检索结果-南通市图书馆

Hippo(YAP)-autophagy axis protects against hepatic ischemia-reperfusion injury through JNK signaling

Chinese Medical Journal 2024年第6期137卷 657-668页

作者： Shuguang Zhu Xiaowen Wang Haoqi Chen Wenfeng Zhu Xuejiao Li Ruiwen Cui Xiaomeng Yi Xiaolong Chen Hua Li Genshu Wang Department of Hepatic Surgery Liver TransplantationThe Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong 510630China Department of Hepatology lab The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong 510630China Department of General Surgery The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong 510630China Department of Organ Transplantation The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong 510630China Department of Renal Transplantation Guangdong Provincial Hospital of Chinese MedicineGuangzhouGuangdong 510630China Department of Surgical Intensive Care Unit The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong 510630China Department of Hepatic Surgery Liver TransplantationGuangdong Provincial Hospital of Chinese MedicineGuangzhouGuangdong 510630China

Background:Hepatic ischemia-reperfusion injury(HIRI)remains a common complication during liver transplantation(LT)in patients.As a key downstream effector of the Hippo pathway,Yes-associated protein(YAP)has been reported to be involved in various physiological and pathological processes.However,it remains elusive whether and how YAP may control autophagy activation during ischemia-reperfusion.Methods:Human liver tissues from patients who had undergone LT were obtained to evaluate the correlation between YAP and autophagy activation.Both an in vitro hepatocyte cell line and in vivo liver-specific YAP knockdown mice were used to establish the hepatic ischemia-reperfusion models to determine the role of YAP in the activation of autophagy and the mechanism of regulation.Results:Autophagy was activated in the post-perfusion liver grafts during LT in patients,and the expression of YAP positively correlated with the autophagic level of hepatocytes.Liver-specific knockdown of YAP inhibited hepatocytes autophagy upon hypoxia-reoxygenation and HIRI(P<0.05).YAP deficiency aggravated HIRI by promoting the apoptosis of hepatocytes both in the in vitro and in vivo models(P<0.05).Attenuated HIRI by overexpression of YAP was diminished after the inhibition of autophagy with 3-methyladenine.In addition,inhibiting autophagy activation by YAP knockdown exacerbated mitochondrial damage through increasing reactive oxygen species(P<0.05).Moreover,the regulation of autophagy by YAP during HIRI was mediated by AP1(c-Jun)N-terminal kinase(JNK)signaling through binding to the transcriptional enhanced associate domain(TEAD).Conclusions:YAP protects against HIRI by inducing autophagy via JNK signaling that suppresses the apoptosis of hepatocytes.Targeting Hippo(YAP)-JNK-autophagy axis may provide a novel strategy for the prevention and treatment of HIRI.

关键词： YAP-signaling proteins Autophagy c-Jun N-terminal kinase ischemia-reperfusion injury Liver transplantation

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

HSP110 aggravates ischemia-reperfusion injury after liver transplantation by promoting NF-κB pathway

引用

Hepatobiliary & Pancreatic Diseases International 2024年第4期23卷 344-352页

作者： Qing-Zhi Hu Zhen-Rui Cao Wei-Xiong Zheng Min-Jie Zhao Jun-Hua Gong Cong Chen Zhong-Jun Wu Rui Tao Department of Hepatobiliary Surgery Bishan Hospital of Chongqing Medical UniversityChongqing 402760China Department of Cardiothoracic Surgery the First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China c Department of Hepatobiliary Surgery the First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China Department of Hepatobiliary Surgery the Second Affiliated Hospital of Chongqing Medical UniversityChongqing 400010China

Background:ischemia-reperfusion injury(IRI)poses a significant challenge to liver transplantation(LT).The underlying mechanism primarily involves overactivation of the immune system.Heat shock protein 110(HSP110)functions as a molecular chaperone that helps stabilize protein structures.Methods:An IRI model was established by performing LT on Sprague-Dawley rats,and HSP110 was silenced using siRNA.Hematoxylin-eosin staining,TUNEL,immunohistochemistry,ELISA and liver enzyme analysis were performed to assess IRI following LT.Western blotting and quantitative reverse transcription-polymerase chain reaction were conducted to investigate the pertinent molecular changes.Results:Our findings revealed a significant increase in the expression of HSP110 at both the mRNA and protein levels in the rat liver following LT(P<0.05).However,when rats were injected with siRNAHSP110,IRI subsequent to LT was notably reduced(P<0.05).Additionally,the levels of liver enzymes and inflammatory chemokines in rat serum were significantly reduced(P<0.05).Silencing HSP110 with siRNA resulted in a marked decrease in M1-type polarization of Kupffer cells in the liver and downregulated the NF-κB pathway in the liver(P<0.05).Conclusions:HSP110 in the liver promotes IRI after LT in rats by activating the NF-κB pathway and inducing M1-type polarization of Kupffer cells.Targeting HSP110 to prevent IRI after LT may represent a promising new approach for the treatment of LT-associated IRI.

关键词： ischemia-reperfusion injury Liver transplantation Inflammation HSP110 Heat shock proteins NF-κB

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Gasdermin D-mediated pyroptosis in myocardial ischemia and reperfusion injury:Cumulative evidence for future cardioprotective strategies

引用

Acta Pharmaceutica Sinica B 2023年第1期13卷 29-53页

作者： Panat Yanpiset Chayodom Maneechote Sirawit Sriwichaiin Natthaphat Siri-Angkul Siriporn C.Chattipakorn Nipon Chattipakorn Cardiac Electrophysiology Research and Training Center Faculty of MedicineChiang Mai UniversityChiang Mai 50200Thailand Cardiac Electrophysiology Unit Department of PhysiologyFaculty of MedicineChiang Mai UniversityChiang Mai 50200Thailand Center of Excellence in Cardiac Electrophysiology Research Chiang Mai UniversityChiang Mai 50200Thailand Department of Oral Biology and Diagnostic Sciences Faculty of DentistryChiang Mai UniversityChiang Mai 50200Thailand

Cardiomyocyte death is one of the major mechanisms contributing to the development of myocardial infarction(MI)and myocardial ischemia/reperfusion(MI/R)injury.Due to the limited regenerative ability of cardiomyocytes,understanding the mechanisms of cardiomyocyte death is necessary.Pyroptosis,one of the regulated programmed cell death pathways,has recently been shown to play important roles in MI and MI/R injury.Pyroptosis is activated by damage-associated molecular patterns(DAMPs)that are released from damaged myocardial cells and activate the formation of an apoptosisassociated speck-like protein containing a CARD(ASC)interacting with NACHT,LRR,and PYD domains-containing protein 3(NLRP3),resulting in caspase-1 cleavage which promotes the activation of Gasdermin D(GSDMD).This pathway is known as the canonical pathway.GSDMD has also been shown to be activated in a non-canonical pathway during MI and MI/R injury via caspase-4/5/11.Suppression of GSDMD has been shown to provide cardioprotection against MI and MI/R injury.Although the effects of MI or MI/R injury on pyroptosis have previously been discussed,knowledge concerning the roles of GSDMD in these settings remains limited.In this review,the evidence from in vitro,in vivo,and clinical studies focusing on cardiac GSDMD activation during MI and MI/R injury is comprehensively summarized and discussed.Implications from this review will help pave the way for a new therapeutic target in ischemic heart disease.

关键词： Pyroptosis Gasdermin D Heart ischemia ischemia-reperfusion injury Myocardial infarction

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

An ischemic area-targeting,peroxynitrite-responsive,biomimetic carbon monoxide nanogenerator for preventing myocardial ischemia-reperfusion injury

引用

Bioactive Materials 2023年第10期28卷 480-494页

作者： Jinyan Zhang Liwei Liu Zhen Dong Xicun Lu Wenxuan Hong Jin Liu Xiaoyi Zou Jinfeng Gao Hao Jiang Xiaolei Sun Kai Hu Youjun Yang Junbo Ge Xiao Luo Aijun Sun Department of Cardiology Zhongshan HospitalFudan UniversityChina Shanghai Institute of Cardiovascular Diseases ShanghaiChina Institutes of Biomedical Sciences Fudan UniversityShanghaiChina NHC Key Laboratory of Viral Heart Diseases ShanghaiChina Key Laboratory of Viral Heart Diseases Chinese Academy of Medical SciencesChina State Key Laboratory of Bioreactor Engineering Shanghai Key Laboratory of Chemical BiologySchool of PharmacyEast China University of Science and TechnologyShanghai200237China Shanghai Engineering Research Center of Molecular Therapeutics and New Drug Development School of Chemistry and Molecular EngineeringEast China Normal UniversityShanghaiChina

Myocardial ischemia-reperfusion (MI/R) injury is common in patients who undergo revascularization therapy for myocardial infarction, often leading to cardiac dysfunction. Carbon monoxide (CO) has emerged as a therapeutic molecule due to its beneficial properties such as anti-inflammatory, anti-apoptotic, and mitochondrial biogenesis-promoting properties. However, its clinical application is limited due to uncontrolled release, potential toxicity, and poor targeting efficiency. To address these limitations, a peroxynitrite (ONOO􀀀 )-triggered CO donor (PCOD585) is utilized to generate a poly (lactic-co-glycolic acid) (PLGA)-based, biomimetic CO nanogenerator (M/PCOD@PLGA) that is coated with the macrophage membrane, which could target to the ischemic area and neutralize proinflammatory cytokines. In the ischemic area, local produced ONOO􀀀 triggers the continuous release of CO from M/PCOD@PLGA, which efficiently ameliorates MI/R injury by clearing harmful ONOO􀀀 , attenuating the inflammatory response, inhibiting cardiomyocyte apoptosis, and promoting mitochondrial biogenesis. This study provides a novel insight into the safe therapeutic use of CO for MI/R injury by utilizing a novel CO donor combined with biomimetic technology. The M/PCOD@PLGA nanogenerator offers targeted delivery of CO to the ischemic area, minimizing potential toxicity and enhancing therapeutic efficacy.

关键词： ischemia-reperfusion injury Macrophage membrane Mitochondria Inflammation Peroxynitrite

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Effi cacy of partial and complete resuscitative endovascular balloon occlusion of the aorta in the hemorrhagic shock model of liver injury

引用

World Journal of Emergency Medicine 2024年第1期15卷 10-15页

作者： Yi Shan Yang Zhao Chengcheng Li Jianxin Gao Guogeng Song Tanshi Li Department of Emergency Medicine Chinese PLA Medical SchoolBeijing 100853China Department of Emergency Medicine the Sixth Medical Center of PLA General HospitalBeijing 100048China Department of Emergency Medicine School of MedicineSouth China University of TechnologyGuangzhou 510006China Department of Emergency Medicine the First Medical Center of PLA General HospitalBeijing 100853China

BACKGROUND:Resuscitative endovascular balloon occlusion of the aorta(REBOA)can temporarily control traumatic bleeding.However,its prolonged use potentially leads to ischemia-reperfusion injury(IRI).Partial REBOA(pREBOA)can alleviate ischemic burden;however,its security and eff ectiveness prior to operative hemorrhage control remains unknown.Hence,we aimed to estimate the effi cacy of pREBOA in a swine model of liver injury using an experimental sliding-chamber ballistic gun.METHODS:Twenty Landrace pigs were randomized into control(no aortic occlusion)(n=5),intervention with complete REBOA(cREBOA)(n=5),continuous pREBOA(C-pREBOA)(n=5),and sequential pREBOA(S-pREBOA)(n=5)groups.In the cREBOA and C-pREBOA groups,the balloon was inflated for 60 min.The hemodynamic and laboratory values were compared at various observation time points.Tissue samples immediately after animal euthanasia from the myocardium,liver,kidneys,and duodenum were collected for histological assessment using hematoxylin and eosin staining.RESULTS:Compared with the control group,the survival rate of the REBOA groups was prominently improved(all Pinjury,a 60-minute pREBOA resulted in improved survival rate and was effective in maintaining reliable aortic pressure,despite persistent hemorrhage.Extended tolerance time for aortic occlusion in Zone I for non-compressible torso hemorrhage was feasible with both continuous partial and sequential partial measures,and the significant improvement in the severity of acidosis and distal organ injury was observed in the sequential pREBOA.

关键词： Non-compressible torso hemorrhage Liver injury ischemia-reperfusion injury Resuscitative endovascular balloon occlusion of the aorta

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

TRPC6 Knockout Alleviates Renal Fibrosis through PI3K/AKT/GSK3B Pathway

引用

Current Medical Science 2024年第3期44卷 589-602页

作者： An-bang SUN Fang-hua LI Lin ZHU Xi-xi ZENG Min ZHU Qing-hua LEI Yan-hong LIAO Department of Anatomy School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China Department of Transfusion Medicine Wuhan Hospital of Traditional Chinese and Western MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China Department of Nephrology The First Affiliated Hospital of Zhengzhou UniversityZhengzhou450052China Department of Thoracic Surgery Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China National Basic Medical Teaching Demonstration Center Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China Key Laboratory of Neurological Diseases of Ministry of Education Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China

Objective Renal fibrosis is the ultimate pathway of various forms of acute and chronic kidney damage.Notably,the knockout of transient receptor potential channel 6(TRPC6)has shown promise in alleviating renal fibrosis.However,the regulatory impact of TRPC6 on renal fibrosis remains unclear.Methods In vivo,TRPC6 knockout(TRPC6−/−)mice and age-matched 129 SvEv(WT)mice underwent unilateral renal ischemia-reperfusion(uIR)injury surgery on the left renal pedicle or sham operation.Kidneys and serum were collected on days 7,14,21,and 28 after euthanasia.In vitro,primary tubular epithelial cells(PTECs)were isolated from TRPC6−/−and WT mice,followed by treatment with transforming growth factorβ1(TGFβ1)for 72 h.The anti-fibrotic effect of TRPC6−/−and the underlying mechanisms were assessed through hematoxylin-eosin staining,Masson staining,immunostaining,qRT-PCR,and Western blotting.Results Increased TRPC6 expression was observed in uIR mice and PTECs treated with TGFβ1.TRPC6−/−alleviated renal fibrosis by reducing the expression of fibrotic markers(Col-1,α-SMA,and vimentin),as well as decreasing the apoptosis and inflammation of PTECs during fibrotic progression both in vivo and in vitro.Additionally,we found that the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT)/glycogen synthase kinase 3 beta(GSK3β)signaling pathway,a pivotal player in renal fibrosis,was down-regulated following TRPC6 deletion.Conclusion These results suggest that the ablation of TRPC6 may mitigate renal fibrosis by inhibiting the apoptosis and inflammation of PTECs through down-regulation of the PI3K/AKT/GSK3βpathway.Targeting TRPC6 could be a novel therapeutic strategy for preventing chronic kidney disease.

关键词： transient receptor potential channel 6 ischemia-reperfusion injury renal fibrosis renal tubular epithelial cells

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Effect of Autophagy Inhibition on the Protection of ischemia Preconditioning against Myocardial ischemia/reperfusion injury in Diabetic Rats

引用

Chinese Medical Journal 2018年第14期131卷 1702-1709页

作者： Ya-Yang Liu Chao Sun Fu-Shan Xue Gui-Zhen Yang Hui-Xian Li Qing Liu Xu Liao Department of Anesthesiology Plastic Surgery Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100041 China

Background： ischemia preconditioning （IPC） remains the most powerful intervention of protection against myocardial ischemiaJreperfusion injury （IRI）, but diabetes can weaken or eliminate its cardioprotective effect and detailed mechanisms remain unclear. In this study, we aimed to explore whether changes of autophagy in the diabetic condition are attributable to the decreased cardioprotective effect of I PC. Methods： Sixty diabetic male Sprague-Dawley rats were randomly divided into the control （C）, IRI, rapamycin （R）, wortmannin （W）, rapamycin ＋ IPC （R ＋ IPC）, and wortmannin ＋ IPC （W ＋ IPC） groups. The in vivo rat model of myocardial IRI was established by ligaturing and opening the left anterior descending coronary artery via the left thoracotomy. Durations of ischemia and reperfusion are 30 min and 120 min, respectively. Blood samples were taken at 120 min of reperfusion for measuring serum concentrations of troponin I （TnI） and creatine kinase isoenzyme MB （CK-MB） using the enzyme-linked immunosorbent assay. The infarct size was assessed by Evans blue and triphenyltetrazolium chloride staining. The expressions ofLC3-11, beclin- 1, phosphoinositide 3-kinase （PI3K）, naammalian target of rapamycin （mTOR）, and P-Akt/Akt ratio in the ischemic myocardium were assessed by Western blotting. Results： Compared to the IRI group, infarct size （56.1% ± 6.1% vs. 75.4 ± 7.1%, P 〈 0.05）, serum cTnl （0.61 ± 0.21 vs. 0.95 ±0.26 ng/ml, P 〈 0.05）, and CK-MB levels （6.70 ± 1.25 vs. 11.51 ±2.35 ng/ml, P 〈 0.05） obviously decreased in the W ＋ IPC group. Compared with the C group, myocardial expressions of LC3-11 （0.46 ± 0.04 and 0.56 ± 0.04 vs. 0.36 ± 0.04, P 〈 0.05） and beclin- 1 （0.34 ± 0.08 and 0.38 ± 0.07 vs. 0.24 ±0.03, P 〈 0.05） evidently increased, and myocardial expressions of mTOR （0.26 ± 0.08 and 0.25 ± 0.07 vs. 0.38 ± 0.06, P 〈 0.05）, PI3K （0.29 ± 0.04 and 0.30 ±0.03 vs. 0.38 ± 0.02, P 〈 0.05）, and P-Akt/Akt ratio （0.49 ± 0.10 and 0.48 ± 0.06 vs. 0.72 ± 0.07, P 〈 0.05） markedly decreased in the IRI and R groups, indicati

关键词： Autophagy Diabetes ischemia Preconditioning ischemia-reperfusion injury

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Melatonin attenuates hepatic ischemia-reperfusion injury in rats by inhibiting NF-κB signaling pathway

引用

Hepatobiliary & Pancreatic Diseases International 2021年第6期20卷 551-560页

作者： Yao Gao Zhi-Tao Li Li Jin Jie Lin Zheng-Lei Fan Zhong Zeng Han-Fei Huang Organ Transplantation Center the First Affiliated Hospital of Kunming Medical UniversityKunming 650032China

Background:The sterile inflammatory response is one of the key mechanisms leading to hepatic ischemia-reperfusion injury.Melatonin has been shown to prevent organ injuries,but its roles in the inflammatory response after hepatic ischemia-reperfusion injury have not been fully explored,especially in late ischemia-reperfusion injury.The present study aimed to investigate the roles and possible mechanisms of melatonin in the inflammatory response after hepatic ischemia-reperfusion injury.Methods:Sixty Sprague-Dawley rats were randomly divided into a sham group,ischemia-reperfusion injury group(I/R group),and melatonin-treated group(M+I/R group).The rats in the I/R group were subjected to 70%hepatic ischemia for 45 min,followed by 5 or 24 h of reperfusion.The rats in the M+I/R group were injected with melatonin(10 mg/kg,intravenous injection)15 min prior to ischemia and immediately before reperfusion.Serum and samples of ischemic liver lobes were harvested for future analysis,and the 7-day survival rate was assessed after hepatic ischemia-reperfusion surgery.Results:In comparison with the I/R group,the M+I/R group showed markedly decreased expression levels of inflammatory cytokines(IL-6 and TNF-α)and numbers of apoptotic hepatocytes(Pischemia-reperfusion injury,alleviated the inflammatory response,protected the liver from ischemia-reperfusion injury,and increased the survival rate.

关键词： Melatonin ischemia-reperfusion injury Inflammation NF-κB Liver

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Protection Against Hepatic ischemia-reperfusion injury in Rats by Oral Pretreatment With Quercetin

引用

Biomedical and Environmental Sciences 2003年第1期16卷 1-8页

作者： JUN-FENG SU, CHANG-JIANG GUO , JING-YU WEI, JI-JUN YANG, YU-GANG JIANG, AND YUN-FENG LIDepartment of Nutrition, Institute of Hygiene and Environmental Medicine, Tianjin 300050, China Department of Nutrition Institute of Hygiene and Environmental MedicineTianjin 天津 300050

Objective To investigate the possible protection provided by oral quercetin pretreatment against hepatic ischemia-reperfusion injury in rats. Methods The quercetin （0.13 mmol/kg） was orally administrated in 50 min prior to hepatic ischemia-reperfusion injury. Ascorbic acid was also similarly administered. The hepatic content of quercetin was assayed by high performance liquid chromatography （HPLC）. Plasma glutamic pyruvic transaminase （GPT）, glutamic oxaloacetic transaminase （GOT） activities and malondialdehyde （MDA） concentration were measured as markers of hepatic ischemia-reperfusion injury. Meanwhile, hepatic content of glutathione （GSH）, activities of superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px） and xanthine oxidase （XO）, total antioxidant capacity （TAOC）, contents of reactive oxygen species （ROS） and MDA, DNA fragmentation were also determined. Results Hepatic content of quercetin after intragastric administration of quercetin was increased significantly. The increases in plasma GPT

关键词： Quercetin ischemia-reperfusion injury Lipid peroxidation Liver

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Tongxinluo Ameliorates Myocardial ischemia-reperfusion injury Mainly via Activating Parkin-Mediated Mitophagy and Downregulating Ubiquitin-Proteasome System

引用

Chinese Journal of Integrative Medicine 2021年第7期27卷 542-550页

作者： YANG Hong-xing WANG Peng WANG Ning-ning LI Shao-dan YANG Ming-hui Dongzhimen Hospital Beijing University of Chinese MedicineBeijing100029China Institute of Radiation Medicine Academy of Military Medical SciencesBeijing100850China Department of Traditional Chinese Medicine Chinese People's Liberation Army General HospitalBeijing100853China

Objective To investigate the protective effects and mechanism of Chinese herbal compound Tongxinluo Capsule(通心络胶囊,TXL)on the Parkin-mediated mitophagy and the ubiquitin-proteasome system in a rat model of myocardial ischemia-reperfusion injury(MIRI).Methods Seventy adult male Sprague-Dawley rats were randomly divided into 7 groups:sham group,MIRI group,low-and high-dose TXL(0.5 and 1 g·kg^(-1)·d^(-1),respectively)groups,atorvastatin(ATV)group(7.2 g·kg^(-1)·d^(-1)),chloroquine(CQ)group(10 g·kg^(-1)·d^(-1)),and highdose TXL+CQ group.After pharmacological administration for 7 days,rats underwent left anterior descending artery ligation surgery to establish the MIRI models with 50 min ischemia followed by 4 h reperfusion.Blood was taken for cardiac troponin I(cTnI)detection and hearts were harvested for infarct staining and apoptosis detection.The autophagy or mitophagy proteins and ubiquitinated proteins were detected by Western blotting.Results Compared with the sham group,the MIRI group exhibited a larger infarcted area(27.13%±0.01%,P<0.01),a higher apoptotic index(34.33%±2.03%vs.1.81%±0.03%,P<0.01),and higher cTnI expression(14.18±1.01 vs.7.96±0.32,P<0.01).The mitochondrial integrity was damaged in the MIRI group,while TXL and ATV alleviated the damage of MIRI.More autophagosomes were observed in the high-dose TXL group than in the MIRI group(7.00±0.58 vs.4.33±1.15,P<0.05).More amounts of PTEN-induced putative kinase protein 1(PINK1)and Parkin translocated onto the mitochondria were detected in the high-dose TXL group than in the MIRI group(P<0.05).The ubiquitin response was signifificantly downregulated in the high-dose TXL group relative to the MIRI group(P<0.05).CQ administration abolished the activation of autophagy flux and the PINK1/Parkin pathway induced by high-dose of TXL.Conclusions TXL ameliorates MIRI via activating Parkin-mediated mitophagy in rats.The downregulation of the ubiquitin-proteasome system is also involved.

关键词： Chinese medicine mitophagy ischemia-reperfusion injury Parkin ubiquitin

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：