Maresin1 alleviates neuroinflammation by inhibiting caspase-3/ GSDME-mediated pyroptosis in mice cerebral ischemia-reperfusion model.

Objective: To explore the mechanism of Maresin1 in reducing cerebral ischemia-reperfusion injury.

Materials And Methods: Male C57BL/6 mice were randomly divided (n = 5 in each group), and focal middle cerebral artery occlusion (MCAO) model was used to simulate cerebral ischemia/reperfusion injury. TTC and the Longa score were used to detect the degree of neurological deficits.

Maresin1 alleviates liver ischemia/reperfusion injury by reducing liver macrophage pyroptosis.

Background: Cell pyroptosis has a strong proinflammatory effect, but it is unclear whether pyroptosis of liver macrophages exacerbates liver tissue damage during liver ischemia‒reperfusion (I/R) injury. Maresin1 (MaR1) has a strong anti-inflammatory effect, and whether it can suppress liver macrophage pyroptosis needs further study.

Methods: This study aimed to investigate whether MaR1 can alleviate liver I/R injury by inhibiting macrophage pyroptosis.

CXCR3 alleviates renal ischemia‑reperfusion injury via increase of Tregs.

Increasing evidence has demonstrated that regulatory T cells (Tregs) suppress innate immunity, as well as protect the kidneys from ischemia‑reperfusion injury (IRI) and offer a potentially effective strategy to prevent or alleviate renal IRI. The present study explored whether C‑X‑C motif chemokine receptor 3 (CXCR3) alleviated renal IRI by increasing Tregs. Male C57BL/6J mice were divided into sham‑surgery, IRI, CXCR3 overexpression (OE‑CXCR3)+IRI, PC61+IRI and OE‑CXCR3+PC61+IRI groups.

Higd1a Protects Cells from Lipotoxicity under High-Fat Exposure.

Hypoxia-inducible gene domain family member 1A (Higd1a) has recently been reported to protect cells from hypoxia by helping to maintain normal mitochondrial function. The potential induction of Higd1a under high-fat exposure and whether it could protect cells from oxidative stress attracted our attention. Initially, 0.

Maresin 1 attenuates the inflammatory response and mitochondrial damage in mice with cerebral ischemia/reperfusion in a SIRT1-dependent manner.

Maresin 1 (MaR1) confers brain-protective effects against cerebral ischemia/reperfusion (I/R) injury. Activation of silent information regulator 1 (SIRT1) signaling has also been demonstrated to inhibit cerebral I/R injury. We hypothesize that MaR1 may protect against cerebral I/R injury by activating SIRT1 signaling.

DAPK1-ERK signal mediates oxygen glucose deprivation reperfusion induced apoptosis in mouse N2a cells.

Aims: Death-associated protein kinase 1 (DAPK1) is a kinase found to promote neuronal apoptosis induced by ischemia. Extracellular signal-regulated kinase (ERK) was identified as a key molecule in DAPK1 signaling. However, the mechanisms of neuronal ischemia reperfusion injury remain unknown.

MiR-221 mediates the epithelial-mesenchymal transition of hepatocellular carcinoma by targeting AdipoR1.

Recent studies have shown that miRNAs play vital roles in tumorigenesis. However, their effects on the epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma (HCC) need to be better understood. Our present study demonstrates that miR-221, which is overexpressed in HCC tissues, promotes EMT in HCC cell lines by targeting a new gene, AdipoR1.

Carvedilol for portal hypertension in cirrhosis: systematic review with meta-analysis.

Objective: To assess the clinical and haemodynamic effects of carvedilol for patients with cirrhosis and portal hypertension.

Design: A systematic review and meta-analysis.

Data Sources: We searched PubMed, Cochrane library databases, EMBASE and the Science Citation Index Expanded through December 2015.

The pro-resolving lipid mediator Maresin 1 protects against cerebral ischemia/reperfusion injury by attenuating the pro-inflammatory response.

Inflammation plays a crucial role in acute ischemic stroke pathogenesis. Macrophage-derived Maresin 1 (MaR1) is a newly uncovered mediator with potent anti-inflammatory abilities. Here, we investigated the effect of MaR1 on acute inflammation and neuroprotection in a mouse brain ischemia reperfusion (I/R) model.

Resolvin D1 promotes the interleukin-4-induced alternative activation in BV-2 microglial cells.

Background: Microglia play key roles in innate immunity, homeostasis, and neurotropic support in the central nervous system. Similar to macrophages, microglia adopt two different activation phenotypes, the classical and alternative activation. Resolvin D1 (RvD1) is considered to display potent anti-inflammatory and pro-resolving actions in inflammatory models.