Mitochondrial damage is a critical contributor to cardiac ischemia/reperfusion(I/R)injury.Mitochondrial quality control(MQC)mechanisms,a series of adaptive responses that preserve mitochondrial structure and function,...Mitochondrial damage is a critical contributor to cardiac ischemia/reperfusion(I/R)injury.Mitochondrial quality control(MQC)mechanisms,a series of adaptive responses that preserve mitochondrial structure and function,ensure cardiomyocyte survival and cardiac function after I/R injury.MQC includes mitochondrial fission,mitochondrial fusion,mitophagy and mitochondria-dependent cell death.The interplay among these responses is linked to pathological changes such as redox imbalance,calcium overload,energy metabolism disorder,signal transduction arrest,the mitochondrial unfolded protein response and endoplasmic reticulum stress.Excessive mitochondrial fission is an early marker of mitochondrial damage and cardiomyocyte death.Reduced mitochondrial fusion has been observed in stressed cardiomyocytes and correlates with mitochondrial dysfunction and cardiac depression.Mitophagy allows autophagosomes to selectively degrade poorly structured mitochondria,thus maintaining mitochondrial network fitness.Nevertheless,abnormal mitophagy is maladaptive and has been linked to cell death.Although mitochondria serve as the fuel source of the heart by continuously producing adenosine triphosphate,they also stimulate cardiomyocyte death by inducing apoptosis or necroptosis in the reperfused myocardium.Therefore,defects in MQC may determine the fate of cardiomyocytes.In this review,we summarize the regulatory mechanisms and pathological effects of MQC in myocardial I/R injury,highlighting potential targets for the clinical management of reperfusion.展开更多
In the present study, three new triterpenoids, 23-hydroxyurs-12, 18-dien-28-oic acid 3β-O-α-L-arabinopyranoside(1), 23-hydroxyurs-12, 18-dien-28-oic acid 3β-O-β-D-glucuronopyranoside-6-O-methyl ester(2), and urs-1...In the present study, three new triterpenoids, 23-hydroxyurs-12, 18-dien-28-oic acid 3β-O-α-L-arabinopyranoside(1), 23-hydroxyurs-12, 18-dien-28-oic acid 3β-O-β-D-glucuronopyranoside-6-O-methyl ester(2), and urs-12, 18-dien-28-oic acid 3β-O-β-D-glucuronopyranoside-6-O-methyl ester(3), and a known triterpenoid, 3β-hydroxy-urs-2, 18-dien-28-oic acid(4, randialic acid B), were isolated from the aerial parts of Ilex cornuta. Their structures were identified by the spectroscopic analyses(IR, ESI-MS, HR-ESI-MS, and 1D and 2D NMR) and chemical reactions. Compound 4 showed significant cell-protective effects against H_2O_2-induced H9c2 cardiomyocyte injury. Compounds 1-4 did not show any significant DPPH radical scavenging activity.展开更多
Objective To investigate whether exogenous hydrogen sulfide（H2S）protects high glucose（HG）-inducedH9c2 cardiomyocyte injury and inflammation response by inhibiting reactive oxygen species（ROS）-Toll-like receptor ...Objective To investigate whether exogenous hydrogen sulfide（H2S）protects high glucose（HG）-inducedH9c2 cardiomyocyte injury and inflammation response by inhibiting reactive oxygen species（ROS）-Toll-like receptor 4（TLR4）pathway.Methods Cell counter kit-8（CCK-8）assay was used to measure the cell viability,展开更多
基金partially supported by the China Postdoctoral Science Foundation(2019TQ0128)the National Natural Science Foundation of China(NSFC81900252,81900254 and 81870249)
文摘Mitochondrial damage is a critical contributor to cardiac ischemia/reperfusion(I/R)injury.Mitochondrial quality control(MQC)mechanisms,a series of adaptive responses that preserve mitochondrial structure and function,ensure cardiomyocyte survival and cardiac function after I/R injury.MQC includes mitochondrial fission,mitochondrial fusion,mitophagy and mitochondria-dependent cell death.The interplay among these responses is linked to pathological changes such as redox imbalance,calcium overload,energy metabolism disorder,signal transduction arrest,the mitochondrial unfolded protein response and endoplasmic reticulum stress.Excessive mitochondrial fission is an early marker of mitochondrial damage and cardiomyocyte death.Reduced mitochondrial fusion has been observed in stressed cardiomyocytes and correlates with mitochondrial dysfunction and cardiac depression.Mitophagy allows autophagosomes to selectively degrade poorly structured mitochondria,thus maintaining mitochondrial network fitness.Nevertheless,abnormal mitophagy is maladaptive and has been linked to cell death.Although mitochondria serve as the fuel source of the heart by continuously producing adenosine triphosphate,they also stimulate cardiomyocyte death by inducing apoptosis or necroptosis in the reperfused myocardium.Therefore,defects in MQC may determine the fate of cardiomyocytes.In this review,we summarize the regulatory mechanisms and pathological effects of MQC in myocardial I/R injury,highlighting potential targets for the clinical management of reperfusion.
文摘In the present study, three new triterpenoids, 23-hydroxyurs-12, 18-dien-28-oic acid 3β-O-α-L-arabinopyranoside(1), 23-hydroxyurs-12, 18-dien-28-oic acid 3β-O-β-D-glucuronopyranoside-6-O-methyl ester(2), and urs-12, 18-dien-28-oic acid 3β-O-β-D-glucuronopyranoside-6-O-methyl ester(3), and a known triterpenoid, 3β-hydroxy-urs-2, 18-dien-28-oic acid(4, randialic acid B), were isolated from the aerial parts of Ilex cornuta. Their structures were identified by the spectroscopic analyses(IR, ESI-MS, HR-ESI-MS, and 1D and 2D NMR) and chemical reactions. Compound 4 showed significant cell-protective effects against H_2O_2-induced H9c2 cardiomyocyte injury. Compounds 1-4 did not show any significant DPPH radical scavenging activity.
文摘Objective To investigate whether exogenous hydrogen sulfide（H2S）protects high glucose（HG）-inducedH9c2 cardiomyocyte injury and inflammation response by inhibiting reactive oxygen species（ROS）-Toll-like receptor 4（TLR4）pathway.Methods Cell counter kit-8（CCK-8）assay was used to measure the cell viability,
