hyperoside and Reperfusion-Injury

Hyperoside (Hyp), one of the active flavones from. To explore the effect of Hyp on vasodilatation in the cerebral basilar artery (CBA) of Sprague-Dawley (SD) rats suffering with ischaemic-reperfusion (IR) injury.. Sprague-Dawley rats were randomly divided into sham, model, Hyp, Hyp + channel blocker and channel blocker groups. Hyp (50 mg/kg, IC. Hyp treatment significantly ameliorated the brain damage induced by IR and evoked endothelium-dependent vasodilation rate (47.93 ± 3.09% vs. 2.99 ± 1.53%) and hyperpolarization (-8.15 ± 1.87 mV vs. -0.55 ± 0.42 mV) by increasing the expression of IP3R, PKC, transient receptor potential vanilloid channel 4 (TRPV4), IK. Although Hyp showed protective effect in ischaemic stroke, more clinical trial certification is needed due to the difference between animals and humans.

Topics: Animals; Antineoplastic Agents; Brain Ischemia; Endothelial Cells; Humans; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Stroke; TRPV Cation Channels; Vasodilation

Ischemia/reperfusion (IR) is a common cause of acute kidney injury (AKI). However, effective therapies for IR-induced AKI are lacking. Hyperoside is an active constituent in the flowers of

Topics: Apoptosis; Drugs, Chinese Herbal; Humans; Kidney; Mitochondria; Oxidative Stress; Plants; Quercetin; Reperfusion Injury

Role of hyperoside in protecting cardiomyocytes from ischemia/reperfusion induced injury has been proved. However, possible protecting mechanisms remain unclear. To fix the problem, an essential pro-apoptotic protein Bnip3 was studied in our experiments.. Neonatal rat cardiomyocytes were used and submitted to hypoxia for 8h followed by reoxygenation for 2h to simulate the ischemia/reperfusion injury. Hypoxia/reoxygenation(H/R) induced damage to cardiomyocytes and the protective effect of hyperoside were examined by means of MTT assay. H/R-induced apoptosis was assessed by Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling(TUNEL) and DNA Ladder assay. mRNA expression of Bnip3 was determined by use of quantitative real-time reverse transcription polymerase chain reaction assay. Protein levels of Bnip3, Bax, Bcl-2 and cleaved caspase-3 were examined using western-blot assay. Our results showed that H/R caused great damage to cardiomyocytes, upregulated the protein expressions of Bnip3, Bax, cleaved caspase3, and decreased the expression of the anti-apoptotic protein of Bcl-2. Whereas, compared with the H/R group, a decrease in activities of Bnip3, Bax, cleaved caspase3, and a promoting expression of Bcl-2 were detected in the H/R goup pretreated with hyperoside.. It was concluded in our study that H/R-induced apoptotic effect in cardiomyocytes could be attenuated by hyperoside, and the protective role of hyperoside, if not completely, could be partly through the suppression of the pro-apoptotic gene Bnip3.

Topics: Animals; Apoptosis; Cardiotonic Agents; Membrane Proteins; Mitochondrial Proteins; Myocardial Infarction; Myocytes, Cardiac; Plants, Medicinal; Quercetin; Rats; Rats, Sprague-Dawley; Reperfusion Injury

Hyperoside is a flavonoid compound and widely used in clinic to relieve pain and improve cardiovascular functions. However, the effects of hyperoside on ischemic neurons and the molecular mechanisms remain unclear. Here, we used an in vitro ischemic model of oxygen-glucose deprivation followed by reperfusion (OGD-R) to investigate the protective effects of hyperoside on ischemic neuron injury and further explore the possible related mechanisms. Our results demonstrated that hyperoside protected cultured cortical neurons from OGD-R injury, it also relieved glutamate-induced neuronal injury and NMDA-induced [Ca(2+)](i) elevation. As for the mechanisms, hyperoside firstly attenuated the phosphorylation of CaMKII caused by OGD-R lesions. Meanwhile, hyperoside lessened iNOS expression induced by OGD-R via inhibition of NF-κB activation. Furthermore, ameliorating of ERK, JNK and Bcl-2 family-related apoptotic signaling pathways were also involved in the neuroprotection of hyperoside. Taken together, these studies revealed that hyperoside had protective effects on neuronal ischemia-reperfusion impairment, which was related to the regulation of nitric oxide signaling pathway.

Topics: Animals; Apoptosis; Calcium; Cell Hypoxia; Cells, Cultured; Cerebral Cortex; Glucose; Neurons; Neuroprotective Agents; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II; Quercetin; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Signal Transduction

To investigate the protective effect of hyperin (Hyp) on focal cerebral ischemia reperfusion injury in rats.. Sixty Wistar male rats were randomly divided into sham-operated group, untreated group, and high-, medium- and low-dose Hyp-treated groups (50, 25 and 12.5 mg x kg(-1) x d(-1)) and ginkgo leaf-treated group. The animals were intragastrically administered with drugs for 5 days. Thirty minutes after the end administration, the operation was performed to induce the middle cerebral artery occlusion (MCAO) model in rats with the method of intraluminal thread. The middle cerebral artery blood flow was blocked for 2 hours, and then reperfused. Twenty-four hours later, the rats' neurology score was observed. Brain triphenyltetrazolium chloride (TTC) staining and dried wet method were carried out to measure the infarct size and the water content of rat brain tissue respectively.. The above-mentioned indexes in the untreated group showed significant differences compared with those in the sham-operated group (P<0.01).The infarct sizes of rat brain tissue in the high- and medium-dose Hyp-treated groups were obviously decreased compared with that in the untreated group (P<0.01, P<0.05). The water content of rat brain and the neurology score were also obviously reduced compared with those in the untreated group (P<0.05 or P<0.01).. Hyp could obviously reduce the brain infarct size and cerebral edema degree in focal cerebral ischemia reperfusion injury rats. Hyp has significant protective effect on focal cerebral ischemia reperfusion injury.

Topics: Animals; Brain; Cerebral Infarction; Male; Neuroprotective Agents; Phytotherapy; Quercetin; Random Allocation; Rats; Rats, Wistar; Reperfusion Injury

The protective effect of hyperin (Hyp) against cerebral ischemia-reperfusion injury was studied. On the cerebral ischemia-reperfusion model in mice, Hyp (50, 100 mg.kg-1, i.p.) was shown to markedly and dose-dependently inhibit the decrease of lactate dehydrogenase (LDH) in cerebrum and improve the learning and memory impairment on the step down test. On the four-vessel occlusion model in rats, Hyp(50 and 100 mg.kg-1, i.p.) significantly reduced the decreases of glutathione peroxidase(GSH-Px), superoxide dismutase(SOD) and LDH activities in the cerebrum. Hyp was also shown to inhibit the increase of nitric oxide (NO) and malondialdehyde (MDA) contents in the cerebrum and promote the recovery of EEG activities. These results suggest that Hyp has protective effect against cerebral ischemia-reperfusion injury via attenuating free radical and NO.

Topics: Animals; Brain; Brain Ischemia; Calcium Channel Blockers; Female; L-Lactate Dehydrogenase; Male; Malondialdehyde; Mice; Nitric Oxide; Quercetin; Rats; Rats, Sprague-Dawley; Reperfusion Injury