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Protection of Ndrg2 deficiency on renal ischemia-reperfusion injury via activating PINK1/Parkin-mediated mitophagy

中华医学杂志(英文版) 2024年第21期137卷 2603页

作者： Liu Min Chen Jianwen Sun Miao Zhang Lixia Yu Yao Mi Weidong Ma Yulong Wang Guyan Department of Anesthesiology Beijing Tongren Hospital Capital Medical University Beijing China Department of Nephrology The First Medical Center of Chinese PLA General Hospital Nephrology Institute of the Chinese People’s Liberation Army State Key Laboratory of Kidney Diseases National Clinical Research Center for Kidney Diseases Beijing Key Laboratory of Kidney Disease Research Beijing China Department of Anesthesiology The First Affiliated Hospital Jinzhou Medical University Jinzhou Liaoning China Department of Burn and Plastic Surgery The Fourth Medical Center of Chinese PLA General Hospital Beijing China Department of Anesthesiology Peking University Third Hospital Beijing China Department of Anesthesiology Chinese PLA General Hospital Beijing China Department of Anesthesiology The First Medical Center of Chinese PLA General Hospital Beijing China

Background: Renal ischemia-reperfusion (R-I/R) injury is the most prevalent cause of acute kidney injury, with high mortality and poor prognosis. However, the underlying pathological mechanisms are not yet fully understood. Therefore, this study aimed to investigate the role of N-myc downstream-regulated gene 2 (Ndrg2) in R-I/R ***: We examined the expression of Ndrg2 in the kidney under normal physiological conditions and after R-I/R injury by immunofluorescence staining, real-time polymerase chain reaction, and western blotting. We then detected R-I/R injury in Ndrg2-deficient (Ndrg2-/-) mice and wild type (Ndrg2+/+) littermatesin vivo, and detected oxygen and glucose deprivation and reperfusion (OGD-R) injury in HK-2 cells. We further conducted transcriptomic sequencing to investigate the role ofNdrg2 in R-I/R injury and detected levels of oxidative stress and mitochondrial damage by dihydroethidium staining, biochemical assays, and western blot. Finally, we measured the levels of mitophagy inNdrg2+/+ andNdrg2-/- mice after R-I/R injury or HK-2 cells in OGD-R ***: Ndrg2 was primarily expressed in renal proximal tubules and its expression was significantly decreased 24 h after R-I/R ***2-/- mice exhibited significantly attenuated R-I/R injury compared toNdrg2+/+ mice. Transcriptomics profiling showed thatNdrg2 deficiency induced perturbations of multiple signaling pathways, downregulated inflammatory responses and oxidative stress, and increased autophagy following R-I/R injury. Further studies revealed thatNdrg2 deficiency reduced oxidative stress and mitochondrial damage. Notably,Ndrg2 deficiency significantly activated phosphatase and tensin homologue on chromosome ten-induced putative kinase 1 (PINK1)/Parkin-mediated mitophagy. The downregulation of NDRG2 expression significantly increased cell viability after OGD-R injury, increased the expression of heme oxygenase-1, decreased the expression of nicotinamide adenine dinucleotide

关键词： ischemia-reperfusion injury N-myc downstream-regulated gene 2 Mitophagy Oxidative stress Renoprotection Oxygen and glucose deprivation

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

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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

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

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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 *** 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 *** was taken for cardiac troponin I(cTnI)detection and hearts were harvested for infarct staining and apoptosis *** autophagy or mitophagy proteins and ubiquitinated proteins were detected by Western *** 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 *** 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 ameliorates MIRI via activating Parkin-mediated mitophagy in *** downregulation of the ubiquitin-proteasome system is also involved.

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

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Reducing the oxidative stress mediates the cardioprotection of bicyclol against ischemia-reperfusion injury in rats

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2013年第6期14卷 487-495页

作者： Jie CUI Zhi LI Ling-bo QIAN Qin GAO Jue WANG Meng XUE Xiao-e LOU Iain C.BRUCE Qiang XIA Hui-ping WANG Department of Physiology School of MedicineZhejiang University Department of Physiology Xuzhou Medical College Department of Physiology Zhejiang Medical College

Objective:To investigate the beneficial effect of bicyclol on rat hearts subjected to ischemia-reperfusion(IR) injuries and its possible ***:Male Sprague-Dawley rats were intragastrically administered with bicyclol(25,50 or 100 mg/(kg·d)) for 3 *** IR was produced by occlusion of the coronary artery for 1 h and reperfusion for 3 *** ventricular hemodynamics was continuously *** the end of reperfusion,myocardial infarct was measured by 2,3,5-triphenyltetrazolium chloride(TTC) staining,and serum lactate dehydrogenase(LDH) level and myocardial superoxide dismutase(SOD) activity were determined by *** ventricular myocytes from adult rats were exposed to 60 min anoxia and 30 min reoxygenation to simulate IR *** reperfusion,cell viability was determined with trypan blue;reactive oxygen species(ROS) and mitochondrial membrane potential of the cardiomyocytes were measured with the fluorescent *** mitochondrial permeability transition pore(mPTP) opening induced by Ca2+(200 μmol/L) was measured with the absorbance at 520 nm in the isolated myocardial ***:Low dose of bicyclol(25 mg/(kg·d)) had no significant improving effect on all cardiac parameters,whereas pretreatment with high bicyclol markedly reduced the myocardial infarct and improved the left ventricular contractility in the myocardium exposed to IR(P<0.05).Medium dose of bicyclol(50 mg/(kg·d)) markedly improved the myocardial contractility,left ventricular myocyte viability,and SOD activity,as well decreased infarct size,serum LDH level,ROS production,and mitochondrial membrane potential in rat myocardium exposed to *** reduction of ventricular myocyte viability in IR group was inhibited by pretreatment with 50 and 100 mg/(kg·d) bicyclol(P<0.05 ***),but not by 25 mg/(kg·d) *** opening of mPTP evoked by Ca2+ was significantly inhibited by medium ***:Bicyclol exerts cardioprotection against IR injur

关键词： ischemia-reperfusion injury Cardioprotection Oxidative stress Mitochondrial permeability transition pore Bicyclol

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Extraction and Identification of Ginsenoside Re and Its Effects and Mechanism of Protecting Acute Renal ischemia-reperfusion injury in Rats

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Chemical Research in Chinese Universities 2011年第4期27卷 584-588页

作者： GU Xin-quan CHEN Yan-ping HU Ting-ting LU Xiu-hua LI Xi-qian DU Xiao-hui CAO Xia WANG Wei-hua XU Zhong-gao China-Japan Union Hospital of Jilin University Changchun 130033 P. R. China College of Chemistry Jilin University Changchun 130012 P. R. China College of Pharmacy Jilin University Changchun 130021 P. R. China The First Hospital of Jilin University Changchun 130021 P. R. China

This paper studies the extraction and identification of ginsenoside Re from ginseng fruits and investigates the effect and mechanism of ginsenoside Re of protecting acute renal ischemia-reperfusion injury in *** been smashed,the ginseng fruits were ultrasonically extracted twice with 95% ethanol for 30min *** been concentrated,the solution was dissolved with distilled water and separated by two-column chromatography,of which one was packed with macroporous resin D4020,and the other was packed with macroporous resin *** raw product was dissolved with methanol and was purified by elution on a Si gel column,finally ginsenoside Re was *** structure of the ginsenoside Re was analyzed by the thin-layer chromatography and NMR methods,and HPLC was carried for the content *** model of acute renal ischemia-reperfusion injury in rats was established after ischemia for 1 h and reperfusion for 1 h or 24 h,serum SOD（superoxide dismutase）,MDA（malondialdehyde） and plasma TXB2（thromboxane B2） and 6-keto-PGF1α were *** results show that it has accurately,fast,convenient merits and so *** Re has a protective effect on acute renal ischemia-reperfusion injury in rats,the mechanism may be related to improving the imbalance of thromboxane A2（TXA2）/prostacyclin（PGI2） and inhibiting lipid peroxidation reaction.

关键词： Ginsenoside Re Extraction Identification Kidney ischemia-reperfusion injury

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

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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 *** 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 *** present study aimed to investigate the roles and possible mechanisms of melatonin in the inflammatory response after hepatic ischemia-reperfusion ***: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 *** rats in the M+I/R group were injected with melatonin(10 mg/kg,intravenous injection)15 min prior to ischemia and immediately before *** and samples of ischemic liver lobes were harvested for future analysis,and the 7-day survival rate was assessed after hepatic ischemia-reperfusion ***: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

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Deficiency of anti-inflammatory cytokine IL-4 leads to neural hyperexcitability and aggravates cerebral ischemia-reperfusion injury

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Acta Pharmaceutica Sinica B 2020年第9期10卷 1634-1645,1802页

作者： Xiaoling Chen Jingliang Zhang Yan Song Pan Yang Yang Yang Zhuo Huang Kewei Wang Department of Molecular and Cellular Pharmacology State Key Laboratory of Natural and Biomimetic DrugsPeking University School of Pharmaceutical SciencesBeijing 100191China Department of Pharmacology Qingdao University School of PharmacyQingdao 266021China Department of Medicinal Chemistry and Molecular Pharmacology Purdue University College of PharmacyWest LafayetteIN 47907USA Institute of Innovative Drugs Qingdao University School of PharmacyQingdao 266021China

Systematic administration of anti-inflammatory cytokine interleukin 4(IL-4)has been shown to improve recovery after cerebral ischemic ***,whether IL-4 affects neuronal excitability and how IL-4 improves ischemic injury remain largely *** we report the neuroprotective role of endogenous IL-4 in focal cerebral ischemia-repertusion(I/R)*** multi-electrode array(MEA)recordings,IL-4 reduces spontaneous firings and network activities of mouse primary cortical ***-4 mRNA and protein expressions are upregulated after I/R *** deletion of 11-4 gene aggravates I/R injury in vivo and exacerbates oxygen-glucose deprivation(OGD)injury in cortical ***,supplemental IL-4 protects 11-4-/-cortical neurons against OGD ***,cortical pyramidal and stellate neurons common for ischemic penumbra after I/R injury exhibit intrinsic hyperexcitability and enhanced excitatory synaptic transmissions in Il-4-/-***,upregulation of Nav1.1 channel,and downregulations of KCa3.1 channel and a6 subunit of GABAA receptors are detected in the cortical tissues and primary cortical neurons from Il-4-/-*** together,our findings demonstrate that IL-4 deficiency results in neural hyperexcitability and aggravates I/R injury,thus activation of IL-4 signaling may protect the brain against the development of permanent damage and help recover from ischemic injury after stroke.

关键词： Anoxic depolarization IL-4 ischemia-reperfusion injury Neuronal excitability Synaptic transmissions

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

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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 *** shock protein 110(HSP110)functions as a molecular chaperone that helps stabilize protein ***:An IRI model was established by performing LT on Sprague-Dawley rats,and HSP110 was silenced using ***-eosin staining,TUNEL,immunohistochemistry,ELISA and liver enzyme analysis were performed to assess IRI following *** blotting and quantitative reverse transcription-polymerase chain reaction were conducted to investigate the pertinent molecular ***: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 *** 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

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

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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

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Pretreatment with erythropoietin reduces hepatic ischemia-reperfusion injury

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Hepatobiliary & Pancreatic Diseases International 2009年第3期8卷 294-299页

作者： Luo, Yu-Hong Li, Zheng-Dong Liu, Li-Xin Dong, Gao-Hong Jinan Univ Dept Hepatobiliary Surg Affiliated Hosp 1 Guangzhou 510630 Peoples R China

BACKGROUND: During hepatectomy, a period of ischemia and restoration of the blood supply can result in hepatic ischemia-reperfusion injury (IRI). Current research indicates that erythropoietin (EPO) has a protective effect in animal models of cerebral ischemia, myocardial infarction, and renal IRI. However there is lack of research into the role of EPO in hepatic IRI. This study aimed to explore the role of EPO in hepatic IRI and its possible mechanism of action. METHODS: Thirty male Sprague-Dawley rats were divided into three groups: (1) ten rats in the experimental group were given 1000 IU/kg EPO one day before the operation; (2) ten rats in a control group were given normal saline preoperatively as a placebo; and (3) ten rats served as a sham-operated group. Hepatic IRI was induced by occluding the hepatic arteries of the three cephalad hepatic segments and the portal vein for about 45 minutes, while in the sham-operated group only laparotomy was performed. The levels of ALT and AST were tested 24 hours pre- and post-operation. All rats were sacrificed 24 hours after the operation to assess the pathologic changes in the liver and measure the expression of heme oxygenase-1 (HO-1) through Western blotting and RT-PCR. RESULTS: Hepatic IRI was markedly mitigated in the experimental group as compared with the control group. Moreover, the expression of HO-1 at the level of both transcription and protein increased prominently (Pinjury through its anti-inflammatory property. (Hepatobiliary Pancreat Dis Int 2009; 8: 294-299)

关键词： erythropoietin ischemia-reperfusion injury heme oxygenase-1

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