Epoxyeicosatrienoic acid ameliorates cerebral ischemia-reperfusion injury by inhibiting inflammatory factors and pannexin-1

Abstract

Epoxyeicosatrienoic acid (EET) has wide applications due to the unique biological effects of anti‑hyperlipidemia, inhibition of platelet aggregation, anti‑inflammation, anti‑cancer, anti‑lipid oxidation and the promotion of brain tissue development. The present study investigated whether EET ameliorates cerebral ischemia‑reperfusion injury (CIRI) by inhibiting inflammatory factors and pannexin. Specific pathogen‑free 7‑week‑old male Sprague‑Dawley rats were randomly divided into three groups: Sham, CIRI and EET. Neurological deficit scores, cerebral infarct volume and cerebral edema were assessed in CIRI rats. Enzyme‑linked immunosorbent assays were performed to detect tumor necrosis factor‑α, interleukin‑6, nuclear factor‑κB and inducible nitric oxide synthase (iNOS) levels, and western blot analysis was performed also used to assess cleaved caspase‑3, phospholipase A2 (PLA2), cyclooxygenase‑2 and prostaglandin E2 (PGE2) protein expression levels. EET ameliorated cerebral injury and CIRI‑induced cleaved caspase‑3 protein expression levels in rats. EET additionally suppressed CIRI‑induced inflammation reactions and iNOS protein expression in rats. Furthermore, the protein expression levels of PLA2, PGE2 and pannexin‑1 in CIRI rats were inhibited by treatment with EET. These results indicated that EET reduces CIRI by inhibiting inflammation and levels of cleaved caspase‑3, PLA2, PGE2 and pannexin-1.

Overexpression of microRNA-202-3p in bone marrow mesenchymal stem cells improves cerebral ischemia-reperfusion injury by promoting angiogenesis and inhibiting inflammation

“…CIRI can activate the NF-κB pathway and promote large-scale expression of various inflammatory factors (IFs), such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Studies also found that there are some important transcription factor binding sites in the IL-10 promoter region, such as those for NF-κB, c-Jun [ 14 , 15 ].…”

Inhibition of soluble epoxide hydrolase induces POTCs to enhance the dentin-pulp complex regeneration mediated by crosstalk between vascular endothelial cells and dental pulp stem cells

“…Increasing EETs levels through genetic modi cation signi cantly increased the number of microvessels in liver and lung tissues [29]. EETs effectively ameliorate cerebral ischemia by increasing the microcirculation of brain tissue and improving the nutritional supply of brain nerves [30,31]. Our in vitro experiments indicated that TPPU enhanced the migration and tubule formation potentials of cocultured DPSCs and ECs.…”

Reduced Levels of A20 Protein Prompted RIPK1-Dependent Apoptosis of Vascular Endothelial Cells and Blood–Brain Barrier Breakdown in CIRI

“…The apoptosis marker cleaved caspase 3 (CC3) was employed in this study to evaluate the effect of RDA on BBB destruction during the progression of ischemia-reperfusion injury (Liu Z et al 2017;Liu C et al 2018). Immunoblotting data showed that an inactive mutant form of RIPK1 (Ripk1 D138N ) inhibited the initiation of RDA in mice after MCAO treatment; however, the RDA features remained intact in the Ripk3 −/− mice (Fig.…”