Lignin only accounts for about 6%of total mass in tobacco stem,but it inuences the harmful substances in the side stream smoke of cigarette in a significant way.Traditional researches focus only on the determination o...Lignin only accounts for about 6%of total mass in tobacco stem,but it inuences the harmful substances in the side stream smoke of cigarette in a significant way.Traditional researches focus only on the determination of lignin content.In the present work,we investigate four typical imidazolium-based ionic liquids for efficient extraction of lignin under mild conditions and 1-ethyl-3-methylimidazolium diethylphosphate([Emim][DEP])shows the best results.The pretreatment of stem using water at 80℃for 30 min can not only remove most of the sugars but also loose the microbers.The extractive rate of lignin reaches 85.38%at 150℃for 4 h and the purity of lignin is 90.21%.展开更多
Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion （I/R） injury and microRNAs （miRNAs） could act on various facets of cardiac function. However, the role of miRNA...Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion （I/R） injury and microRNAs （miRNAs） could act on various facets of cardiac function. However, the role of miRNAs in the cardioprotection by electroacupuncture pre-treatment on myocardial I/R injury remains unknown. The purpose of the study was to examine whether miR-214 was involved in cardio-protection by electroacupuncture. Methods Using rat myocardial I/R model, we examined the role of electroacupuncture pretreatment in myocardial I/R injury and analyzed the changes in the expression of miR-214. In addition, I/R was simulated in vitro by performing oxy-gen-glucose deprivation （OGD） on H9c2 cell cultures, and the effect of electroacupuncture pretreatment on I/R injury as well as expressional level of miR-214 were examined in vitro. Furthermore, the miR-214 mimic was transfected into OGD-treated H9c2 cells, we analyzed the cell apoptosis, lactate dehydrogenase （LDH） and creatine kinase （CK） activities, intracellular free Ca2＋concentration （[Ca2＋]i） as well as the relative protein levels of sodium/calcium exchanger 1（NCX1）, BCL2-like 11 （BIM）, calmodulin-dependent protein kinase IIδ（CaMKIIδ） and Cyclophilin D （CypD）. Results The in vivo results revealed that compared with the I/R group, the electroacupuncture pretreatment group showed significant decreased myocardial infarct size, as well as the increased indices of the cardiac function, including heart rate, mean arterial pressure, left ventricular systolic pressure and maximal rate for left ventricular pressure rising and declining （±dp/dt max）. In addition, electroacupuncture pretreatment could inhibit the elevation of LDH and CK activities induced by I/R injury. The quantitative PCR （qPCR） results demonstrated electroacupuncture pretreatment could provide cardioprotection against myocardial I/R injury in rats with miR-214 up-regulation. In the meanwhile, in vitro, electroacupuncture pretreatment protected H9c2 cells from OGD-induced injury. Trans-fection of miR-214 mimic showed protective effects on OGD-induced injury to H9c2 cells by reducing apoptosis, decreasing LDH and CK activities, rescuing the OGD-induced Ca2＋and down-regulating elevated protein levels of NCX1, BIM, CaMKIIδand CypD. Conclusions Our findings firstly demonstrated that electroacupuncture pretreatment promotes the expression of miR-214 in myocardial I/R injury and miR-214 contributes to the protective effect of electroacupuncture on myocardial I/R injury.展开更多
Acute myocardial infarction （AMI） is the leading cause of death and disability worldwide. Timely reperfusion is the standard of care and results in decreased infarct size, improving patient survival and prognosis. H...Acute myocardial infarction （AMI） is the leading cause of death and disability worldwide. Timely reperfusion is the standard of care and results in decreased infarct size, improving patient survival and prognosis. However, 25% of patients proceed to develop heart failure （HF） after myocardial infarction （MI） and 50% of these will die within five years. Since the size of the infarct is the major predictor of the outcome, including the development of HF, therapies to improve myocardial salvage have great potential. Over the past three decades, a number of stimuli have been discovered that activate endogenous cardioprotective pathways. In ischemic preconditioning （IPC） and ischemic postconditioning, ischemia within the heart initiates the protection. Brief reversible episodes of ischemia in vascular beds remote from the heart can also trigger cardioprotection when applied before, during, or immediately after myocardial ischemia-- known as remote ischemic pre-, per-, and post-conditioning, respectively. Although the mechanism of remote ischemic preconditioning （RIPC） has not yet been fully elucidated, many mechanistic components are shared with IPC. The discovery of RIPC led to research into the use of remote non-ischemic stimuli including nerve stimulation （spinal and vagal）, and electroacupuncture （EA）. We discovered and, with others, have elucidated mechanistic aspects of a non- ischemic phenomenon we termed remote preconditioning of trauma （RPCT）. RPCT operates via neural stimulation of skin sensory nerves and has similarities and differences to nerve stimulation and EA conducted at acupoints. We show herein that RPCT can be mimicked using electrical stimulation of the abdominal midline （EA-like treatment） and that this modality of activating cardioprotection is powerful as both a preconditioning and a postconditioning stimulus （when applied at reperfusion）. Investigations of these cardioprotective phenomena have led to a more integrative understanding of mechanisms related to cardioprotection, and in the last five to ten years, it has become clear that the mechanisms are similar, whether induced by ischemic or non-ischemic stimuli. Taking together much of the data in the literature, we propose that all of these cardioprotective ＂conditioning＂ phenomena represent activation from different entry points of a cardiac conditioning network that converges upon specific mediators and effectors of myocardial cell survival, including NF-KB, Stat3/5, protein kinase C, bradykinin, and the mitoKA^P channel. Nervous system pathways may represent a novel mechanism for initiating conditioning of the heart and other organs. IPC and RIPC have proven difficult to translate clinically, as they have associated risks and cannot be used in some patients. Because of this, the use of neural and nociceptive stimuli is emerging as a potential non-ischemic and non-traumatic means to initiate cardiac conditioning. Clinical relevance is underscored by the demonstration of postconditioning with one of these modalities, supporting the conclusion that the development of pharmaceuticals and electroceuticals for this purpose is an area ripe for clinical development.展开更多
Objective： We compare the cardioprotective effects of anesthetic preconditioning by propofol and/or isoflurane in rats with ischemia-reperfusion injury. Methods： Male adult Wistar rats were subjected to 60 min of an...Objective： We compare the cardioprotective effects of anesthetic preconditioning by propofol and/or isoflurane in rats with ischemia-reperfusion injury. Methods： Male adult Wistar rats were subjected to 60 min of anterior descending coronary artery occlusion followed by 120 rain of reperfusion. Before the long ischemia, anesthetics were administered twice for 10 min followed by 5 min washout. Isoflurane was inhaled at 1 MAC （0.016） in I group, whereas propofol was inhaled intravenously at 37.5 mg/（kg.h） in P group. A combination ofisoflurane and propofol was administered simultaneously in I＋P group. Results： In control （without anesthetic preconditioning, C group）, remarkable myocardial infarction and apoptosis accompanied by an increased level of cardiac troponin T were noted 120 min aider ischemia-reperfusion. As compared to those of control group, I and P groups had comparable cardioprotection. In addition, I＋P group shares with I and P groups the comparable cardioprotective effects in terms of myocardial infarction and cardiac troponin T elevation. Conclusion： A combination of isoflurane and propofol produced no additional cardioprotection.展开更多
基金supported by the China Postdoctoral Science Foundation (BH2060000062)China Tobacco Anhui Industrial Co.,LTD
文摘Lignin only accounts for about 6%of total mass in tobacco stem,but it inuences the harmful substances in the side stream smoke of cigarette in a significant way.Traditional researches focus only on the determination of lignin content.In the present work,we investigate four typical imidazolium-based ionic liquids for efficient extraction of lignin under mild conditions and 1-ethyl-3-methylimidazolium diethylphosphate([Emim][DEP])shows the best results.The pretreatment of stem using water at 80℃for 30 min can not only remove most of the sugars but also loose the microbers.The extractive rate of lignin reaches 85.38%at 150℃for 4 h and the purity of lignin is 90.21%.
基金This study was supported by a grant from the Hainan Provincial Nature Science Foundation
文摘Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion （I/R） injury and microRNAs （miRNAs） could act on various facets of cardiac function. However, the role of miRNAs in the cardioprotection by electroacupuncture pre-treatment on myocardial I/R injury remains unknown. The purpose of the study was to examine whether miR-214 was involved in cardio-protection by electroacupuncture. Methods Using rat myocardial I/R model, we examined the role of electroacupuncture pretreatment in myocardial I/R injury and analyzed the changes in the expression of miR-214. In addition, I/R was simulated in vitro by performing oxy-gen-glucose deprivation （OGD） on H9c2 cell cultures, and the effect of electroacupuncture pretreatment on I/R injury as well as expressional level of miR-214 were examined in vitro. Furthermore, the miR-214 mimic was transfected into OGD-treated H9c2 cells, we analyzed the cell apoptosis, lactate dehydrogenase （LDH） and creatine kinase （CK） activities, intracellular free Ca2＋concentration （[Ca2＋]i） as well as the relative protein levels of sodium/calcium exchanger 1（NCX1）, BCL2-like 11 （BIM）, calmodulin-dependent protein kinase IIδ（CaMKIIδ） and Cyclophilin D （CypD）. Results The in vivo results revealed that compared with the I/R group, the electroacupuncture pretreatment group showed significant decreased myocardial infarct size, as well as the increased indices of the cardiac function, including heart rate, mean arterial pressure, left ventricular systolic pressure and maximal rate for left ventricular pressure rising and declining （±dp/dt max）. In addition, electroacupuncture pretreatment could inhibit the elevation of LDH and CK activities induced by I/R injury. The quantitative PCR （qPCR） results demonstrated electroacupuncture pretreatment could provide cardioprotection against myocardial I/R injury in rats with miR-214 up-regulation. In the meanwhile, in vitro, electroacupuncture pretreatment protected H9c2 cells from OGD-induced injury. Trans-fection of miR-214 mimic showed protective effects on OGD-induced injury to H9c2 cells by reducing apoptosis, decreasing LDH and CK activities, rescuing the OGD-induced Ca2＋and down-regulating elevated protein levels of NCX1, BIM, CaMKIIδand CypD. Conclusions Our findings firstly demonstrated that electroacupuncture pretreatment promotes the expression of miR-214 in myocardial I/R injury and miR-214 contributes to the protective effect of electroacupuncture on myocardial I/R injury.
基金supported by grants from the National Institutes of Health (NIHR01 HL091478) for W.Keith Jonesthe National Natural Science Foundation of China (81470425) for Xiaoping Ren
文摘Acute myocardial infarction （AMI） is the leading cause of death and disability worldwide. Timely reperfusion is the standard of care and results in decreased infarct size, improving patient survival and prognosis. However, 25% of patients proceed to develop heart failure （HF） after myocardial infarction （MI） and 50% of these will die within five years. Since the size of the infarct is the major predictor of the outcome, including the development of HF, therapies to improve myocardial salvage have great potential. Over the past three decades, a number of stimuli have been discovered that activate endogenous cardioprotective pathways. In ischemic preconditioning （IPC） and ischemic postconditioning, ischemia within the heart initiates the protection. Brief reversible episodes of ischemia in vascular beds remote from the heart can also trigger cardioprotection when applied before, during, or immediately after myocardial ischemia-- known as remote ischemic pre-, per-, and post-conditioning, respectively. Although the mechanism of remote ischemic preconditioning （RIPC） has not yet been fully elucidated, many mechanistic components are shared with IPC. The discovery of RIPC led to research into the use of remote non-ischemic stimuli including nerve stimulation （spinal and vagal）, and electroacupuncture （EA）. We discovered and, with others, have elucidated mechanistic aspects of a non- ischemic phenomenon we termed remote preconditioning of trauma （RPCT）. RPCT operates via neural stimulation of skin sensory nerves and has similarities and differences to nerve stimulation and EA conducted at acupoints. We show herein that RPCT can be mimicked using electrical stimulation of the abdominal midline （EA-like treatment） and that this modality of activating cardioprotection is powerful as both a preconditioning and a postconditioning stimulus （when applied at reperfusion）. Investigations of these cardioprotective phenomena have led to a more integrative understanding of mechanisms related to cardioprotection, and in the last five to ten years, it has become clear that the mechanisms are similar, whether induced by ischemic or non-ischemic stimuli. Taking together much of the data in the literature, we propose that all of these cardioprotective ＂conditioning＂ phenomena represent activation from different entry points of a cardiac conditioning network that converges upon specific mediators and effectors of myocardial cell survival, including NF-KB, Stat3/5, protein kinase C, bradykinin, and the mitoKA^P channel. Nervous system pathways may represent a novel mechanism for initiating conditioning of the heart and other organs. IPC and RIPC have proven difficult to translate clinically, as they have associated risks and cannot be used in some patients. Because of this, the use of neural and nociceptive stimuli is emerging as a potential non-ischemic and non-traumatic means to initiate cardiac conditioning. Clinical relevance is underscored by the demonstration of postconditioning with one of these modalities, supporting the conclusion that the development of pharmaceuticals and electroceuticals for this purpose is an area ripe for clinical development.
文摘Objective： We compare the cardioprotective effects of anesthetic preconditioning by propofol and/or isoflurane in rats with ischemia-reperfusion injury. Methods： Male adult Wistar rats were subjected to 60 min of anterior descending coronary artery occlusion followed by 120 rain of reperfusion. Before the long ischemia, anesthetics were administered twice for 10 min followed by 5 min washout. Isoflurane was inhaled at 1 MAC （0.016） in I group, whereas propofol was inhaled intravenously at 37.5 mg/（kg.h） in P group. A combination ofisoflurane and propofol was administered simultaneously in I＋P group. Results： In control （without anesthetic preconditioning, C group）, remarkable myocardial infarction and apoptosis accompanied by an increased level of cardiac troponin T were noted 120 min aider ischemia-reperfusion. As compared to those of control group, I and P groups had comparable cardioprotection. In addition, I＋P group shares with I and P groups the comparable cardioprotective effects in terms of myocardial infarction and cardiac troponin T elevation. Conclusion： A combination of isoflurane and propofol produced no additional cardioprotection.
