved situation in clinical practice, especially in the field of solid organ transplantation. Hydrogen sulfide (H2S) is the third gaseous signaling molecule and plays a broad range of physiological and pathophysiological roles in mammals. H2S could protect against I/R injury in many organs and tissues, such as heart, liver, kidney, brain, intestine, stomach, hind-limb, lung, and retina. The goal of this review is to highlight recent findings regarding the role of H2S in I/R injury. In this review, we present the production and metabolism of H2S and further discuss the effect and mechanism of H2S in I/R injury.

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Section: H 2 S and I/r Injurymentioning

confidence: 99%

Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury

Wang

et al. 2015

Oxidative Medicine and Cellular Longevity

122

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“…The abovementioned EDHF‐mediated cerebral relaxation of TFR suggested an involvement of K Ca channel in the protective effect of TFR. In rat middle cerebral artery VSMCs, it was found that TFR significantly enhanced K Ca channel current indeed, suggesting mediation of K Ca channel in the protection of TFR against cerebral ischaemic injury.…”

Section: Introductionmentioning

confidence: 99%

Total flavones of Rhododendron simsii Planch flower protect rat hippocampal neuron from hypoxia-reoxygenation injury via activation of BKCa channel

Guo

Chen

et al. 2020

Journal of Pharmacy and Pharmacology

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Objectives To study the effects of total flavones of Rhododendra simsii Planch flower (TFR) on hypoxia/reoxygenation (H/R) injury in rat hippocampal neurons and its underlying mechanism. Method Model of H/R was established in newborn rat primary cultured hippocampal neuron. Lactate dehydrogenase (LDH) and neuron‐specific enolase (NSE) activity as well as malondialdehyde (MDA) content in cultured supernatants of the neurons were examined. Methyl thiazolyl tetrazolium assay and Hoechst33258 staining were, respectively, used to detect cell viability and apoptosis of neurons. Protein expression and current of BKCa channel were assessed by using Western blotting and whole‐cell patch‐clamp methods, respectively. Key findings In the ranges of 3.7–300 mg/l, TFR significantly inhibited H/R‐induced decrease of neuronal viability and increases of LDH, NSE and MDA in the supernatants as well as apoptosis; TFR 33.3, 100 and 300 mg/l markedly increased current of BKCa channel rather than the BKCa channel protein expression in the neurons. Conclusions Total flavones of R. simsii Planch flower had a protective effect against H/R injury in rat hippocampal neuron, and activation of BKCa channel may contribute to the neuroprotection.

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“…Total flavones of Rhododendron (TFR) is the effective flavonoid component extracted from Rhododendron flowers and its main ingredients are matteucinol, quercetin, rutin, hyperoside, and flavonoids. TFR has a positive effect on anticerebral ischemic injury by reducing the area of cerebral infarction, alleviating cerebral edema and cerebral cell apoptosis [ 15 , 16 ]. Our previous studies have demonstrated that TFR induces EDHF-mediated vasodilatation and smooth muscle cell membrane hyperpolarization in the cerebral basilar artery of rats with cerebral ischemia-reperfusion (CIR) injury and that the effect of TFR on brain blood vessels in rats was inhibited by the nonspecific TRPV4 blocker ruthenium red (RR) [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Total Flavone of Rhododendron Improves Cerebral Ischemia Injury by Activating Vascular TRPV4 to Induce Endothelium‐Derived Hyperpolarizing Factor‐Mediated Responses

Han

Chen

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Background Total flavonoids of Rhododendron (TFR) is extracted from Rhododendron, a herbal medicine widely used in China. The main components are flavone compounds such as warfarin, rutin, quercetin, and hyperoside. We investigated the role of TRPV4 channel in the TFR induced endothelium-dependent hyperpolarizing factor- (EDHF-) mediated responses against ischemia/reperfusion injury (IR) in cerebral IR (CIR) rats. Methods The morphological changes of cerebral cortex, the relaxation of cerebral basal artery (CBA), and cell membrane potential recording were studied in CIR rats. The outward potassium current in smooth muscle cell was recorded by whole-cell patch clamp recording. The protein expression of TRPV4, SKca, and IKca was determined. Confocal laser was used to measure the Ca2+ fluorescence intensity. Results After treatment with TFR, the number of pyramidal cells in brain tissue increased and the number of empty or lightly stained cells decreased and these effects were eliminated by using HC-067047, Apamin, or TRAM-34. TFR induced and EDHF-mediated dilatation and hyperpolarization in CBA were also attenuated by using these inhibitors. The increased outward current density elicited by TFR in acutely isolated CBA smooth muscle cells was abolished by using TRAM-34 and Apamin. TFR upregulated the protein expression of TRPV4, SKca, and IKca that was also eliminated by these inhibitors. Laser scanning showed that the increased mean fluorescence intensity of Ca2+ by CIR was decreased by using TFR and that this effect was again eliminated by the above inhibitors. Conclusions We conclude that in the CBA of the CIR rats the protective effect of TFR on ischemic cerebrovascular injury may be related to the activation of the TRPV4 in both endothelium and smooth muscle by increasing its expression and activity. The activation of TRPV4 channel in the endothelium may be linked to the opening of endothelial IKca/SKca channels that induces EDHF-mediated relaxation and hyperpolarization in the smooth muscle cell. In addition, the activation of TRPV4 in the smooth muscle cell in CBA may be linked with the activation of BKCa channel through a TRPV4-dependent pathway, reduce Ca2+ concentration in the cell, and relaxes the vessel. These findings may form a new therapeutic target for protection of ischemic brain injury and facilitate the use of Chinese medicine in brain protection.

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Protective Effect and Mechanism of Total Flavones from Rhododendron simsii Planch on Endothelium‐Dependent Dilatation and Hyperpolarization in Cerebral Ischemia‐Reperfusion and Correlation to Hydrogen Sulphide Release in Rats

Cited by 9 publications

References 45 publications

Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury

Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury

Total flavones of Rhododendron simsii Planch flower protect rat hippocampal neuron from hypoxia-reoxygenation injury via activation of BKCa channel

Total Flavone of Rhododendron Improves Cerebral Ischemia Injury by Activating Vascular TRPV4 to Induce Endothelium‐Derived Hyperpolarizing Factor‐Mediated Responses

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