Necroptosis was found in a rat ischemia/reperfusion injury flap model

Abstract

Background: Necroptosis is a new form of cell death that has been identified as a third pathway causing cell death. In this study, necrostatin-1 (Nec-1) was used to determine whether necroptosis exists in a rat ischaemia/reperfusion injury flap model. Methods: In this study, twenty male Sprague-Dawley rats were divided randomly into two groups: a control group (CTL group) and a Nec-1 group. Each abdominal skin flap underwent 3 h of ischaemia and then reperfusion. Fifteen minutes before and after reperfusion, phosphate buffer saline (PBS) was administered intraperitoneally to the CTL group, while Nec-1 was administered intraperitoneally to the Nec-1 group. Twenty-four hours after reperfusion, the whole flap was divided equally into 54 sections. Flap blood perfusion was measured. One sample was taken randomly from each row. Morphological changes, apoptosis, receptor-interacting protein-1 (RIP-1) expression and caspase-3 activity were observed and detected. The measurements between the two groups were compared with the independent t -test, and a P value of <0.05 was considered statistically significant. Results: Compared to flaps in the CTL group, flaps in the Nec-1 group showed longer survival rates, better blood perfusion and less inflammatory infiltration. The total flap area considered to have survived was 70.88 ± 10.28% in the CTL group, whereas 80.56 ± 5.40% of the area was found to be living in the Nec-1 group (Nec-1 vs. CTL, t = –2.624, P < 0.05). For some rows, there were significant differences in cell apoptosis between the two groups, the apoptosis index (AI) in rows “9 cm”, “7 cm”, “6 cm” and “5 cm” was significantly lower in the Nec-1 group than that in the CTL group (Nec-1 vs. CTL, P < 0.05). RIP-1 expression was much lower in the Nec-1 group than that in the CTL group in rows “5 cm” to “9 cm” (Nec-1 vs. CTL, P < 0.05). No significant differences in caspase-3 activity were found. Conclusion: According to the results, necroptosis was present in a rat abdominal ischaemia/reperfusion injury flap model.

Cyclic helix B peptide promotes random‐pattern skin flap survival via TFE3‐mediated enhancement of autophagy and reduction of ROS levels

“…This newly identified programmed necrosis is called ‘necroptosis’ (Vandenabeele et al, 2010). Furthermore, some studies have detected necroptosis in the skin flaps in agreement with the data of RNA sequencing analysis obtained in the present study (Geng et al, 2020; Liu, Zhang, Dong, et al, 2019; Liu, Zhang, Liu, et al, 2019). Thus, we measured the levels of necroptosis by western blotting, immunohistochemistry and immunofluorescence.…”

CircANXA2 Promotes Myocardial Apoptosis in Myocardial Ischemia-Reperfusion Injury via Inhibiting miRNA-133 Expression

“…Various revascularization methods can alleviate myocardial injury and necrosis caused by ischemia by restoring myocardial perfusion in time and effectively. However, restoration of blood reperfusion after myocardial ischemia can itself further lead to myocardial cell damage and even necrosis, a phenomenon known as myocardial ischemia-reperfusion injury [ 14 – 18 ]. However, up to now, there is still no effective clinical treatment method to avoid myocardial ischemia-reperfusion injury, which seriously restricts the therapeutic effect of coronary heart disease.…”

Extracellular vesicles from hypoxia-pretreated adipose-derived stem cells regulate hypoxia/reoxygenation-induced human dermal microvascular endothelial apoptosis and autophagy in vitro

“…And the death of HDMECs is an important feature of reperfusion injury of free skin flap transplantation. At the reperfusion stage, high levels of ROS, endothelium-derived relaxing factor, and pro-inflammatory cytokines such as tumor necrosis factor α and interleukin-1 are released from ischemic tissues [ 25 ], resulting in leukocyte infiltration, interstitial edema, apoptosis and autophagy [ 26 ]. Reperfusion can also cause mitochondrial respiratory chain dysfunction by damaging complexes I, II and IV, resulting in mitochondrial membrane depolarization and mitochondrial outer membrane rupture, leading to the release of cytochrome C into the cytoplasm and activation of the autophagy and apoptosis pathway.…”