Hyperbaric oxygen protects against myocardial reperfusion injury via the inhibition of inflammation and the modulation of autophagy

Chen, Chunxia; Chen, Wan; Li, Yaoxuan; Dong, Yanling; Xiaoming, Teng; Nong, Zhihuan; Pan, Xiaorong; Lv, Liwen; Gao, Ying; Wu, Guangwei

doi:10.18632/oncotarget.22869

Cited by 17 publications

(10 citation statements)

References 56 publications

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“…Consistently, a recent study has shown that HBOT (2ATA, 60 minutes, once daily for 5 days) significantly increased autophagic flux as indicated by increased LC3-II and decreased p62 via inhibiting the mechanistic target of the rapamycin (mTOR) pathway in rats with spinal nerve ligation (SNL) compared to sham-SNL rats [ 30 ]. Contrary to our findings, HBOT preconditioning (2.5ATA, 1hr, one time per day for 14days) could reduce Beclin-1 and increased mTOR expression resulting in the inhibition of exaggerated autophagy in rats with myocardial ischemia reperfusion injury [ 31 ]. The discrepancy between a previous study and ours might be owing to the difference between the models (MIRI vs aging rats) and the pressure used for HBOT (2.5ATA vs 2ATA).…”

Section: Discussioncontrasting

confidence: 91%

Hyperbaric oxygen therapy effectively alleviates D-galactose-induced-age-related cardiac dysfunction via attenuating mitochondrial dysfunction in pre-diabetic rats

Bo-Htay

Shwe

Jaiwongkam

et al. 2021

Aging

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Currently, the prevalence of obesity in aging populations is fast growing worldwide. Aging induced by D-galactose (D-gal) is proven to cause the worsening of cardiac dysfunction in pre-diabetic rats via deteriorating cardiac mitochondrial function. Hyperbaric oxygen therapy (HBOT) has been shown to attenuate D-gal-induced cognitive deterioration through decreased inflammation and apoptosis. We tested the hypothesis that HBOT alleviates D-gal induced cardiac dysfunction via improving mitochondrial function in pre-diabetic rats. Wistar rats (n=56) were fed normal diet or high-fat diet for 12 weeks. For subsequent 8 weeks, they were subcutaneously injected either vehicle (0.9% normal saline) or D-gal (150mg/kg/day). Rats were randomly subdivided into 7 groups at week 21: sham-treated (normal diet fed rats with vehicle (NDV), high-fat diet fed rats with vehicle (HFV), normal diet fed rats with D-gal (NDDg), high-fat diet fed rats with D-gal (HFDg)) and HBOT-treated (HFV, NDDg, HFDg). Sham rats received ambient pressure of oxygen while HBOT-treated ones received 100% oxygen given once daily for 60 minutes at 2 atmosphere absolute. HBOT reduced metabolic impairments, mitochondrial dysfunction and increased autophagy, resulting in an improvement of cardiac function in aged pre-diabetic rats.

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Section: Discussioncontrasting

confidence: 91%

Hyperbaric oxygen therapy effectively alleviates D-galactose-induced-age-related cardiac dysfunction via attenuating mitochondrial dysfunction in pre-diabetic rats

Bo-Htay

Shwe

Jaiwongkam

et al. 2021

Aging

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“…Previous studies have shown that TLR4 can activate the NF-κB pathway, and thus result in the secretion of pro-inflammatory cytokines (24,25). In the present study, it was found that the overexpression of miR-93 negatively influenced the expression of TLR4 in LPS-treated chondrocytes.…”

Section: Resultsmentioning

confidence: 99%

MicroRNA‑93 inhibits chondrocyte apoptosis and inflammation in osteoarthritis by targeting the TLR4/NF‑κB signaling pathway

et al. 2018

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Osteoarthritis (OA) is a serious disease of the articular cartilage, and inflammation has been implicated in its pathogenesis. Previously, microRNAs (miRNAs) have been proposed as novel regulators of inflammation, however, the functional role of microRNAs in regulating inflammation in OA remains to be fully elucidated. The aim of the present study was to investigate the roles of miRNAs in OA inflammation and the underlying molecular mechanism. Firstly, the miRNA expression patterns were analyzed in the articular cartilage tissues from experimental OA mice using an miRNA microarray. miRNA (miR)-93 was identified with particular interest due to its reported effects on apoptosis and inflammation suppression. Subsequently, the expression of miR-93 was further validated in the articular cartilage tissues of OA mice and lipopolysaccharide (LPS)-stimulated primary chondrocytes. Using this LPS-induced chondrocyte injury model, the overexpression of miR-93 enhanced cell viability, improved cell apoptosis and attenuated the inflammatory response, as reflected by reductions in pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6. In addition, Toll-like receptor 4 (TLR4), an important regulator of the nuclear factor-κB (NF-κB) signaling pathway, was identified as a direct target of miR-93 in chondrocytes. Furthermore, the restoration of TLR4 markedly abrogated the inhibitory effects of miR-93 on the chondrocyte apoptosis and inflammation induced by LPS. In addition, the overexpression of miR-93 by agomir-miR-93 significantly inhibited the levels of pro-inflammatory cytokines and cell apoptosis, whereas antagomir-93 exacerbated apoptosis and inflammation in vivo. Taken together, the results of the study suggested that miR-93 may be a promising therapeutic target for the treatment of human OA.

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“…Autophagy or 'self-devouring' is the natural, regulated, destructive mechanism of the cell that removes unnecessary or dysfunctional components (41). It is a constitutive housekeeping process involved in the progression of cardiovascular disease (42,43). A number of studies have revealed the role of miRNAs in regulating autophagy in cardiomyocytes (44,45).…”

Section: Discussionmentioning

confidence: 99%

Effects of miR‑103a‑3p on the autophagy and apoptosis of cardiomyocytes by regulating Atg5

Zhang

Wang

et al. 2019

Int J Mol Med

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Autophagy and apoptosis are associated with cardiovascular diseases. Emerging evidence shows that microRNAs (miRs) are critical in the development of pathological processes underlying cardiovascular diseases by regulating the induction of apoptosis and autophagy. The present study aimed to investigate the role of miR-103a-3p in cardiomyocyte injury through autophagy and apoptosis. H9c2 cells were cultured under hypoxia and reoxygenation (H/R) conditions and were used to mimic cells under ischemia. The transfection of cells with miR-103a-3p (mimics and inhibitors) was performed to examine its function in cardiomyocytes. The expression levels of miR-103a-3p were evaluated by reverse transcription-quantitative polymerase chain reaction analysis. Cell viability was determined using an MTT assay, and the lactate dehydrogenase assay (LDH) was used to investigate cell injury. The expression levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, Beclin-1, autophagy-related 5 ( Atg5 ), cleaved caspase-3 and cleaved caspase-9 were detected using western blotting. Immunofluorescence assays were performed to detect the expression of LC3 as a marker of autophagy. The target gene of miR-103a-3p was identified using dual-luciferase reporter assays. The results revealed that the expression levels of miR-103a-3p were significantly downregulated in cardiomyocytes under H/R conditions. Injury of the cardiomyocytes was evaluated under H/R conditions. Following transfection of the cells with miR-103a-3p inhibitors, cell injury was increased, as determined by LDH and MTT assays. The expression levels of apoptotic proteins were consistent with the results obtained in the LDH and cell viability assays. The induction of autophagy was increased in cells under H/R conditions and cells with miR-103a-3p inhibitor transfection, whereas the induction of autophagy was decreased in cells transfected with miR-103a-3p mimics. In addition, the data indicated that miR-103a-3p directly targeted Atg5 , which regulated the induction of autophagy and apoptosis. Taken together, these findings indicate that, following the inhibition of miR-103a-3p, Atg5 promotes autophagy and apoptosis in cardiomyocytes by directly targeting Atg5 . Therefore, miR-103a-3p can be considered a potential therapeutic target for myocardial ischemia.

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Hyperbaric oxygen protects against myocardial reperfusion injury via the inhibition of inflammation and the modulation of autophagy

Cited by 17 publications

References 56 publications

Hyperbaric oxygen therapy effectively alleviates D-galactose-induced-age-related cardiac dysfunction via attenuating mitochondrial dysfunction in pre-diabetic rats

Hyperbaric oxygen therapy effectively alleviates D-galactose-induced-age-related cardiac dysfunction via attenuating mitochondrial dysfunction in pre-diabetic rats

MicroRNA‑93 inhibits chondrocyte apoptosis and inflammation in osteoarthritis by targeting the TLR4/NF‑κB signaling pathway

Effects of miR‑103a‑3p on the autophagy and apoptosis of cardiomyocytes by regulating Atg5

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