Hyperbaric oxygen protects against myocardial ischemia‑reperfusion injury through inhibiting mitochondria dysfunction and autophagy

Abstract

our previous study demonstrated that hyperbaric oxygen (HBo) improves heart function predominantly through reducing oxygen stress, modulating energy metabolism and inhibiting cell apoptosis. The present study aimed to investigate the protective effects of HBo on mitochondrial function and autophagy using rats with a ligated left anterior descending artery. The cardioprotective effects of HBo were mainly evaluated using ELISA, fluorescent probes, transmission electron microscopy and reverse transcription-quantitative Pcr (rT-qPcr). HBo pretreatment for 14 days (once a day) using a 0.25 MPa chamber improved mitochondrial morphology and decreased the number of autophagic vesicles, as observed using a transmission electron microscope. HBO pretreatment significantly increased the levels of aTP, adP, energy charge and the opening of the mitochondrial permeability transition pore, but decreased the levels of aMP, cytochrome c and reactive oxygen species. Moreover, HBo pretreatment significantly increased the gene or protein expression levels of eiF4e-binding protein 1, mammalian target of rapamycin (mTor), mitochondrial dna, nadH dehydrogenase subunit 1, mitofusin 1 and mitofusin 2, whereas it decreased the gene or protein expression levels of autophagy-related 5 (atg5), cytochrome c, dynamin-related protein 1 and p53, as determined using rT-qPcr or immunohistochemistry. in conclusion, HBo treatment was observed to protect cardiomyocytes during myocardial ischemia-reperfusion injury (Miri) by preventing mitochondrial dysfunction and inhibiting autophagy. Thus, these results provide novel evidence to support the use of HBo as a potential agent for the mitigation of Miri.

High Throughput Proteomic Exploration of Hypothermic Preservation Reveals Active Processes within the Cell Associated with Cold Ischemia Kinetic

“…Moreover, the well-described association between these pathways and cell death pathways (apoptosis, necrosis) as well as the activation of the immune system [ 61 ] provides increased quality to the description of ischemia-reperfusion injury, a key issue in transplantation as well as other pathologies. Among these pathways, recent work highlights the interplay between NADP and mTOR in survival and protection against ischemia-reperfusion [ 62 , 63 ] as well as the benefits of NADPH supplementation [ 64 ]; this is concordant with our results regarding the NADP pathways and the role of TKT. Moreover, we demonstrate that RhoGTPases are impacted, a pathway recently highlighted to play a critical role in kidney disease, notably podocytopathy [ 65 ].…”

Xihuang Pill inhibits the development of DMBA combined estrogen and progesterone induced breast precancerous lesions rats by PI3K/AKT/mTOR signaling pathway

“…In invasive tumor tissues, the gene expression was decreased, and the transcription level of TSC2 in normal tissues was apparently higher than that in tumor. the activation of mTOR promotes the phosphorylation of its downstream effectors, including phosphorylation of eIF4E binding protein 1 (4EBP1) and activation of p70 ribosomal S6 protein kinase (p70S6K), which phosphorylates S6 ribosomal protein, hus inducing cell proliferation, angiogenesis and metastasis [30]. Studies have shown that when eIF4E increases, the protein expression of VEGF also increases accordingly.…”

Xihuang Pill Inhibits The Development of DMBA Combined With Oestrogen- And Progesterone-Induced Precancerous Breast lesions In Rats By The PI3K/AKT/mTOR Signaling Pathway

“…In invasive tumour tissues, the gene expression was decreased, and the transcription level of TSC2 in normal tissues was apparently higher than the transcription level of TSC2 in tumours. Activation of mTOR promotes the phosphorylation of its downstream effectors, including phosphorylation of eIF4E binding protein 1 (4EBP1) and activation of p70 ribosomal S6 protein kinase (p70S6K), which phosphorylates S6 ribosomal protein and induces cell proliferation, angiogenesis and metastasis [30]. Studies have shown that when eIF4E increases, the protein expression of VEGF also increases accordingly.…”