Intake of hot water–extracted apple protects against myocardial injury by inhibiting apoptosis in an ischemia/reperfusion rat model

Kim, Mi Young; Lim, Sun Ha; Lee, Jongwon

doi:10.1016/j.nutres.2014.08.007

Cited by 15 publications

(13 citation statements)

References 46 publications

(70 reference statements)

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“…The neutral monosaccharide composition of WE was 1% arabinose, 1.6% xylose, 0.7% galactose, and 77.1% glucose (wt%). The composition of neutral monosaccharides in the arabinogalactan-peptide and WE was assessed as previously described9.…”

Section: Methodsmentioning

confidence: 99%

“…Assessments of IS, apoptotic cells, LV wall thickness, collagen content, and expansion index were performed as previously described91021. The MDA levels in the AAR were measured as previously described61.…”

Section: Methodsmentioning

confidence: 99%

“…The sample size in the MI experiments was pre-determined using a power analysis (G*Power 3.1.7 program) as previously described9. The data are expressed as the mean ± SEM.…”

Section: Methodsmentioning

confidence: 99%

“…Previously, we showed that the hot water extract of apple9 and apple pectin10, a cell wall polysaccharide, protects against ischaemia-reperfusion (IR) injury by inhibiting the apoptotic cascade in a rat MI model. Based on these results, we hypothesize that cell wall polysaccharides, which are the predominant constituents of dietary fibre in plant-based diets, contribute to the reduction of CHD risk by blocking postocclusion steps.…”

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confidence: 99%

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Plant-based foods containing cell wall polysaccharides rich in specific active monosaccharides protect against myocardial injury in rat myocardial infarction models

Lim

Kim

Yun

et al. 2016

Sci Rep

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Many cohort studies have shown that consumption of diets containing a higher composition of foods derived from plants reduces mortality from coronary heart disease (CHD). Here, we examined the active components of a plant-based diet and the underlying mechanisms that reduce the risk of CHD using three rat models and a quantitative proteomics approach. In a short-term myocardial infarction (MI) model, intake of wheat extract (WE), the representative cardioprotectant identified by screening approximately 4,000 samples, reduced myocardial injury by inhibiting apoptosis, enhancing ATP production, and maintaining protein homeostasis. In long-term post-MI models, this myocardial protection resulted in ameliorating adverse left-ventricular remodelling, which is a predictor of heart failure. Among the wheat components, arabinose and xylose were identified as active components responsible for the observed efficacy of WE, which was administered via ingestion and tail-vein injections. Finally, the food components of plant-based diets that contained cell wall polysaccharides rich in arabinose, xylose, and possibly fucose were found to confer protection against myocardial injury. These results show for the first time that specific monosaccharides found in the cell wall polysaccharides in plant-based diets can act as active ingredients that reduce CHD by inhibiting postocclusion steps, including MI and heart failure.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…The sample size in the MI experiments was pre-determined using a power analysis (G*Power 3.1.7 program) as previously described9. The data are expressed as the mean ± SEM.…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Plant-based foods containing cell wall polysaccharides rich in specific active monosaccharides protect against myocardial injury in rat myocardial infarction models

Lim

Kim

Yun

et al. 2016

Sci Rep

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“…We could not abandon the profit of percutaneous coronary intervention, coronary artery bypass grafting or thrombolytic agents but rescue reperfusion injury. The procedure of MIRI refers to a series of complicated pathological processes, including inflammatory response ( 3 ), calcium overload ( 4 ), complement activation ( 5 ), cell autophagy ( 6 ) and apoptosis ( 7 ). The inflammatory response with Toll-like receptor (TLR) signaling is considered to be a pivotal link to myocardial ischemia/reperfusion induced tissue injury ( 8 , 9 ).…”

Section: Introductionmentioning

confidence: 99%

RP105 alleviates myocardial ischemia reperfusion injury via inhibiting TLR4/TRIF signaling pathways

Yang

et al. 2018

Int J Mol Med

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The Toll-like receptor 4 (TLR4) signal pathway-induced inflammation is considered to be a crucial link to myocardial ischemia reperfusion injury (MIRI). Our previous study proved that radioprotective 105 kDa protein (RP105), a negative regulator of TLR4, performed a protective role in MIRI by anti-apoptosis approach. However, the mechanism of RP105 cardioprotection of anti-inflammation is still unclear. This study aimed to explore the underlying mechanism of RP105 anti-inflammation effect in MIRI. We established a rat model of MIRI induced by ligation of the left anterior descending coronary artery for 30 min followed by 2 h reperfusion. Animals were pre-infected with Ad-EGFP-RP105, Ad-EGFP or saline at the apex of the heart. All rats were sacrificed to collect blood samples and myocardial tissue and assessed by immunofluorescence, blood biochemical analysis, Evans blue/triphenyltetrazolium chloride (TTC), hematoxylin and eosin (H&E) staining, enzyme-linked immuno sorbent assay (ELISA), western blot analysis, quantitative PCR and electrophoretic mobility shift assay (EMSA). RP105 overexpression with adenovirus vectors reduced serum myocardial enzyme (CK-MB and LDH) activities, decreased myocardial infarct size, mitigated inflammatory factors interferon-β and tumor necrosis factor-α during MIRI. We also found that Ad-RP105 group exerted distinct repression of TLR4/TRIF signal pathway related proteins and mRNAs (TRIF, TBK-1, IRF3 and p-IRF3) with a low transcriptional activity of IRF3. These findings first expounded that RP105 could alleviate the ischemia reperfusion induced inflammatory status in heart via inhibiting TLR4/TRIF signaling pathway and provided a theoretical foundation of RP105 gene in MIRI.

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microRNA‐183 improve myocardial damager via NF‐kb pathway: In vitro and in vivo study

Xing

Xie

Wang

et al. 2018

J of Cellular Biochemistry

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Aim: The aim of this study is to evaluate the effects of microRNA-183 (miRNA-183) in myocardial damager.Methods: In the cell experiment, the H9C2 cell was divided into three groups: NC group, Model group, and miRNA group. The cell apoptosis and relative proteins' expressions were measured by flow cytometry and Western blot assay. The in vivo study of the rats was divided into three groups: Sham group, Model group, and miRNA group. The pathology, Infarct size, cell apoptosis, and relative protein expressions were evaluated by hematoxylin and eosin staining, nitro blue tetrazolium staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, and immunohistochemistry. Results: Compared with NC groups, the in vitro and in vivo study showed that cell apoptosis rate of miRNA groups was significantly suppressed (P < 0.05). The pathology and infarct size of miRNA group were significantly improved compared with the NC group. Meanwhile, the relative proteins expression (nuclear factor-κB [NF-kb], caspase-3, Bax, and Bcl-2) of miRNA groups were significantly different compared with those of NC groups (P < 0.05). Conclusion:In vitro and in vivo study revealed that miRNA-183 improves myocardial damager through the NF-κb pathway.

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Intake of hot water–extracted apple protects against myocardial injury by inhibiting apoptosis in an ischemia/reperfusion rat model

Cited by 15 publications

References 46 publications

Plant-based foods containing cell wall polysaccharides rich in specific active monosaccharides protect against myocardial injury in rat myocardial infarction models

Plant-based foods containing cell wall polysaccharides rich in specific active monosaccharides protect against myocardial injury in rat myocardial infarction models

RP105 alleviates myocardial ischemia reperfusion injury via inhibiting TLR4/TRIF signaling pathways

microRNA‐183 improve myocardial damager via NF‐kb pathway: In vitro and in vivo study

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