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Protective Effect and Mechanism of Kuntai Capsule on angiotensin II-Induced Hypertension in Ovariectomized Rats

Chinese Journal of Integrative Medicine 2023年第6期29卷 526-533页

作者： GE Xiao-fen LI Sha-sha LIU Yan-hua LU Mei-qiu SU Hui-na YANG Xin SUN Xiao-wan Department of Obstetrics and Gynecology Peking University People's HospitalBeijing(100044)China Department of Obstetrics and Gynecology Dongying People's HospitalDongyingShandong Province(257000)China

Objective To explore the protective effect and mechanism of Kuntai(KT)Capsule on angiotensin II(Ang ii)-induced hypertension in ovariectomized(OVX)rats.Methods Fifty-four rats were randomly divided into 6 groups according to a random number table,9 in each group:control,OVX sham+Ang ii,OVX,OVX+Ang ii,OVX+Ang ii+E2,and OVX+Ang ii+KT.OVX rats model was constructed by retroperitoneal bilateral ovariectomy.After 4 weeks of pretreatment with KT Capsule[0.8 g/(kg·d)and 17-β-estradiol(E2,1.2 mg/(kg·d)]respectively,Ang ii was injected into a micro-osmotic pump with a syringe to establish a hypertensive rat model.Blood pressure of rat tail artery was measured in a wake state of rats using a non-invasive sphygmomanometer.Blood pressure changes were compared between the intervention groups(OVX+Ang ii+KT,OVX+Ang ii+E2)and the negative control group(OVX+Ang ii).Serum malondialdehyde(MDA)level and superoxide dismutase(SOD)activity were detected respectively.The expressions of oxidative stress-related protein superoxide dismutase2(SOD2)and anti-thioredoxin(TRX),autophagy marker protein[beclin1,light chain(LC)3 ii/I ratio and autophagy canonical pathway protein phosphatidylinositol 3-kinase(PI3K)/serine/threonine kinase(AKT)-mammalian target of rapamycin(mTOR)]were evaluated by Western blotting.Results Compared with the OVX+Ang ii group,the systolic blood pressure of OVX+Ang ii+KT group was significantly lowered(Pii+KT group compared with the OVX+Ang ii group(Pii+KT group,respectively(Pii group,the levels of cardiac proteins beclin-1 and LC3ii/LC3 I in OVX+Ang ii+KT group were also up-regulated(Pii-induced OVX rats by inhibiting

关键词： Kuntai Capsule Chinese medicine perimenopausal hypertension angiotensin II

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Biological function of miRNA-145-5p in angiotensin II induced renal inflammation

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BIOCELL 2024年第4期48卷 601-611页

作者： BIN LI YUCHENG SHENG XIAOYING XU SHENGCUN WANG HONGYAN SONG JINGYUAN LI HAONAN JI QINGHUA WANG XIAODI ZHOU LONGJU QI Department of Pediatrics Affiliated Hospital of Nantong UniversityNantong226001China Department of Science and Education Affiliated Nantong Hospitalof Nantong UniversityNantong226001China Laboratory Animal Center Nantong UniversityNantong226001China Department of Gynecology and Obstetrics and Department of Oncology Hai’an Hospital Affiliated to Nantong UniversityNantong226600China

Objective:Chronic kidney disease(CKD)is a progressive disorder characterized by intricate structural and functional alterations in the kidneys,attributable to diverse causative factors.Notably,the therapeutic promise of miR-145-5p in addressing renal pathologies has been discerned.This investigation seeks to elucidate the functional role of miR-145-5p in injured kidneys by subjecting human glomerular mesangial cells(HGMCs)to stimulation with angiotensin II(Angii).Materials and Methods:Cellular viability and the levels of inﬂammatory mediators were evaluated utilizing Cell Counting Kit-8(CCK-8),quantitative real-time polymerase chain reaction(qRT-PCR),and western blot methodologies,both in the presence of Angii incubation and in scenarios of miR-145p overexpression and downregulation.Furthermore,the cell cycle dynamics were elucidated through Fluorescence-activated Cell Sorting(FACS)analysis.Results:Angii incubation induced an upregulation of miR-145-5p and inﬂammatory factors including Intercellular Adhesion Molecule 1(ICAM-1),Interleukin 6(IL-6),Interleukin 8(IL-8),and Interleukin 1β(IL-1β).Additionally,it elevated the expression of Cyclin A2,Cyclin D1,and the G2/M cell cycle ratio.Conversely,inhibition of miR-145-5p heightened the levels of inﬂammatory factors and cell cycle regulators induced by Angii incubation.Reduced expression of miR-145-5p correlated with a downregulation of Interleukin 10(IL-10)expression,concurrently promoting HGMC proliferation under Angii stimulation.Moreover,ectopic miR-145-5p expression demonstrated a reduction in inﬂammatory factors,cell cyclin regulators,G2/M cell cycle ratio,and overall proliferation.Conclusion:MiR-145-5p exhibited inhibitory effects on the inﬂammatory response and proliferation induced by angiotensin II in HGMCs,showcasing its potential as a therapeutic avenue for the treatment of kidney injury.

关键词： miR-145-5p Kidney angiotensin II Cell cycle Inflammation

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F：lole of Jaggedl-Heyl Signal in angiotensin II-induced Impairment of Myocardial Angiogenesis

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Chinese Medical Journal 2017年第3期130卷 328-333页

作者： Ai-Li Guan Tao He Yi-Bing Shao Yi-Fan Chi Hong-Yan Dai Yan Wang Li Xu Xuan Yang Hua-Min Ding Shang-Lang Cai Department of Cardiology Heart Center Qingdao Municipal Hospital Qingdao University Qingdao Shandong 266071 China Department of Cardiology Affiliated Hospital of Qingdao University Qingdao Shandong 266005 China

Background： angiotensin II （Ang ll） is a major contributor to the development of heart failure. However, the molecular and cellular mechanisms that underlie this process remain elusive. Inadequate angiogenesis in the myocardium leads to a transition from cardiac hypertrophy to dysfunction, and our previous study showed that Ang ii significantly impaired the angiogenesis response. The current study was designed to examine the role of Jaggedl-Notch signaling in the effect of Ang ii during impaired angiogenesis and cardiac hypertrophy. Methods： Ang ii was subcutaneously infused into 8-week-old male C57BL/6 mice at a dose of 200 ng·kg^-1·min^-1 for 2 weeks using Alzet micro-osmotic pumps. N-[N-（3, 5-difluorophenacetyl）-L-alanyl]-S-phenylglycine tert-butyl ester （DAPT）, a y-secretase inhibitor, was injected subcutaneously during Ang ii infusion at a dose of 10.0 mg.kg^-1·d^-1. Forty mice were divided into four groups （n = 10 per group）： control group; Ang 11 group, treated with Ang I1; DAPT group, treated with DAPT; and Ang ii ＋ DAPT group, treated with both Ang I1 and DAPT. At the end of experiments, myocardial （left ventricle [LV]） tissue from each experimental group was evaluated using immunohistochemistry, Western blotting, and real-time polymerase chain reaction, Data were analyzed using one-way analysis of variance test followed by the least significant difference method or independent samples t-test. Results： Ang ii treatment significantly induced cardiac hypertrophy and impaired the angiogenesis response compared to controls, as shown by hematoxylin and eosin （HE） staining and immunohistochemistry fbr CD31, a vascular marker （P 〈 0.05 for both）. Meanwhile, Jaggedl protein was significantly increased, but gene expression for both Jagl and Heyl was decreased in the LV following Ang ii treatment, compared to that in controls （relative ratio for Jag1 gene： 0.45 ± 0.13 vs. 0.84± 0.15; relative ratio for Heyl gene： 0.51 ± 0.08 vs. 0.91 ± 0.09; P 〈 0.05）. All these cellular and molecular effects induced by Ang ii in

关键词： y-secretase angiotensin II Cardiac Angiogenesis Hey Jaggedl

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Human paraoxonase gene cluster overexpression alleviates angiotensin II-induced cardiac hypertrophy in mice

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Science China(Life Sciences) 2016年第11期59卷 1115-1122页

作者： Jian-Fei Pei Yun-Fei Yan Xiaoqiang Tang Yang Zhang Shen-Shen Cui Zhu-Qin Zhang Hou-Zao Chen De-Pei Liu State Key Laboratory of Medical Molecular Biology Department of Biochemistry and Molecular Biology Institute of Basic Medical SciencesChinese Academy of Medical Sciences & Peking Union Medical College

Cardiac hypertrophy is the strongest predictor of the development of heart failure, and anti-hypertrophic treatment holds the key to improving the clinical syndrome and increasing the survival rates for heart failure. The paraoxonase(PON) gene cluster(PC) protects against atherosclerosis and coronary artery diseases. However, the role of PC in the heart is largely unknown. To evaluate the roles of PC in cardiac hypertrophy, transgenic mice carrying the intact human PON1, PON2, and PON3 genes and their flanking sequences were studied. We demonstrated that the PC transgene(PC-Tg) protected mice from cardiac hypertrophy induced by Ang ii; these mice had reduced heart weight/body weight ratios, decreased left ventricular wall thicknesses and increased fractional shortening compared with wild-type(WT) control. The same protective tendency was also observed with an Apoe^(-/-)background. Mechanically, PC-Tg normalized the disequilibrium of matrix metalloproteinases(MMPs)/tissue inhibitors of MMPs(TIMPs) in hypertrophic hearts, which might contribute to the protective role of PC-Tg in cardiac fibrosis and, thus, protect against cardiac remodeling. Taken together, our results identify a novel anti-hypertrophic role for the PON gene cluster, suggesting a possible strategy for the treatment of cardiac hypertrophy through elevating the levels of the PON gene family.

关键词： cardiac hypertrophy fibrosis paraoxonase gene cluster angiotensin II

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Sulfur Dioxide Inhibits Extracellular Signal-regulated Kinase Signaling to Attenuate Vascular Smooth Muscle Cell Proliferation in angiotensin II-induced Hypertensive Mice

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Chinese Medical Journal 2016年第18期129卷 2226-2232页

作者： Hui-Juan Wu Ya-Qian Huang Qing-Hua Chen Xiao-Yu Tian Jia Liu Chao-Shu Tang Hong-Fang Jin Jun-Bao Du Department of Pediatrics Peking University First Hospital Beijing 100034 China Department of Physiology and Pathophysiology Peking University Health Science Centre Beijing 100191 China Key Laboratory of Molecular Cardiology Ministry of Education Beijing 100091 China

Background： Clarifying the mechanisms underlying vascular smooth muscle cell （VSMC） proliferation is important for the prevention and treatment of vascular remodeling and the reverse of hyperplastic lesions. Previous research has shown that the gaseous signaling molecule sulfur dioxide （SO2） inhibits VSMC proliferation, but the mechanism for the inhibition of the angiotensin Ⅱ （Angll）-induced VSMC proliferation by SO, has not been fully elucidated. This study was designed to investigate if SO2 inhibited VSMC proliferation in mice with hypertension induced by Angll. Methods： Thirty-six male C57 mice were randomly divided into control, Angll, and Angll ＋ SO2 groups. Mice in Angll group and Angl I ＋ SO2 group received a capsule-type Angll pump implanted under the skin of the back at a slow-release dose of 1000 ng-kg^-1min In addition, mice in Angll ＋ SO2 received intraperitoneal injections of SO., donor. Arterial blood pressure of tail artery was determined. The thickness of the aorta was measured by elastic fiber staining, and proliferating cell nuclear antigen （PCNA） and phosphorylated-extracellular signal-regulated kinase （P-ERK） were detected in aortic tissues. The concentration of SO~ in serum and aortic tissue homogenate supernatant was measured using high-performance liquid chromatography with fluorescence determination. In the in vio＇o study, VSMC of A7R5 cell lines was divided into six groups： control, Angll, Angll ＋ SO2 PD98059 （an inhibitor of ERK phosphorylation）, Angll ＋ PD98059, and Angll ＋ SO, ＋ PD98059. Expression of PCNA, ERK, and P-ERK was determined by Western blotting. Results： In animal experiment, compared with the control group, Angll markedly increased blood pressure （P 〈 0.01 ） and thickened the aortic wall in mice （P 〈 0.05） with an increase in the expression of PCNA （P 〈 0.05）. SO2 however, reduced the systemic hypertension and the wall thickness induced by AnglI （P 〈 0.05）. It inhibited the increased expression of PCNA and P-ERK induced by AnglI （P 〈 0.05）. In cell experiment, PD98059, an

关键词： angiotensin II Hypertension Proliferation Sulfur Dioxide Vascular Smooth Muscle Cell

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Impacts of angiotensin II on retinal artery changes in apolipoprotein E deficient mice

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International Journal of Ophthalmology(English edition) 2024年第1期17卷 16-24页

作者： Li-Hui Meng Shi-Yu Cheng He Chen Yue-Lin Wang Wen-Fei Zhang Huan Chen Xin-Yu Zhao You-Xin Chen Department of Ophthalmology Peking Union Medical College HospitalChinese Academy of Medical SciencesBeijing 100730China Key Lab of Ocular Fundus Diseases Chinese Academy of Medical SciencesBeijing 100730China

AIM:To investigate the impacts of angiotensin II(Ang ii)on retinal artery changes in apolipoprotein E deficient(apoE^(-/-))mice.METHODS:ApoE^(-/-)male mice were infused by minipumps with Ang ii at 1000 ng/kg·min(Ang ii group)or saline(control group)for 28d.They were underwent ophthalmic fundus examination on day 0,14,and 28 of infusion.Histopathologic examination,ribonucleic acid(RNA)sequencing and local Ang ii measurement of retinas were conducted.RESULTS:Ophthalmic fundus examination showed Ang ii infusion promoted the formation of retinal arterial aneurysm-like lesions on day 28.Optical coherence tomography revealed the ganglion cell and inner plexiform layer(GCIPL)thickness in the control group was significantly thinner than that in Ang ii group(Pii group.Transmission electron microscopy showed Ang ii infusion caused aggravation of atherosclerotic lesions,including increased swelling,roughness,disorganization of the retinal vasculature,and vacuoles formation.RNA-sequencing and gene ontology enrichment analysis demonstrated that the structure and function of cellular membrane might be disturbed and visual function might be compromised by Ang ii.The local level of Ang ii was higher in Ang ii infusion group but did not show significant differences compared to the control group(P=0.086).CONCLUSION:Ang ii infusion promotes the formation of retinal arterial aneurysm-like lesions in apoE^(-/-)mice,causing aggravation of atherosclerotic lesions,more severe disorganization of the retinal vasculature and disturbance of the cellular membrane.

关键词： angiotensin II retinal artery aneurysm apoE^(-/-)mice

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MicroRNA-155 mediates endogenous angiotensin II type 1 receptor regulation:implications for innovative type 2 diabetes mellitus management

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世界糖尿病杂志:英文版(电子版) 2023年第9期14卷 1334-1340页

作者： Konstantinos I Papadopoulos Alexandra Papadopoulou Tar-Choon Aw Department of R&D THAI StemLifeBangkok 10310Thailand Occupational and Environmental Health Services Feelgood LundLund 223-63SkåneSweden Department of Laboratory Medicine Changi General HospitalSingapore 529889SingaporeSingapore Department of Medicine National University of SingaporeSingapore 119228SingaporeSingapore

Type 2 diabetes mellitus(T2DM)is a lifelong condition and a threat to human health.Thorough understanding of its pathogenesis is acutely needed in order to devise innovative,preventative,and potentially curative pharmacological interventions.MicroRNAs(miRNA),are small,non-coding,one-stranded RNA molecules,that can target and silence around 60%of all human genes through translational repression.MiR-155 is an ancient,evolutionarily well-conserved miRNA,with distinct expression profiles and multifunctionality,and a target repertoire of over 241 genes involved in numerous physiological and pathological processes including hematopoietic lineage differentiation,immunity,inflammation,viral infections,cancer,cardiovascular conditions,and particularly diabetes mellitus.MiR-155 Levels are progressively reduced in aging,obesity,sarcopenia,and T2DM.Thus,the loss of coordinated repression of multiple miR-155 targets acting as negative regulators,such as C/EBPβ,HDAC4,and SOCS1 impacts insulin signaling,deteriorating glucose homeostasis,and causing insulin resistance(IR).Moreover,deranged regulation of the renin angiotensin aldosterone system(RAAS)through loss of angiotensin II Type 1 receptor downregulation,and negated repression of ETS-1,results in unopposed detrimental angiotensin II effects,further promoting IR.Finally,loss of BACH1 and SOCS1 repression abolishes cytoprotective,anti-oxidant,anti-apoptotic,and anti-inflam matory cellular pathways,and promotesβ-cell loss.In contrast to RAAS inhibitor treatments that further decrease already reduced miR-155 Levels,strategies to increase an ailing miR-155 production in T2DM,e.g.,the use of metformin,mineralocorticoid receptor blockers(spironolactone,eplerenone,finerenone),and verapamil,alone or in various combinations,represent current treatment options.In the future,direct tissue delivery of miRNA analogs is likely.

关键词： angiotensin II angiotensin II type 1 receptor Arginase 2 L-type calcium channel Mineralocorticoid receptor MiRNA-155 Renin-angiotensin aldosterone system Type 1/2 diabetes mellitus Verapamil

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Effects of chronic peripheral pretreatment with an angiotensin II type-1 receptor blocker on apoptosis-related molecules in rats with cerebral ischemia/reperfusion injury

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Neural Regeneration Research 2010年第15期5卷 1150-1155页

作者： Jingping Shi Jingde Dong Jie Lu Yingdong Zhang Department of Neurology Nanjing Brain Hospital Nanjing Medical University Nanjing 210029 Jiangsu Province China

Chronic systemic treatment with blockers of angiotensin II type-1 （AT1） receptors inhibits ischemia-induced apoptosis and reduces ischemic neuronal damage. However, the molecular mechanisms of AT1 receptor blockers in modulating neuronal apoptosis remain poorly understood. Pretreatment with irbesartan significantly suppressed cell apoptosis at 1-7 days following cerebral ischemia/reperfusion, increased levels of brain-derived neurotrophic factor, and elevated the ratios of Bcl-2/Bax and phosphorylated cyclic adenosine monophosphate response element-binding protein （pCREB）/CREB in the ischemic cortex at 1 day after reperfusion, as well as suppressing caspase-3 activation. Cerebral ischemia increased the mRNA expression of AT1 and AT2 receptors in the ischemic cortex, whereas irbesartan blocked this increase in AT1 expression but potentiated the expression of AT2. Therefore, this AT1 receptor blocker was neuroprotective by increasing the ratios of Bcl-2/Bax and pCREB/CREB, increasing brain-derived neurotrophic factor levels, inhibiting caspase-3 activation, and modulating AT receptor expression.

关键词： angiotensin II cerebral ischemia receptor apoptosis brain-derived neurotrophic factor brain injury neural regeneration

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Effect of angiotensin II receptor 1 antisense oligodoexynucleotides on physiological and pathophysiological growth of cardiomyocytes

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Acta Pharmacologica Sinica 2004年第5期25卷 19-27页

作者： Ying WANG2, Jin-ming WANG2, Shu-xun Yan3, Ming-jiang LI2,4, Jian-jun LI22Department of Cardiology, Renmin Hospital, Wuhan University, Wuhan 430060, China 3Hubei College of Traditional Chinese Medicine, Wuhan 430061,China Department of Cardiology Renmin Hospital Wuhan University Wuhan 430060 Hubei College of Traditional Chinese Medicine Wuhan 430061

AIM: To evaluate the role of angiotensin II receptor 1 antisense oligodexynucleotides (AT1R-AS-ODNs) on physi-ological and pathophysiological growth of cardiomyocytes from normotensive rats. METHODS: Cardiomyocyteswere transfected with AT1R-AS-ODNs (200 nmol/L) followed by treatment with or without angiotensin II (1 mol/L).In situ hybridization and Western blot were used for AT1R mRNA and protein detection, respectively. c-Jun N-terminal protein kinase (JNK) activity was characterized by immune complex kinase assay. c-Jun protein expres-sion was examined by immunocytochemistry. DNA content was detected by flow cytometric assay. Atrial natri-uretic factor (ANF) expression was identified by radioimmunoassay. RESULTS: Treatment with AT1R-AS-ODNsfor 24 h resulted in 51.2 % decrease in AT1R mRNA and 60.7 % in protein (Pangiotensin II for 30 min, both p46JNK and p54JNK wererobustly activated. By 2 h, c-Jun protein expression was increased. By 24 h, angiotensin II caused a markedincrease both in G0/G1 and G2/M DNA content, and increased ANF expression by 1.8-fold. All these were inhibitedby AT1R-AS-ODNs pretreatment. In contrast, sense sequence was ineffective. CONCLUSION: Decrease ofAT1R expression by AS-ODNs did not interfere with normal growth, but protected cardiomyocytes from angio-tensin ii-dependent pathophysiological growth.

关键词： antisense oligodeoxynucleotides angiotensin receptors angiotensin II myocardium hypertrophy mitogen-activated protein kinases

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angiotensin II stimulates phosphorylation of 4E-binding protein 1 and p70 S6 kinase in cultured vascular smooth muscle cells

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Acta Pharmacologica Sinica 2004年第5期25卷 51-54页

作者： Na LI1, Ke-gui WU, Xiang-yu WANG, Liang-di XIE, Chang-sheng XU, Hua-jun WANGHypertension Institute, First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China Hypertension Institute First Affiliated Hospital Fujian Medical University Fuzhou 350005

AIM: To examine the regulatory effects of angiotensin II (Ang ii) on the phosphorylation of 4E-binding protein 1(4E-BP1) and p70 S6 kinase in cultured vascular smooth muscle cells (VSMC), and the contribution ofphosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) signaling pathway in this process. METHODS: VSMCobtained from rat thoracic aortas were cultured. The phosphorylation of 4E-BP1 and p70 S6 kinase was detectedby immunoblotting. RESULTS: Ang ii significantly increased the phosphorylation of 4E-BP1 and p70 S6 kinase,with the peaks occurring at, respectively, 10 min and 30 min, after stimulation with Ang ii. The stimulatory effectof Ang ii on 4E-BP1 and p70 S6 kinase phosphorylation was abrogated by Ang ii type 1 receptor (AT1 receptor)antagonist losartan, and suppressed by PI3K inhibitor LY294002 in a concentration-dependent manner.CONCLUSION: Ang ii treatment of VSMC induces the phosphorylation of 4E-BP1 and p70 S6 kinase via AT1receptor, and PI3K signaling pathway is involved in this process.

关键词： angiotensin II 4E-binding protein 1 p70 S6 kinase phosphatidylinositol 3-kinase vascular smoothmuscle

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