Down-Regulation of Long Non-Coding RNA AK139328 Reduces Cell Inflammation and Apoptosis in Cerebral Ischemia Reperfusion Injury

Cerebral ischemia-reperfusion injury (CIRI) refers to the phenomenon that the ischemic injury of brain leads to the injury of brain cells, and ischemic injury is further aggravated after the recovery of blood reperfusion. In this study, we first constructed Oxygen and glucose deprivation/reoxygenation (OGD/R) injury model of PC12 cells, we found that the expression of LncRNA AK139328 in model cells was significantly increased through RT-qPCR. Subsequently, we interfered LncRNA AK139328 in model cells by plasmid transfection and found that interfering LncRNA AK139328 could significantly reduce the expression of inflammatory factors, including TNF a, IL-1β, IL-6, McP-1, and oxidative stress-related factors, including ROS, MDA, LDH, while the expressions of SOD and GSHPx were significantly increased. Flow cytometry was used to detect cell apoptosis, and apoptosisrelated proteins bcl-2, Bax, cleaved-caspase3 and cleaved PARP-1 were detected by western blot. Results show that interfering LncRNA AK139328 could reduce the apoptosis rate of OGD/R cells and the expression of Bax, cleaved caspase3 and cleaved PARP-1, while increasing the expression of bcl-2. Meanwhile, we found that after interfering LncRNA AK139328, the expressions of Nrf2, HO-1, NQO-1 and phosphorylated-P65 increased, while P65 showed no significant changes. This may be related to Nrf2/HO-1 and NF-κB signaling pathways. In a word, our study showed that interfering with LncRNA AK139328 can reduce cell inflammation and apoptosis in CIRI.

Etomidate Alleviates Ischemia-Anoxia Reperfusion Injury in Intestinal Epithelial Cells by Inhibiting the Activation of traf6-Regulated NF-KB Signaling

Objective: The present study aimed to investigate the role of etomidate in intestinal cell ischemia and hypoxia-reperfusion injury and potential mechanisms. Method: In this study, we establish the intestinal epithelial cells ischemia-reperfusion model in vitro. CCK8 was used to detect cell viability and flow cytometry assay was used to detect apoptosis levels of treated OGD/R model cells. ELISA measured the expression level of oxidative stress factors and inflammatory factors. Furthermore, western blot assay was used to detect the expression the apoptosis-related factors and TNFR-associated factors in treated OGD/R model cells. Result: Etomidate does not affect the activity of intestinal epithelial cells, and can protect intestinal epithelial cells to reduce ischemiareperfusion injury, and the expression of inflammatory factors and oxidative stress in cells with mild intestinal epithelial ischemia-reperfusion injury. Etomidate alleviates apoptosis of intestinal epithelial ischemia-reperfusion injury cells. Etomidate inhibits the activation of traf6-mediated NF-κB signal during ischemia-anoxia reperfusion of intestinal epithelial cells. Conclusion: Taken together, our study demonstrated that etomidate attenuates inflammatory response and apoptosis in intestinal epithelial cells during ischemic hypoxia-reperfusion injury and inhibits activation of NF-κB signaling regulated by TRAF6.

Recent Advance on Drug Therapy Related to Myocardial Ischemia Reperfusion Injury

Myocardial ischemia reperfusion injury (MIRI) means complete or partial artery obstruction of coronary artery, and ischemic myocardium will be recirculating in a period of time. Although the ischemic myocardium can be restored to normal perfusion, its tissue damage will instead be progressive. An aggravated pathological process. MIRI is a complex entity where many inflammatory mediators play different roles, both to enhance myocardial infarction-derived damage and to heal injury. Therefore, the research and development of drugs for the prevention and treatment of this period has also become the focus. This article first studied pathophysiology of MIRI, and reviewed the research progress of MIRI-related drugs. Research results show that: MIRI is inevitable for myocardial ischemia, with the possible to double damage via the ischemic condition. Therefore, it is a serious complication and one of the most popular diseases in the world. It has always been difficult to find an effective treatment for this disease, because it is difficult to explore the inflammation behind its pathophysiology.

Effect of different storage solutions on oxidative stress in human saphenous vein grafts

Background Ischemia–reperfusion injury of saphenous vein grafts (SVG) during coronary artery bypass grafting surgery negatively impacts endothelial integrity and functionality and is associated with vein graft failure. The aim of this study was to evaluate the level of oxidative stress in human SVG segments following ischemic storage in three intraoperative graft storage solutions: saline (S), autologous heparinized blood (HB) and DuraGraft (DG). Methods 3 mm tissue rings derived from surplus SVG segments from 50 patients were stored at room temperature for 30 min in DG, S or HB. Total oxidative status (TOS) and total antioxidant status (TAS) levels were determined from which the oxidative stress index (OSI: TOS/TAS ratio) was calculated. A p-value < 0.017 was considered significant implementing a Bonferroni correction. Results TOS values were significantly lower for DG stored samples in comparison to both S and HB; there was no difference between S and HB (DG: 32.6 ± 1.8, S: 39.6 ± 2.8 and HB: 40.6 ± 2.4 µmol H2O2 eqv.; DG vs. S and DG vs. HB p < 0.0001, S vs. HB p = 0.047). TAS was higher for both DG and HB in comparison to S (DG: 8.9 ± 0.9, S: 6.9 ± 1.0 and HB: 8.6 ± 0.9 mmol Trolox eqv.; DG vs S p < 0.0001, DG vs. HB p = 0.263, S vs. HB p < 0.0001). OSI differed between all groups with the lowest value for DG (DG: 3.7 ± 0.2, S: 5.8 ± 0.4 and HB: 4.7 ± 0.2 µmol H2O2 eqv./mmol Trolox eqv.; all p < 0.0001). Conclusions Saphenous veins grafts stored in DuraGraft had a lower oxidative level, higher antioxidant level and a lower oxidative stress index in comparison to saphenous vein grafts stored in saline or heparinized blood. ClinicalTrials.gov Identifier NCT02922088.

Pathophysiology, Diagnosis, and Management of Coronary No-Reflow Phenomenon

Coronary no-reflow phenomenon is a lethal mechanism of ongoing myocardial injury following successful revascularization of an infarct-related coronary artery. Incidence of this phenomenon is high following percutaneous intervention and is associated with adverse in-hospital and long-term outcomes. Several mechanisms such as ischemia-reperfusion injury and distal microthromboembolism in genetically susceptible patients and those with preexisting endothelial dysfunction have been implicated. However, the exact mechanism in humans is still poorly understood. Several investigative and treatment strategies within and outside the cardiac catheterization laboratory have been proposed, but they have not uniformly shown success in reducing mortality or in preventing adverse left ventricular remodeling resulting from this condition. The aim of this article is to provide a brief and concise review of the current understanding of the pathophysiology, clinical predictors, and investigations and management of coronary no-reflow phenomenon.