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κ-opioid receptor activation promotes mitochondrial fusion and enhances myocardial resistance to ischemia and reperfusion injury via STAT3-OPA1 pathway

κ-opioid receptor activation promotes mitochondrial fusion ...

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2019中国生理学会学术年会暨张锡钧基金第十五届全国青年优秀生理学学术论文交流会及第十三届全国青年生理学工作者学术会议

作者：王凯燕 jianming pei Haitao Guo Department of Physiology and Pathophysiology National Key Discipline of Cell BiologyFourth Military Medical University

Mitochondrial dynamics, determining mitochondrial morphology, quality and abundance, have recently been implicated in myocardial ischemia and reperfusion(MI/R) *** roles of κ-opioid receptor activation in cardioprotection have been confirmed in our previous studies, while the underlying mechanism associated with mitochondrial dynamics remains *** study aims to investigate the effect of κ-opioid receptor activation on the pathogenesis of MI/R and elucidate the underlying mechanisms related to mitochondrial ***/R mouse model and hypoxia-reoxygenation cardiomyocyte model were *** dynamics were analyzed by transmission electron microscopy in vivo and by confocal microscopy in ***3 phosphorylation and OPA1 expression were detected by Western *** results suggested thatκ-opioid receptor activation with the selective agonist U50,488 H promoted mitochondrial fusion and enhanced myocardial resistance to MI/R injury, while the protective effects of κ-opioid receptor activation were blocked by nor-BNI, a selective κ-opioid receptor *** addition, κ-opioid receptor activation increased STAT3 phosphorylation and OPA1 expression, which were blocked by ***, inhibition of STAT3 phosphorylation by stattic, a specific STAT3 inhibitor,repressed the effects of κ-opioid receptor activation on promoting OPA1 expression and mitochondrial fusion, as well as cell apoptosis and oxidative stress both in vivo and in vitro during MI/R ***, our data for the first time provide evidence that κ-opioid receptor activation promotes mitochondrial fusion and enhances myocardial resistance to MI/R injury via the STAT3/OPA1 *** the effects of κ-opioid receptor activation on mitochondrial dynamics may be a potential therapeutic strategy for MI/R injury.

关键词： κ-opioid receptor STAT3 Mitochondrial dynamics OPA1

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P53/PANK1/miR-107 signaling pathway bridges the gap between metabolic reprogramming and insulin resistance induced by high-fat diet

P53/PANK1/miR-107 signaling pathway bridges the gap between ...

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2019中国生理学会学术年会暨张锡钧基金第十五届全国青年优秀生理学学术论文交流会及第十三届全国青年生理学工作者学术会议

作者：杨璐 Li Chen Xinju Wang jianming pei Department of Physiology Fourth Military Medical University Department of Aerospace Physiology Fourth Military Medical University Battalion 5 of Cadets Fourth Military Medical University

Background: High-fat diet(HFD) leads to obesity, type II diabetes mellitus(T2 DM) and increases the coincidence of cardiovascular diseases and *** resistance(IR) is considered as the "common soil" of those ***, people on HFD showed restrained glycolysis and enhanced fatty acid oxidation which is the so-called metabolic ***, the relationship between metabolic reprogramming and IR induced by HFD is still ***:The C57 BL/6 mice were fed on HFD for 16 *** glucose and insulin tolerance tests were *** AML12 hepatocyte were treated with palmitate acid(PA) for 24 *** levels of P53, pantothenate kinase 1(PANK1) and miR-107 in the liver tissues and cells were *** P53 was regulated by agonist or antagon *** intervention of PANK1 or miR-107, the mRNA expression and activity of key enzymes in glycolysis and gluconeogenesis were analyzed, the insulin signaling was ***: Here, we demonstrate that PANK1 and miR-107 were upregulated in the liver tissue of mice on HFD for 16 weeks and involved in metabolic reprogramming induced by palmitate acid(PA) ***, miR-107 within an intron of PANK1 gene facilitated IR by targeting caveolin-1 in AML12 cells upon PA ***, we identify that HFD enhanced P53 expression, and activation of P53 with nutlin-3 a induced PANK1 and miR-107 expression simultaneously in transcriptional level, leading to metabolic reprogramming and IR, ***, inhibition of P53 with pifithrin-α hydrobromide ameliorated PA induced metabolic reprogramming and ***: Thus, our results revealing a new mechanism by which P53 regulate *** addition, the results distinguished the different role of PANK1 and its intron miR-107 in metabolic regulation, which will provide more accurate intervention targets for the treatment of metabolic diseases.

关键词： High-fat diet Metabolic reprogramming Insulin resistance P53 PANK1 MiR-107

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The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion

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The Journal of Biomedical Research 2023年第4期37卷 230-254页

作者： Natalia V.Naryzhnaya Leonid N.Maslov Ivan A.Derkachev Huijie Ma Yi Zhang NRajendra Prasad Nirmal Singh Feng Fu jianming pei Akpay Sarybaev Akylbek Sydykov Laboratory of Experimental Cardiology Cardiology Research InstituteTomsk National Research Medical CenterRussian Academy of ScienceTomskTomsk Region 634012Russia Department of Physiology Hebei Medical UniversityShijiazhuangHebei 050017China Department of Biochemistry and Biotechnology Faculty of ScienceAnnamalai UniversityAnnamalainagarTamilnadu 608002India Department of Pharmaceutical Sciences and Drug Research Punjabi UniversityPatialaPunjabi 147002India Department of Physiology and Pathophysiology National Key Discipline of Cell BiologySchool of Basic Medicinethe Fourth Military Medical UniversityXi'anShaanxi 710032China Department of Mountain and Sleep Medicine and Pulmonary Hypertension National Center of Cardiology and Internal MedicineBishkek 720040Kyrgyzstan Kyrgyz-Indian Mountain Biomedical Research Center Bishkek 720033Kyrgyzstan Department of Internal Medicine Excellence Cluster Cardio-Pulmonary Institute(CPI)Member of the German Center for Lung Research(DZL)Justus Liebig University of GiessenGiessenHessen 35392Germany Department of Mountain and Sleep Medicine and Pulmonary Hypertension National Center of Cardiology and Internal MedicineBishkek 720040Kyrgyzstan.

The acute myocardial infarction(AMI)and sudden cardiac death(SCD),both associated with acute cardiac ischemia,are one of the leading causes of adult death in economically developed *** development of new approaches for the treatment and prevention of AMI and SCD remains the highest priority for medicine.A study on the cardiovascular effects of chronic hypoxia(CH)may contribute to the development of these *** hypoxia exerts both positive and adverse *** positive effects are the infarct-reducing,vasoprotective,and antiarrhythmic effects,which can lead to the improvement of cardiac contractility in *** adverse effects are pulmonary hypertension and right ventricular *** review presents a comprehensive overview of how CH enhances cardiac tolerance to ischemia/*** is an in-depth analysis of the published data on the underlying mechanisms,which can lead to future development of the cardioprotective effect of CH.A better understanding of the CH-activated protective signaling pathways may contribute to new therapeutic approaches in an increase of cardiac tolerance to ischemia/reperfusion.

关键词： heart vessels infarct size arrhythmias chronic hypoxia

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Do reactive oxygen species damage or protect the heart in ischemia and reperfusion?Analysis on experimental and clinical data

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The Journal of Biomedical Research 2023年第4期37卷 255-267页

作者： Leonid N.Maslov Natalia V.Naryzhnaya Maria Sirotina Alexandr V.Mukhomedzyanov Boris K.Kurbatov Alla A.Boshchenko Huijie Ma Yi Zhang Feng Fu jianming pei Viacheslav N.Azev Vladimir A.Pereverzev Cardiology Research Institute Tomsk National Research Medical Centerthe Russian Academy of SciencesTomskTomsk Region 634012Russia Department of Physiology Hebei Medical UniversityShijiazhuangHebei 050017China Department of Physiology and Pathophysiology National Key Discipline of Cell BiologySchool of Basic Medicinethe Fourth Military Medical UniversityXi'anShaanxi 710032China The Branch of the Institute of Bioorganic Chemistry Russian Academy of SciencesPushchinoMoscow Oblast 142290Russia Department of Normal Physiology Belarusian State Medical UniversityMinsk 220083Belarus

The role of reactive oxygen species(ROS)in ischemic and reperfusion(I/R)injury of the heart has been discussed for more than 40 *** has been demonstrated that reperfusion triggers a multiple increase in free radical generation in the isolated *** were found to have the ability to mitigate I/R injury of the ***,it is unclear whether their cardioprotective effect truly depends on the decrease of ROS levels in myocardial *** high doses and high concentrations of antioxidants were experimentally used,it is highly likely that the cardioprotective effect of antioxidants depends on their interaction not only with free radicals but also with other *** has been demonstrated that the antioxidant N-2-mercaptopropionyl glycine or NDPH oxidase knockout abolished the cardioprotective effect of ischemic ***,there is evidence that ROS protect the heart against the I/R injury.

关键词： reactive oxygen species free radicals antioxidants heart reperfusion patients

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A historical literature review of coronary microvascular obstruction and intra-myocardial hemorrhage as functional/structural phenomena

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The Journal of Biomedical Research 2023年第4期37卷 268-289页

作者： Leonid N.Maslov Natalia V.Naryzhnaya Sergey V.Popov Alexandr V.Mukhomedzyanov Ivan A.Derkachev Boris K.Kurbatov Andrey V.Krylatov Feng Fu jianming pei Vyacheslav V.Ryabov Evgenii V.Vyshlov Svetlana V.Gusakova Alla A.Boshchenko Akpay Sarybaev Laboratory of Experimental Cardiology Cardiology Research InstituteTomsk National Research Medical Center of the Russian Academy of SciencesTomskTomsk Region 634012Russia Department of Physiology and Pathophysiology National Key Discipline of Cell BiologySchool of Basic Medicinethe Fourth Military Medical UniversityXi'anShaanxi 710032China Siberian State Medical University TomskTomsk Region 634050Russia National Center of Cardiology and Internal Medicine Bishkek 720040Kyrgyzstan.

The analysis of experimental data demonstrates that platelets and neutrophils are involved in the no-reflow phenomenon,also known as microvascular obstruction(MVO).However,studies performed in the isolated perfused hearts subjected to ischemia/reperfusion(I/R)do not suggest the involvement of microembolization and microthrombi in this *** intracoronary administration of alteplase has been found to have no effect on the occurrence of MVO in patients with acute myocardial ***,the major events preceding the appearance of MVO in coronary arteries are independent of microthrombi,platelets,and *** cells appear to be the target where ischemia can disrupt the endothelium-dependent vasodilation of coronary ***,reperfusion triggers more pronounced damage,possibly mediated by *** and intra-myocardial hemorrhage contribute to the adverse post-infarction myocardial ***,pharmacological agents used to treat MVO should prevent endothelial injury and induce relaxation of smooth *** conditioning protocols have been shown to prevent MVO,with L-type Ca2+channel blockers appearing the most effective in treating MVO.

关键词： heart ischemia reperfusion microvascular obstruction intra-myocardial hemorrhage

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胰岛素抵抗与转录因子E3

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临床心血管病杂志 2009年第6期25卷 419-420页

作者：郭海涛张荣怀裴建明第四军医大学基础部生理学教研室西安710032 第四军医大学心内科

胰岛素抵抗(insulin resistance, IR)是指机体组织或靶细胞对内源性或外源性胰岛素的生物学效应低于正常水平的一种现象,是代谢综合征(metabolic syndrome, MS)的中心环节,但其发生的机制尚不十分清楚.

关键词：代谢综合征胰岛素抵抗转录因子E3

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原油蒸馏塔过汽化油的讨论

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石油化工高等学校学报 1996年第1期9卷 30-35页

作者：裴建明广东石油化工高等专科学校广东茂名525000

通过对原油蒸馏塔进科汽化过程的分析与讨论，提出原料进入精馏段的汽相量等于汽化段一次汽化量与塔底二次汽化量之和，从而解释了原油蒸馏塔传统工艺计算中出现的精馏段底部内回流量与所设定的过汽化量严重不符的矛盾，对进一步降低原... 详细信息

通过对原油蒸馏塔进科汽化过程的分析与讨论，提出原料进入精馏段的汽相量等于汽化段一次汽化量与塔底二次汽化量之和，从而解释了原油蒸馏塔传统工艺计算中出现的精馏段底部内回流量与所设定的过汽化量严重不符的矛盾，对进一步降低原油蒸馏塔的能量消耗有一定的指导意义．

关键词：原油蒸馏塔过汽化油汽化段汽化塔底

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固溶时效对节镍型高氮奥氏体不锈钢组织的影响

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金属热处理 2020年第2期45卷 120-124页

作者：常金宝赵英利嵇爽张福利杨现亮裴建明河钢集团钢研总院河北石家庄052165 燕山大学机械工程学院河北秦皇岛066000

对热轧态节镍型高氮奥氏体不锈钢进行固溶及时效处理,利用光学显微镜、电子背散射衍射,结合相图系统分析该材料固溶处理及时效后组织变化规律。结果表明,1050℃固溶处理后,试验钢基体为奥氏体,存在少量的铁素体,奥氏体晶粒形状偏等轴,... 详细信息

对热轧态节镍型高氮奥氏体不锈钢进行固溶及时效处理,利用光学显微镜、电子背散射衍射,结合相图系统分析该材料固溶处理及时效后组织变化规律。结果表明,1050℃固溶处理后,试验钢基体为奥氏体,存在少量的铁素体,奥氏体晶粒形状偏等轴,晶粒内部存在大量孪晶。时效后,析出相主要为Cr2N、CrN、Cr23C6。在时效时间为5 h不变的条件下,温度由650℃升高至800℃,碳化物及氮化物数量呈现先增长后降低的趋势,在750℃时数量最多。而在750℃时效5~10 h范围内,随着时效时间的增加,析出相数量变化不大。析出相的析出过程为:先在晶界交叉处析出胞状析出物,随时间的延长,在晶界逐渐析出条状析出物,在晶内开始出现并逐渐长大,最终形成类珠光体的片层状析出。

关键词：节镍型高氮奥氏体不锈钢固溶处理时效微观组织

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κ阿片受体激动剂U50,488H的利尿作用机制

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西安交通大学学报（医学版） 2005年第6期26卷 541-544页

作者：郭海涛仝黎槐勇毕辉王跃民裴建明第四军医大学基础部生理学教研室陕西西安710032 第四军医大学学员旅十四队陕西西安710032

目的观察κ阿片受体激动剂U50,488H对大鼠的利尿作用并探讨其作用机制。方法用生理学整体实验技术观察U50,488H对尿量的影响;分离大鼠肾动脉,用血管环方法测定肾血管张力的变化;应用放射免疫分析方法观察其对血浆中抗利尿激素(ADH)、血... 详细信息

目的观察κ阿片受体激动剂U50,488H对大鼠的利尿作用并探讨其作用机制。方法用生理学整体实验技术观察U50,488H对尿量的影响;分离大鼠肾动脉,用血管环方法测定肾血管张力的变化;应用放射免疫分析方法观察其对血浆中抗利尿激素(ADH)、血管紧张素Ⅱ(AngⅡ)和心房钠尿肽(ANP)的影响。结果静脉注射U50,488H可显著增加大鼠的尿量,并且使大鼠血浆ADH水平显著性下降;在离体水平,U50,488H可以剂量依赖性地舒张大鼠的肾动脉。以上效应均可被κ阿片受体选择性阻断剂(nor-BNI)所阻断。结论U50,488H通过激动κ阿片受体使大鼠的尿量增加,舒张肾动脉和降低ADH的分泌是其利尿的主要机制。

关键词： κ阿片受体肾动脉利尿抗利尿激素

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油－氢混合物焓温曲线的绘制

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石油化工高等学校学报 1995年第2期8卷 21-23页

作者：裴建明艾红广东石油化工高等专科学校

以催化重整装置为例，介绍一种油－氢混合物焓温曲线的制作方法，并通过实例查出催化重整原料油及循环氢混合物各组分在不同温度下的焓值。

关键词：油氢混合物焓曲线绘制原油

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