Coupling Between Interleukin-1R1 and Necrosome Complex Involves in Hemin-Induced Neuronal Necroptosis After Intracranial Hemorrhage.

Background and Purpose- Accumulated evidence suggests that hemin-a breakdown product of hemoglobin-plays a pivotal role in the inflammatory injuries that result after hemorrhagic stroke through the Toll Like Receptor 2-Toll Like Receptor 4 signal pathway. However, the mechanism of how hemin triggers neuronal necroptosis directly after intracranial hemorrhage (ICH) is still an area of active research. As animal model and preclinical studies have shown, the recombinant interleukin-1 receptor antagonist (IL-1RA) improves clinical outcomes after stroke.

The PXXP domain is critical for the protective effect of BAG3 in cardiomyocytes.

Bcl-2-associated athanogene3(BAG3) protects the heart and cardiomyocytes from ischaemia/reperfusion (I/R) injury. Although the anti-apoptosis effect of BAG3 has been demonstrated in multiple cell types, the structural domain of BAG3, which is responsible for its anti-apoptosis effect, is not well understood. BAG3 protein consists of various characteristic amino acid motifs/regions that permit the interaction of BAG3 with numerous proteins involved in many cellular key pathways.

Endoplasmic Reticulum Stress-Induced NLRP1 Inflammasome Activation Contributes to Myocardial Ischemia/Reperfusion Injury.

Studies have shown that Nod-like receptor protein (NLRP) 3 inflammasome activation contributes to myocardial ischemia/reperfusion (I/R) injury. However, the role and mechanism of NLRP1 inflammasome in myocardial I/R injury remain unknown. Endoplasmic reticulum (ER) stress is involved in the development of myocardial I/R injury.

Inhibition of the ubiquitination of HSF1 by FBXW7 protects the intestine against ischemia-reperfusion injury.

Epithelial apoptosis is an important factor in intestinal ischemia-reperfusion (I/R) injury. Heat shock factor 1 (HSF1) is a classical stress response factor that directly regulates the transcription of heat shock proteins (HSPs) under stress conditions. Although HSPs are involved in protecting the intestine against I/R, the mechanism whereby HSF1 is regulated in I/R is poorly understood.

Melatonin Protects Against Hypoxia/Reoxygenation-Induced Dysfunction of Human Umbilical Vein Endothelial Cells Through Inhibiting Reactive Oxygen Species Generation.

Background: Hypoxia/reoxygenation (H/R) in human umbilical vein endothelial cells (HUVECs) induces oxidative stress and eventually leads to vascular injury.

Objective: The aim of this study was to examine the effect of melatonin on HUVECs injured by H/R and explore the underlying mechanisms.

Materials And Methods: A model of HUVECs under hypoxia/reoxygenation was established.

Autophagy Induction Ameliorates Inflammatory Responses in Intestinal Ischemia-Reperfusion Through Inhibiting NLRP3 Inflammasome Activation.

Intestinal ischemia/reperfusion (I/R)-induced systemic inflammation leads to multiple organ dysfunction syndrome. Previous studies have indicated that the NOD-like receptor protein (NLRP)3 inflammasome modulates intestinal inflammation; however, the pathophysiological mechanisms remain unclear. Autophagy is a critical metabolic mechanism that promotes cellular survival following ischemic injury.

microRNA-423-3p exosomes derived from cardiac fibroblasts mediates the cardioprotective effects of ischaemic post-conditioning.

Aims: A recent study reported the cardioprotective effects mediated by cardiac fibroblasts (CFs) during acute phase of ischaemia-reperfusion injury (IRI). Little is known about whether exosomes/microvesicles mediate this beneficial effect and whether ischaemia post-conditioning (Postcon) can regulate this process. Here, we aimed to investigate the cardioprotective effect of CFs-exosomes/microvesicles and whether Postcon can regulate this effect.

LAMA5 promotes human umbilical vein endothelial cells migration, proliferation, and angiogenesis and is decreased in preeclampsia.

Preeclampsia (PE) is currently thought to associated with oxidative stress and vascular endothelial dysfunction. LAMA5 is associated with the cell migration, proliferation, and vascular endothelial function. The aims of this study are to investigate the expression patterns of LAMA5 in normal and PE pregnancies, as well as evaluating the effects of LAMA5 on human umbilical vein endothelial cells (HUVECs) function.

[Role of poly(ADP-ribose) polymerases-1-mediated blockade of autophagy in ischemia/reperfusion injury of rat cardiomyocytes].

Objective: To investigate the role of poly(ADP-ribose) polymerases-1 (PARP-1)-mediated blockade of autophagic flow in myocardial ischemia-reperfusion injury.

Methods: H9c2 cells, a rat cardiac myocyte line, were divided into control group, hypoxia/ reoxygenation model group (H/R group), PARP-1 inhibitor (PJ34) group, and PJ34 + H/R group. The total protein was extracted from the cells in each group to detect the expressions of pADPr, Bax, the DNA damage marker protein p-YH2ax, and autophagic flow-associated proteins LC3BⅡ/LC3Ⅰ, Beclin-1, and P62 using Western blotting.

Protective effects of the AKT activator SC79 on renal ischemia-reperfusion injury.

Background And Aims: SC79, an AKT activator, has been reported to protect experimental ischemia-elicited neuronal death, brain injury, and myocardiocyte hypoxia/reoxygenation (H/R) injury. However, the protection of SC79 from renal ischemia-reperfusion (I/R) injury and the precise mechanisms involved are unknown. Here, we investigated the effects of SC79 in renal tubular epithelial cells and in mouse kidney following hypoxia-reoxygenation (H/R) and renal I/R injury.

Platycodin D inhibits oxidative stress and apoptosis in H9c2 cardiomyocytes following hypoxia/reoxygenation injury.

Myocardial ischemia/reperfusion (I/R) injury is a complex pathophysiological process related to the occurrence of myocardial infarction (MI). Oxidative stress is known to play a crucial role in the pathogenesis of I/R injury. Platycodin D (PD) is an active natural saponin that possesses strong anti-oxidant activity.

Effect of long non-coding RNA growth arrest-specific 5 on apoptosis in renal ischaemia/reperfusion injury.

Aim: Long non-coding RNA (lncRNAs) have been shown to play a critical role in a variety of pathophysiological processes, such as cell proliferation, apoptosis and migration. However, there were few studies addressing the function of lncRNAs in renal ischaemia/reperfusion (I/R) injury. Apoptosis is an important pathogenesis during I/R injury.

DHA attenuates hepatic ischemia reperfusion injury by inhibiting pyroptosis and activating PI3K/Akt pathway.

Hepatic ischemia reperfusion (I/R) injury is very common in liver transplantation and major liver surgeries and may cause liver failure or even death. Docosahexaenoic acid (DHA) has displayed activities in reducing oxidative stress and inflammatory reaction in many disorders. In the present study, we investigated the protective effects of DHA against I/R-induced injury and the underlying mechanisms.

Overexpression of FGF19 alleviates hypoxia/reoxygenation-induced injury of cardiomyocytes by regulating GSK-3β/Nrf2/ARE signaling.

Fibroblast growth factor 19 (FGF19) has emerged as a crucial cytoprotective regulator that antagonizes cell apoptosis and oxidative stress under adverse conditions. However, whether FGF19 plays a cytoprotective role in preventing myocardial damage during myocardial ischemia/reperfusion injury remains unknown. In this study, we aimed to investigate the potential role of FGF19 in regulating hypoxia/reoxygenation (H/R)-induced injury of cardiomyocytes in vitro.

[The protective effects of Astragaloside Ⅳ on diastolic function of rat thoracic aortic rings impaired by microvesicles].

Objectives: To investigate the effects of Astragaloside IV (AST) on diastolic function of rat thoracic aorta rings which was injured by microvesicles derived from hypoxia/reoxygenation (H/R)-treated human umbilical vein endothelial cells (HUVECs), and the mechanism of AST.

Methods: H/R-induced endothelial microvesicles (H/R-EMVs) were generated from cultured HUVECs under the condition of hypoxia for 12 hour/Reoxygenation for 4 hour, H/R-EMVs were stored in D-Hank's solution. Male Wistar rats were underwent thoracotomy, the thoracic aorta with intact endothelium were carefully removed and cut into 3~4 mm rings.

Protective effect of hydroxysafflor yellow A against acute kidney injury via the TLR4/NF-κB signaling pathway.

This study aimed to evaluate the protective effect of hydroxysafflor yellow A (HSYA) on ischemia/reperfusion (I/R)-induced acute kidney injury via the TLR4/NF-κB pathway, both in vitro and in vivo. Rats were subjected to removal of the right kidney and I/R injury to the left kidney. Rats subjected to renal I/R injury were treated with HSYA at 0.

Hydrogen protects lung from hypoxia/re-oxygenation injury by reducing hydroxyl radical production and inhibiting inflammatory responses.

Here we investigated whether hydrogen can protect the lung from chronic injury induced by hypoxia/re-oxygenation (H/R). We developed a mouse model in which H/R exposure triggered clinically typical lung injury, involving increased alveolar wall thickening, infiltration by neutrophils, consolidation, alveolar hemorrhage, increased levels of inflammatory factors and recruitment of M1 macrophages. All these processes were attenuated in the presence of H.

Remifentanil Induces Cardio Protection Against Ischemia/Reperfusion Injury by Inhibiting Endoplasmic Reticulum Stress Through the Maintenance of Zinc Homeostasis.

Background: Although it is well known that remifentanil (Rem) elicits cardiac protection against ischemia/reperfusion (I/R) injury, the underlying mechanism remains unclear. This study tested if Rem can protect the heart from I/R injury by inhibiting endoplasmic reticulum (ER) stress through the maintenance of zinc (Zn) homeostasis.

Methods: Isolated rat hearts were subjected to 30 minutes of regional ischemia followed by 2 hours of reperfusion.

Polyacetylene glycoside attenuates ischemic kidney injury by co-inhibiting inflammation, mitochondria dysfunction and lipotoxicity.

Aims: Ischemic acute kidney injury (AKI) is a serious clinical problem and no efficient therapeutics is available in clinic now. Natural polyacetylene glycosides (PGAs) had shown antioxidant and anti-inflammatory properties, but their effects on kidney injury have not been evaluated. This study aimed to investigate the protective effect of PGA on ischemic kidney injury in renal tubular epithelial cells (TECs) and mice.

Isorhamnetin protects against hypoxia/reoxygenation-induced injure by attenuating apoptosis and oxidative stress in H9c2 cardiomyocytes.

To unveil the possible protective role of isorhamnetin, an immediate 3'-O-methylated metabolite of quercetin, in cardiomyocyte under hypoxia/reoxygenation (H/R) condition and the underlying mechanisms involved, H9c2 cardiomyocytes were exposed to the vehicle or H/R for 6 h (2 h of hypoxia following by 4 h of reoxygenation) with isorhamnetin (0, 3, 6, 12, 25, 50 μM for 4 h prior to H/R exposure). Apoptosis was evaluated by TUNEL staining, flow cytometry analysis and western blot assay for cleaved caspase-3. Myocardial injure in vivo was determined by infarct size using TTC staining, histological damage using H&E staining and myocardial apoptosis.

Genetic Lineage Tracing of Nonmyocyte Population by Dual Recombinases.

Background: Whether the adult mammalian heart harbors cardiac stem cells for regeneration of cardiomyocytes is an important yet contentious topic in the field of cardiovascular regeneration. The putative myocyte stem cell populations recognized without specific cell markers, such as the cardiosphere-derived cells, or with markers such as Sca1, Bmi1, Isl1, or Abcg2 cardiac stem cells have been reported. Moreover, it remains unclear whether putative cardiac stem cells with unknown or unidentified markers exist and give rise to de novo cardiomyocytes in the adult heart.

Tenecteplase versus Alteplase before Thrombectomy for Ischemic Stroke.

Background: Intravenous infusion of alteplase is used for thrombolysis before endovascular thrombectomy for ischemic stroke. Tenecteplase, which is more fibrin-specific and has longer activity than alteplase, is given as a bolus and may increase the incidence of vascular reperfusion.

Methods: We randomly assigned patients with ischemic stroke who had occlusion of the internal carotid, basilar, or middle cerebral artery and who were eligible to undergo thrombectomy to receive tenecteplase (at a dose of 0.

Alda-1, an ALDH2 activator, protects against hepatic ischemia/reperfusion injury in rats via inhibition of oxidative stress.

Previous studies have proved that activation of aldehyde dehydrogenase two (ALDH2) can attenuate oxidative stress through clearance of cytotoxic aldehydes, and can protect against cardiac, cerebral, and lung ischemia/reperfusion (I/R) injuries. In this study, we investigated the effects of the ALDH2 activator Alda-1 on hepatic I/R injury. Partial warm ischemia was performed in the left and middle hepatic lobes of Sprague-Dawley rats for 1 h, followed by 6 h of reperfusion.

PEDF improves cardiac function in rats subjected to myocardial ischemia/reperfusion injury by inhibiting ROS generation via PEDF‑R.

The prevention and management of myocardial ischemia/reperfusion (MI/R) injury is an essential part of coronary heart disease surgery and is becoming a major clinical problem in the treatment of ischemic heart disease. Previous studies by our group have demonstrated that pigment epithelium‑derived factor (PEDF) improves cardiac function in rats with acute myocardial infarction and reduces hypoxia‑induced cell injury. However, the protective function and mechanisms underlying the effect of PEDF in MI/R injury remain to be fully understood.