polydatin/blödning

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Polydatin, a natural polyphenol, protects arterial smooth muscle cells against mitochondrial dysfunction and lysosomal destabilization following hemorrhagic shock.

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The main objective of this study was to investigate the activity of polydatin on mitochondrial dysfunction and lysosomal stability of arteriolar smooth muscle cells (ASMCs) in severe shock. The experimental animals (rats) were divided into five groups: control, hemorrhagic shock, shock + CsA, shock

Hypotensive resuscitation combined with polydatin improve microcirculation and survival in a rabbit model of uncontrolled hemorrhagic shock in pregnancy.

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BACKGROUND Obstetric hemorrhage remains a leading cause of maternal death internationally. Polydatin is an effective drug in ameliorating microcirculatory insufficiency and increasing survival rate in non-pregnant animal model of controlled hemorrhagic shock. In the present study, we investigated

Polydatin Alleviates Small Intestine Injury during Hemorrhagic Shock as a SIRT1 Activator.

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OBJECTIVE To evaluate the role of SIRT1 in small intestine damage following severe hemorrhagic shock and to investigate whether polydatin (PD) can activate SIRT1 in shock treatment. METHODS The severe hemorrhagic shock model was reproduced in Sprague Dawley rats. METHODS Two hours after drug

Polydatin ameliorates injury to the small intestine induced by hemorrhagic shock via SIRT3 activation-mediated mitochondrial protection.

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Previously, we demonstrated that sirtuin (SIRT)1 plays vital roles in the small intestine (SI), protecting against severe hemorrhagic shock (HS), and that polydatin (PD) can attenuate SI injury via SIRT1 activation. To explore the role of SIRT3 and mitochondria in SI injury after HS, and explore

Polydatin Protecting Kidneys against Hemorrhagic Shock-Induced Mitochondrial Dysfunction via SIRT1 Activation and p53 Deacetylation.

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OBJECTIVE To ascertain if mitochondrial dysfunction (MD) of kidney cells is present in severe hemorrhagic shock and to investigate whether polydatin (PD) can attenuate MD and its protective mechanisms. METHODS Renal tubular epithelial cells (RTECs) from rat kidneys experiencing HS and a cell line

[Effect of polydatin on dynamic changes of excitatory amino acids in cerebrospinal fluid of cerebral hemorrhage rats].

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OBJECTIVE To observe the effects of polydatin on dynamic changes of excitatory amino acids in cerebrospinal fluid and water content of brain tissue of cerebral hemorrhage rats. And to discuss the therapeutic action and mechanisms of polydatin on brain hemorrhagic injured rats. METHODS A quantitative

Effect of Polydatin on Neurological Function and the Nrf2 Pathway during Intracerebral Hemorrhage.

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This study investigates the effect of polydatin on the neurological function of cerebral hemorrhage rats and on the Nrf2 pathway of the endogenous antioxidant system in tissues around cerebral hematoma. Further, the study also aims to provide solid insights for clinical diagnosis and treatment. A

Polydatin--a new mitochondria protector for acute severe hemorrhagic shock treatment.

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OBJECTIVE The aim of the study was find out whether neuronal mitochondrial injury does take place in severe shock and to explore effective therapy for severe shock. METHODS Rats were divided in the following group: sham, shock + normal saline (NS), shock + cyclosporine A (CsA), shock + resveratrol

Polydatin protects hepatocytes against mitochondrial injury in acute severe hemorrhagic shock via SIRT1-SOD2 pathway.

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OBJECTIVE The aim of the study was to determine whether hepatocyte mitochondrial injury instigates severe shock and to explore effective therapy. METHODS Wistar rats were randomly divided into five groups: Control (sham) group, shock + normal saline, shock + cyclosporine A, shock + resveratrol (Res)

Evidence for SIRT1 Mediated HMGB1 Release From Kidney Cells in the Early Stages of Hemorrhagic Shock.

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This study is to explore the effect of SIRT1 deacetylating inactivation on organ-derived high mobility group box 1 (HMGB1) during the development of severe hemorrhagic shock (HS).Hemorrhagic shock model was reproduced in rats by blood shedding and mimicked

Neuroprotective effects of polydatin against mitochondrial-dependent apoptosis in the rat cerebral cortex following ischemia/reperfusion injury.

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The neuroprotective effect of polydatin (PD) against hemorrhagic shock-induced mitochondrial injury has been described previously, and mitochondrial dysfunction and apoptosis were reportedly involved in ischemic stroke. In the present study the neuroprotective effect of PD in preventing apoptosis

Polydatin: a new therapeutic agent against multiorgan dysfunction.

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BACKGROUND Polydatin (PD), a monocrystalline and polyphenolic drug isolated from a traditional Chinese herb (Polygonum cuspidatum), is protective against mitochondrial dysfunction and has been approved for clinical trials in the treatment of shock. However, whether the administration of PD has a

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