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Exercise attenuates angiotensinⅱ-induced muscle atrophy by targeting PPARγ/miR-29b

Journal of Sport and Health Science 2022年第6期11卷 696-707,F0003页

作者： Qi Liu Liyang Chen Xuchun Liang Yuqing Cao Xinyue Zhu Siqi Wang Jin Li Juan Gao Junjie Xiao Cardiac Regeneration and Ageing Lab Institute of Cardiovascular SciencesSchool of Life ScienceShanghai UniversityShanghai 200444China Shanghai Engineering Research Center of Organ Repair School of MedicineShanghai UniversityShanghai 200444China

Background:Exercise is beneficial for muscle atrophy.Peroxisome proliferator-activated receptor gamma(PPARγ) and microRNA-29 b(miR-29 b) have been reported to be responsible for angiotensinⅱ(AngⅡ)-induced muscle atrophy.However,it is unclear whether exercise can protect AngⅡ-induced muscle atrophy by targeting PPARγ/miR-29 b.Methods:Skeletal muscle atrophy in both the control group and the run group was established by AngⅡ infusion;after 1 week of exercise training,the mice were sacrificed,and muscle weight was determined.Myofiber size was measured by hematoxylin-eosin and wheat-germ agglutinin staining.Apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling staining.The expression level of muscle atrogenes,including F-box only protein 32(FBXO32,also called Atrogin-1) and muscle-specific RING-finger 1(MuRF-1),the phosphorylation level of protein kinase B(PKB,also called AKT)/forkhead box 03 A(FOX03 A)/mammalian target of rapamycin(mTOR) pathway proteins,the expression level of PPARγ and apoptosis-related proteins,including B-cell lymphoma-2(Bcl-2),Bcl-2-associated X(Bax),cysteine-aspartic acid protease 3(caspase-3),and cleaved-caspase-3,were determined by western blot.The expression level of miR-29 b was checked by reversetranscription quantitative polymerase chain reaction.A PPARγ inhibitor(T0070907) or adeno-associated virus serotype-8(AAV8)-mediated miR-29 b overexpression was used to demonstrate whether PPARγ activation or miR-29 b inhibition mediates the beneficial effects of exercise in AngⅡ-induced muscle atrophy.Results:Exercise can significantly attenuate AngⅡ-induced muscle atrophy,which is demonstrated by increased skeletal muscle weight,cross-sectional area of myofiber,and activation of AKT/mTOR signaling and by decreased atrogenes expressions and apoptosis.In AngⅡ-induced muscle atrophy mice models,PPARγ was elevated whereas miR-29 b was decreased by exercise.The protective effects of exercise in AngⅡ-induced muscle atrophy were inhibited by a PPARγ inhibitor(T0070907)

关键词： angiotensinⅱ Exercise Muscle atrophy PPARg miR-29b

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Influence ofβ-elemene on the secretion of angiotensin II and expression of AT1R in hepatic stellate cells

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Frontiers of Medicine 2009年第1期3卷 36-40页

作者： Ling YANG Rui ZHU Qingjing ZHU Dan DAN Jin YE Keshu XU Xiaohua HOU Department of Gastroenterology Union HospitalTongji Medical CollegeHuazhong University of Science&TechnologyWuhan 430022China Department of Traditional Chinese Medicine Union HospitalTongji Medical CollegeHuazhong University of Science&TechnologyWuhan 430022China Department of Integrated Traditional Chinese Medicine and Western Medicine Wuhan Municipal Hospital of Infectious DiseasesWuhan 430022China

This study aims to investigate the inﬂuence ofβ-elemene on the secretion of angiotensin II(ANG II)and the expression of angiotensin receptor type 1(AT1R)in hepatic stellate cells(HSCs).In vitro,HSC-T6 were cultured for 24 hours and then treated with different doses ofβ-elemene(2.5,5 and 10 mg/L).A control group was also set up.The secretion of ANG II in the supernatant was detected by radioimmunoassay.The mRNA expression of AT1R at 4,12 and 24 h after treatment was detected by reverse transcription-polymerase chain reaction(RT-PCR),respectively.The protein expression of AT1R was detected by western blot.At the 4th h,the ANG II secretion in the supernatant was signiﬁcantly inhibited by 10 mg/Lβ-elemene compared with the control group(P0.05).At the time point of the 12th h,the secretion of ANG II in the supernatant treated with 10 mg/L and 5.0 mg/Lβ-elemene was signiﬁcantly lower than the control(P<0.01,P<0.05).Following the treatment with 5.0 mg/L and 2.5 mg/Lβ-elemene for 24 h,signiﬁcant inhibition of ANG II secretion was observed(P<0.05),but 10 mg/Lβ-elemene had no such effect.β-elemene signiﬁcantly reduced the amount of AT1R mRNA in HSCs after the treatment for 4,12,and 24 h in a dose-dependent manner.The expression of AT1R protein also decreased after the treatment withβ-elemene for 24 h.β-elemene can inhibit the secretion of ANG II and the gene and protein expression of AT1R,which may be the mechanism by whichβ-elemene prevents the progress of hepaticﬁbrosis.

关键词： liver cirrhosis beta-elemene hepatic stellate cells angiotensinⅱ receptor,angiotensin,type 1

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Oxidative stress-mediated effects of angiotensin Ⅱ in the cardiovascular system

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World Journal of Hypertension 2012年第4期2卷 34-44页

作者： Hairuo Wen Judith K Gwathmey Lai-Hua Xie Department of Cell Biology and Molecular Medicine UMDNJ-New Jersey Medical School Newark NJ 07103 United States GwathmeyInc. CambridgeMA02138 United States School of Optometry Massachusetts CollegeofPharmacyandHealthSciences WorcesterMA01608 United States

angiotensin Ⅱ(Ang Ⅱ), an endogenous peptide hormone, plays critical roles in the pathophysiological modulation of cardiovascular functions. Ang Ⅱ is the principle effector of the renin-angiotensin system for maintaining homeostasis in the cardiovascular system, as well as a potent stimulator of NAD(P)H oxidase, which is the major source and primary trigger for reactive oxygen species(ROS) generation in various tissues. Recent accumulating evidence has demonstrated the importance of oxidative stress in Ang Ⅱ-induced heart diseases. Here, we review the recent progress in the study on oxidative stress-mediated effects of Ang Ⅱ in the cardiovascular system. In particular, the involvement of Ang Ⅱ-induced ROS generation in arrhythmias, cell death/heart failure, ischemia/reperfusion injury, cardiac hypertrophy and hypertension are discussed. Ca2+/calmodulin-dependent protein kinase Ⅱ is an important molecule linking Ang Ⅱ, ROS and cardiovascular pathological conditions.

关键词： angiotensinⅱ Oxidative stress Mitochondria Arrhythmias Ischemia-reperfusion Hypertrophy Hypertension

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Induction of tissue angiotensin Ⅱ-forming activity in two-kidney, one-clip hypertensive hamster model

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World Journal of Hypertension 2013年第2期3卷 9-17页

作者： Yoshinari Uehara Kanta Fujimi Eiji Yahiro Satomi Abe Sankar Devarajan Keijiro Saku Hidenori Urata Department of Cardiology Fukuoka University School of Medicine Fukuoka 814-0180 Japan Department of Cardiovascular Diseases Fukuoka University Chikushi Hospital Chikushino 818-8502 Japan

AIM: To evaluate the role of chymase in blood pressure regulation and its actions on tissue renin-angiotensin system.METHODS: A two-kidney, one-clip(2K1C) hypertension model was developed in Syrian hamsters, which have a human-type chymase. Either an angiotensin(Ang) converting enzyme(ACE) inhibitor(ACE-I; temocapril, 30 mg/kg per day), Ang Ⅱ type 1 receptor antagonist(ARB; CS866, 10 mg/kg per day), or vehicle was administered, beginning 2 wk after renal artery clipping and continued for 16 wk. At the end of this protocol, hearts, aortas, and lungs were removed, and total Ang Ⅱ-forming activities and ACE- and chymasedependent Ang Ⅱ-forming activities were determined.RESULTS: After renal artery clipping, systolic blood pressure in the vehicle group was significantly higher compared with that in a sham-operated group throughoutthe experimental period. Both ACE-I and ARB treatments revealed similar antihypertensive effects. Moreover, in the vehicle group, cardiac total and chymase-dependent Ang Ⅱ-forming activities significantly increased at 18 wk after clipping. Further, cardiac total and chymase-dependent Ang Ⅱ-forming activities decreased significantly after ACE-I or ARB treatment for 16 wk. In addition, chymase-dependent Ang Ⅱ-forming activity significantly increased in the aorta, although these changes were inhibited only by ARB. ARB treatment was more effective compared with ACE-I treatment in reversing the changes in tissue Ang Ⅱ formation, particularly in the aorta, despite their similar antihypertensive effects.CONCLUSION: Chymase does not play a major role in maintaining blood pressure and tissue ACE and chymase are regulated in a tissue-dependent manner in 2K1 C hamster.

关键词： Chymase local renin angiotensin system angiotensinⅱ tissue remodeling hypertension

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Ocular renin-angiotensin system with special reference in the anterior part of the eye

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World Journal of Ophthalmology 2015年第3期5卷 110-124页

作者： Mervi Holappa Heikki Vapaatalo Anu Vaajanen BioMediTech University of Tampere Institute of Biomedicine PharmacologyUniversity of Helsinki Department of Ophthalmology Tampere University Hospital SILK Department of OphthalmologySchool of MedicineUniversity of Tampere

The renin-angiotensin system(RAS) regulates blood pressure(BP) homeostasis, systemic fluid volume and electrolyte balance. The RAS cascade includes over twenty peptidases, close to twenty angiotensin peptides and at least six receptors. Out of these, angiotensin Ⅱ, angiotensin converting enzyme 1 and angiotensin Ⅱ type 1 receptor(AngⅡ-ACE1-AT1R) together with angiotensin(1-7), angiotensin converting enzyme 2 and Mas receptor(Ang(1-7)-ACE2-Mas R) are regarded as the main components of RAS. In addition to circulating RAS, local RA-system exists in various organs. Local RA-systems are regarded as tissue-specific regulatory system accounting for local effects and long term changes in different organs. Many of the central components such as the two main axes of RAS: AngⅡ-ACE1-AT1 R and Ang(1-7)-ACE2-Mas R, have been identified in the human eye. Furthermore, it has been shown that systemic antihypertensive RAS- inhibiting medications lower intraocular pressure(IOP). These findings suggest the crucial role of RAS not only in the regulation of BP but also in the regulation of IOP, and RAS potentially plays a role in the development of glaucoma and antiglaucomatous drugs.

关键词： angiotensin converting enzyme 1 angiotensin converting enzyme 2 angiotensin converting enzyme-inhibitors angiotensinⅱ angiotensin(1-9) angiotensin(1-7) Glaucoma Intraocular pressure Renin-angiotensin system

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angiotensinⅱor epinephrine hemodynamic and metabolic responses in the liver of L-NAME induced hypertension and spontaneous hypertensive rats

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World Journal of Hepatology 2017年第17期9卷 781-790页

作者： Debora Conte Kimura Marcia Regina Nagaoka Durval Rosa Borges Maria Kouyoumdjian Department of Biochemistry Federal University of Sao PauloExperimental Hepatology Laboratory Department of Biosciences Federal University of Sao PauloExperimental Hepatology Laboratory Department of Medicine Federal University of Sao PauloExperimental Hepatology Laboratory

AIM To study hepatic vasoconstriction and glucose release induced by angiotensin(Ang)Ⅱ or Epi in rats with pharmacological hypertension and spontaneously hypertensive rat(SHR).METHODS Isolated liver perfusion was performed following portal vein and vena cava cannulation; AngⅡ or epinephrine(Epi) was injected in bolus and portal pressure monitored; glucose release was measured in perfusate aliquots. RESULTS The portal hypertensive response(PHR) and the glucose release induced by AngⅡ of L-NAME were similar to normal rats(WIS). On the other hand, the PHR inducedby Epi in L-NAME was higher whereas the glucose release was lower compared to WIS. Despite the similar glycogen content, glucose release induced by AngⅡ was lower in SHR compared to Wistar-Kyoto rats although both PHR and glucose release induced by Epi in were similar. CONCLUSION AngⅡ and Epi responses are altered in different ways in these hypertension models. Our results suggest that inhibition of NO production seems to be involved in the hepatic effects induced by Epi but not by AngⅡ; the diminished glucose release induced by AngⅡ in SHR is not related to glycogen content.

关键词： Epinephrine Liver perfusion Spontaneously hypertensive rat Glucose angiotensinⅱ L-NAME

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Protective Effects of Combination of Radix Astragali and Radix Salviae Miltiorrhizae on Kidney of Spontaneously Hypertensive Rats and Renal Intrinsic Cells

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Chinese Journal of Integrative Medicine 2020年第1期26卷 46-53页

作者： LI Wei JIANG Yue-hua WANG Yan ZHAO Meng HOU Guang-jian HU Hong-zhen ZHOU Le Department of Nephrology Affiliated Hospital of Shandong University of Traditional Chinese MedicineJinan 250011China Central Laboratory Affiliated Hospital of Shandong University of Traditional Chinese MedicineJinan 250011China First Clinical Medical College Shandong University of Traditional Chinese MedicineJinan 250355China

Objective: To evaluate the effects of combination of Radix Astragali(RA) and Radix Salviae Miltiorrhizae(RS) on kidney of spontaneously hypertensive rats(SHRs) and renal intrinsic cells. Methods: SHRs were intragastrically administrated with RA(5.09 g/kg) and RS(2.55 g/kg) either alone or with combination for 4 weeks;valsartan(13.35 mg/kg) was used as a positive control. Blood pressure and renal ultrasonography were monitored periodically. The biomarkers [microalbumin(m ALB), cystatin C, angiotensin Ⅱ(Ang Ⅱ), interleukin-1 beta(IL-1β), and β2-microglobulin(β2-Mg), etc.] in serum and urine were measured by enzyme-linked immunosorbent assay(ELISA). The protein expressions [phosphorylated adenosine 5’-monophosphate-activated protein kinase-α1(p-AMPKα1), sestrin-β, calcium/calmodulin-dependent protein kinase kinase-β(Ca MKK-β), phosphoinositide 3-kinases(PI3 K), serine-threonine protein kinase 1(AKT1), and vascular endothelial growth factor receptor 2(VEGFR2)] in renal cortex were determined by Western blot. In vitro, the hypertensive cellular model was established by applying 2×10^-6 mol/L Ang Ⅱ. The primary human podocytes, human glomerular endothelial cells(HRGECs), and human proximal tubular epithelial cells(HK-2 s) were pre-incubated with sulfotanshinone sodium(Tan, 10 μg/m L) and/or calycosin-7-O-β-D-glucoside(Cal, 5 μg/m L). The cellular viability and apoptosis were assayed by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide(MTT) and Annexin V/PI staining, respectively. The level of endothelial nitric oxide synthase(eNOS) in culture supernatant was determined by ELISA. Results: RA+RS significantly decreased the diastolic blood pressure, renal vascular resistance index, and parenchymal thickness, increased 24 h urinary volume as well as lowered the levels of urine m ALB and serum cystatin C, IL-1β and β2-Mg of SHRs(P<0.05 vs. SHRs). The decreased protein levels of p-AMPKα1, sestrinβ and Ca MKK-β and the increased protein levels of PI3 K, AKT1 and VEGFR2 in renal cortex of SHRs were normalized afte

关键词： hypertensive renal damage angiotensinⅱ human glomerular endothelial cells HK-2 Chinese medicine

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Clinical and biochemical indexes from 2019-nCoV infected patients linked to viral loads and lung injury

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Science China(Life Sciences) 2020年第3期63卷 364-374页

作者： Yingxia Liu Yang Yang Cong Zhang Fengming Huang Fuxiang Wang Jing Yuan Zhaoqin Wang Jinxiu Li Jianming Li Cheng Feng Zheng Zhang Lifei Wang Ling Peng Li Chen Yuhao Qin Dandan Zhao Shuguang Tan Lu Yin Jun Xu Congzhao Zhou Chengyu Jiang Lei Liu Shenzhen Key Laboratory of Pathogen and Immunity National Clinical Research Center for Infectious DiseaseState Key Discipline of Infectious DiseaseShenzhen Third People’s HospitalSecond Hospital Affiliated to Southern University of Science and TechnologyShenzhen 518112China Hefei National Laboratory for Physical Sciences at the Microscale and School of Life Sciences University of Science and Technology of ChinaHefei 230027China State Key Laboratory of Medical Molecular Biology Institute of Basic Medical SciencesChinese Academy of Medical SciencesDepartment of BiochemistryPeking Union Medical CollegeBeijing 100005China Institute of Microbiology Chinese Academy of SciencesBeijing 100101China Emergence Department Peking Union Medical College Hospital Beijing 100731China

The outbreak of the 2019-nCoV infection began in December 2019 in Wuhan,Hubei province,and rapidly spread to many provinces in China as well as other countries.Here we report the epidemiological,clinical,laboratory,and radiological characteristics,as well as potential biomarkers for predicting disease severity in 2019-nCoV-infected patients in Shenzhen,China.All 12 cases of the 2019-nCoV-infected patients developed pneumonia and half of them developed acute respiratory distress syndrome (ARDS).The most common laboratory abnormalities were hypoalbuminemia,lymphopenia,decreased percentage of lymphocytes (LYM) and neutrophils (NEU),elevated C-reactive protein (CRP) and lactate dehydrogenase (LDH),and decreased CD8 count.The viral load of 2019-nCoV detected from patient respiratory tracts was positively linked to lung disease severity.ALB,LYM,LYM (%),LDH,NEU (%),and CRP were highly correlated to the acute lung injury.Age,viral load,lung injury score,and blood biochemistry indexes,albumin (ALB),CRP,LDH,LYM (%),LYM,and NEU (%),may be predictors of disease severity.Moreover,the angiotensin Ⅱlevel in the plasma sample from 2019-nCoV infected patients was markedly elevated and linearly associated to viral load and lung injury.Our results suggest a number of potential diagnosis biomarkers and angiotensin receptor blocker (ARB) drugs for potential repurposing treatment of 2019-nCoV infection.

关键词： 2019-nCoV angiotensinⅱ ARDS

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Phosphoinositide-3 kinaseαmediates negative inotropy of angiotensin Ⅱ on mouse heart

Phosphoinositide-3 kinaseαmediates negative inotropy of ang...

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2008北京国际生理科学学术大会

作者： PATEl Mikin M WARD Michael.E BACKX Peter.H Department of Physiology H&S/Richard Lewar CenterUniversity of TorontoKing's College CircleTorontoOntarioCanadaM5S 1A8 Division of Critical Care ST.Michael's HospitalUniversity of TorontoCanada

The effect of angiotensinⅱ(AngⅡ),an important regulator of cardiovascular system,on cardiac contractility is not clear.In Langendorff mouse hearts,perfused at constant pressure,AngⅡ(3 nmol/L)transiently decreased(P0.05,n=5)in hearts from mice lacking PI3Kγ.AngⅡ-induced negative inotropy was not affected(P=0.103,n=4)in hearts from mice with genetic deletion of the NADPH oxidase subunit p47, suggesting a NADPH oxidase-independent pathway.Neither p38 MAP kinase inhibition with 1μmol/L SB-202190 (IC=50 nmol/L for p38αand 100 nmol/L for p38β)nor epidermal growth factor receptor(EGFR)inhibition with 1μmol/L AG 1478(IC=3 nmol/L)affected(P>0.05,n=5)AngⅡ-induced negative inotropy in hearts.The results suggest that AngⅡhas both coronary artery-dependent and-independent

关键词： angiotensinⅱ phosphoinositide-3 kinases cardiac contraction

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Combined effects of hypertension and angiotensin Ⅱ on the risk of coronary heart disease:a population-based prospective cohort study among Inner Mongolians in China

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中国循环杂志 2018年第S1期33卷 111-111页

作者： Yiting Zhou Department of Epidemiology and Biostatistics School of Pubilc HealthMedical College of Soochow UniversitySuzhouJiangsuChina

Objective To investigate the combined effects of hypertension and angiotensinⅱon the risk of coronary heart disease(CHD)on the basis of a 10-year prospective study in an Inner Mongolian population of China.Methods Based on a cross-sectional survey,a prospective cohort study was conducted from June 2003 to July 2012 among 2,530 Mongolian people.

关键词： effects hypertension angiotensinⅱ coronary heart disease(CHD)

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