IL-22 ameliorated cardiomyocyte apoptosis in cardiac ischemia/reperfusion injury by blocking mitochondrial membrane potential decrease, inhibiting ROS and cytochrome C

Che, Yang; Tian, Yu; Chen, Rong; Xia, Lin; Liu, Fang; Su, Zhaoliang

doi:10.1016/j.bbadis.2021.166171

Cited by 28 publications

(11 citation statements)

References 35 publications

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“…Additionally, studies done by other groups also suggest that myocardial apoptosis leads to irreversible loss of cardiomyocytes and cardiac function impairment in cardiovascular diseases. [30][31][32] Therefore, there is a high percentage of irreversible apoptotic cardiomyocytes in Hmgb1 f/f Tg Cre/+ mice, and we believe this massive apoptosis of cardiomyocytes may result in severe myocarditis because cardiomyocytes account for approximately 56% in murine myocardium and up to 70-85% of heart volume. 33,34 It is well known that serum HMGB1 is a proinflammatory factor in VMC.…”

Section: Discussionmentioning

confidence: 97%

Cardiomyocyte‐derived HMGB1 takes a protective role in CVB3‐induced viral myocarditis via inhibiting cardiac apoptosis

2023

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Coxsackievirus B3 (CVB3)‐induced viral myocarditis (VMC) is characterized by immune cell infiltration and myocardial damage. High mobility group box 1 (HMGB1) is a highly conserved nuclear DNA‐binding protein that participates in DNA replication, transcriptional regulation, repair response and inflammatory response in different disease models. To investigate the exact function of HMGB1 in CVB3‐induced VMC, we crossed Hmgb1‐floxed (Hmgb1f/f) mice with mice carrying a suitable Cre recombinase transgenic strain to achieve conditional inactivation of the Hmgb1 gene in a cardiomyocyte‐specific manner and to establish myocarditis. In this study, we found that cardiomyocyte‐specific Hmgb1‐deficient (Hmgb1f/fTgCre/+) mice exhibited exacerbated myocardial injury. Hmgb1‐deficient cardiomyocytes may promote early apoptosis via the p53‐mediated Bax mitochondrial pathway, as evidenced by the higher localization of p53 protein in the cytosol of Hmgb1‐deficient cardiomyocytes upon CVB3 infection. Moreover, cardiomyocyte Hmgb1‐deficient mice are more susceptible to cardiac dysfunction after infection. This study provides new insights into HMGB1 in VMC pathogenesis and a strategy for appropriate blocking of HMGB1 in the clinical treatment of VMC.

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Section: Discussionmentioning

confidence: 97%

Cardiomyocyte‐derived HMGB1 takes a protective role in CVB3‐induced viral myocarditis via inhibiting cardiac apoptosis

2023

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“…Mitochondrial dysfunction under ischemia‐hypoxia conditions leads to the excessive generation of ROS from the mitochondrial electron transport chain (ETC) (Sada et al, 2016). The destroyed ETC causes ATP synthesis to decrease, and the cell loses energy supply resulting in cell apoptosis (Che et al, 2021). Meanwhile, mitochondrial quality plays a key role in microvascular dysfunction and might be a promising cardioprotective target in MI (Chang et al, 2021; Zhou, Ren, Toan, & Mui, 2021; Zhu et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca²⁺ channels

Zhang

et al. 2022

Phytotherapy Research

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Liquiritigenin (Lq) offers cytoprotective effects against various cardiac injuries, but its beneficial effects on myocardial ischemic (MI) injury and the related mechanisms remain unclear. In the in vivo study, an animal model of MI was induced by intraperitoneal injection of isoproterenol (Iso, 85 mg/kg). ECG, heart rate, serum levels of CK and CK‐MB, histopathological changes, and reactive oxygen species (ROS) levels were all measured. In vitro, H9c2 cells were divided into four groups and treated for 24 hr with liquiritigenin (30 μmol/L and 100 μmol/L) followed with CoCl2 (800 μmol/L) for another 24 hr. Cell viability, apoptosis, mitochondrial membrane potential, and intracellular Ca2+ concentration ([Ca2+]i) were then assessed. The L‐type Ca2+ current (ICa‐L) was detected using a patch clamp technique on isolated rat ventricular myocytes. The myocyte contraction and Ca2+ transients were measured using an IonOptix detection system. The remarkable cardiac injury and generation of intracellular ROS induced by Iso were alleviated via treatment with Lq. CoCl2 administration induced cell apoptosis, mitochondrial dysfunction, and Ca2+ overload in H9c2; Lq reduces these deleterious effects of CoCl2. Meanwhile, Lq blocked ICa‐L in a dose‐dependent manner. The half‐maximal inhibitory concentration of Lq was 110.87 μmol/L. Lq reversibly reduced the amplitude of cell contraction as well as the Ca2+ transients. The results show that Lq protects against MI injury by antioxidation, antiapoptosis, counteraction mitochondrial dysfunction, and inhibition of ICa‐L, thus damping intracellular Ca2+.

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“…The level of intracellular ROS was detected as previously described [ 27 ]. The cells of 2 mL were seeded into 6-well plates (1 × 10 6 cells/well) and cultured for 24 h. After medium discarding, 2 mL of the samples (dose levels of 400 and 800 μg/mL) were added to each well to treat the cells for 24 and 48 h, respectively.…”

Section: Methodsmentioning

confidence: 99%

Monosaccharide Composition and In Vitro Activity to HCT-116 Cells of Purslane Polysaccharides after a Covalent Chemical Selenylation

Guan

Lin

et al. 2022

Foods

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The anti-cancer effects of selenylated plant polysaccharides are a focus of research. As a natural plant with extensive biological effects, there have been few studies related to edible purslane (Portulaca oleracea L.). Thus, in this study, soluble P. oleracea polysaccharides (PPS) were extracted from the dried P. oleracea and then selenylated chemically using the HNO3-Na2SeO3 method to obtain two selenylated products, namely, SePPS1 and SePPS2. Compared with the extracted PPS, SePPS1 and SePPS2 had much higher Se contents (840.3 and 1770.5 versus 66.0 mg/kg) while also showing lower contents in three saccharides—arabinose, fucose, and ribose—and higher contents in seven saccharides including galactose, glucose, fructose, mannose, rhamnose, galacturonic acid, and glucuronic acid, but a stable xylose content demonstrated that the performed chemical selenylation of PPS led to changes in monosaccharide composition. Moreover, SePPS1 and SePPS2 shared similar features with respect to monosaccharide composition and possessed higher bioactivity than PPS in human colon cancer HCT-116 cells. Generally, SePPS1 and SePPS2 were more active than PPS with respect to cell growth inhibition, the alteration of cell morphology, disruption of mitochondrial membrane potential, intracellular reactive oxygen species (ROS) generation, the induction of cell apoptosis, and upregulation or downregulation of five apoptosis-related genes and proteins such as Bax, Bcl-2, caspases-3/-9, and cytochrome C, that cause cell apoptosis and growth suppression via the ROS-mediated mitochondrial pathway. SePPS2 consistently showed the highest capacity to exert these observed effects on the targeted cells, suggesting that the performed chemical selenylation of PPS (in particular when higher degrees of selenylation are reached) resulted in an increase in activity in the cells. It can thus be concluded that the performed selenylation of PPS was able to incorporate inorganic Se into the final PPS products, changing their monosaccharide composition and endowing them with enhanced nutraceutical and anti-cancer effects in the colon.

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IL-22 ameliorated cardiomyocyte apoptosis in cardiac ischemia/reperfusion injury by blocking mitochondrial membrane potential decrease, inhibiting ROS and cytochrome C

Cited by 28 publications

References 35 publications

Cardiomyocyte‐derived HMGB1 takes a protective role in CVB3‐induced viral myocarditis via inhibiting cardiac apoptosis

Cardiomyocyte‐derived HMGB1 takes a protective role in CVB3‐induced viral myocarditis via inhibiting cardiac apoptosis

Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca²⁺ channels

Monosaccharide Composition and In Vitro Activity to HCT-116 Cells of Purslane Polysaccharides after a Covalent Chemical Selenylation

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IL-22 ameliorated cardiomyocyte apoptosis in cardiac ischemia/reperfusion injury by blocking mitochondrial membrane potential decrease, inhibiting ROS and cytochrome C

Cited by 28 publications

References 35 publications

Cardiomyocyte‐derived HMGB1 takes a protective role in CVB3‐induced viral myocarditis via inhibiting cardiac apoptosis

Cardiomyocyte‐derived HMGB1 takes a protective role in CVB3‐induced viral myocarditis via inhibiting cardiac apoptosis

Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca2+ channels

Monosaccharide Composition and In Vitro Activity to HCT-116 Cells of Purslane Polysaccharides after a Covalent Chemical Selenylation

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Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L‐type Ca²⁺ channels