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Article: Effects of Xin-Ji-Er-Kang on Anticardiovascular Remodeling in

Wang, Li / Cai, Guo-Wei / Ding, Ling / Hu, Juan / Zhang, Yong-Xue / Huang, Guang-Yao / Cheng, Pan / Gao, Shan

Evidence-based complementary and alternative medicine : eCAM

2018 Volume 2018, Page(s) 8067361

Abstract: Background: Xin-Ji-Er-Kang (XJEK) shows protective effects on the myocardial ischemic diseases ...

Abstract	Background: Xin-Ji-Er-Kang (XJEK) shows protective effects on the myocardial ischemic diseases in our previous reports. We hypothesized that XJEK may exert preventing effects on Methods: After treatment with XJEK for four weeks, cardiac function and cardiovascular pathology changes were evaluated. Then, endothelial-dependent vascular relaxation and serum NO, eNOS, AMDA, SOD, MDA content, and cardiac tissue eNOS expression were detected. Results: The hypertensive mice displayed distinct cardiovascular remodeling including increased HW/BW index (4.7 ± 0.33 versus 5.2 ± 0.34), cross-section area, and collagen deposition. In addition, ED was found manifested by decreased serum NO (20.54 ± 8.05 versus 6.29 ± 2.33), eNOS (28.34 ± 2.36 versus 20.37 ± 2.30), content, and decreased eNOS expression in cardiac tissue and damaged endothelium-dependent diastolic function. Moreover, OS was detected confirmed by decreased SOD activity and increased MDA content in serum. However, treatment with XJEK for 4 wk could reverse cardiovascular remodeling (HW/BW index normalized from 5.2 ± 0.34 to 4.59 ± 0.25), ameliorate and preserve endothelial function (NO: 16.67 ± 7.24 versus 6.29 ± 2.33; eNOS: 16.67 ± 7.24 versus 6.29 ± 2.33), and suppress OS. Conclusion: XJEK has protective effects against cardiovascular remodeling in L-NAME induced hypertensive mice.
Language	English
Publishing date	2018-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2171158-6
ISSN	1741-4288 ; 1741-427X
ISSN (online)	1741-4288
ISSN	1741-427X
DOI	10.1155/2018/8067361
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Xin-Ji-Er-Kang protects myocardial and renal injury in hypertensive heart failure in mice.

Ling, Xin-Xin / Chen, Hua / Fu, Bei-Bei / Ruan, Cheng-Shao / Pana, Ming / Zhou, Kai / Fang, Zhi-Rui / Shao, Jun-Tang / Zhu, Feng-Qin / Gao, Shan

Phytomedicine : international journal of phytotherapy and phytopharmacology

2021 Volume 91, Page(s) 153675

Abstract: Background: Xin-Ji-Er-Kang (XJEK) as a herbal formula of traditional Chinese medicine (TCM) has ...

Abstract	Background: Xin-Ji-Er-Kang (XJEK) as a herbal formula of traditional Chinese medicine (TCM) has shown the protective effects on myocardial function as well as renal function in mouse models of myocardial infarction. Hypothesis/purpose: We investigated the effects of XJEK on cardiovascular- and renal-function in a heart failure mouse model induced by high salt (HS) and the associated mechanisms. Study design: For the purpose of assessing the effects of XJEK on a hypertensive heart failure model, mice were fed with 8% high salt diet. XJEK was administered by oral gavage for 8 weeks. Cardiovascular function parameters, renal function associated biomarkers and XJEK's impact on renin-angiotensin-aldosterone system (RAAS) activation were assessed. To determine the underlying mechanism, the calpain1/junctophilin-2 (JP2)/sarcoplasmic reticulum Ca Results: Mice on HS-diet exhibited hypertensive heart failure along with progressive kidney injury. Similar to fosinopril, XJEK ameliorated hypertension, cardiovascular-and renal- dysfunction in mice of HS-diet group. XJEK inhibited HS-induced activation of RAAS and reversed the abnormal expression pattern of calpain1and JP2 protein in heart tissues. XJEK significantly improved cell viability of angiotensin II-challenged AC16 cells. Moreover, XJEK's impact on calpain1/JP2 pathway was partly diminished in AC16 cells transfected with calpastatin siRNA. Conclusion: XJEK was found to exert cardiovascular- and renal protection in HS-diet induced heart failure mouse model. XJEK inhibited HS-diet induced RAAS activation by inhibiting the activity and expression of calpain1 and protected the junctional membrane complex (JMC) in cardiomyocytes.
MeSH term(s)	Animals ; Blood Pressure ; Calpain ; Drugs, Chinese Herbal/pharmacology ; Heart Failure/drug therapy ; Hypertension/drug therapy ; Kidney/drug effects ; Kidney/physiology ; Membrane Proteins ; Mice ; Muscle Proteins ; Oxidative Stress ; Sarcoplasmic Reticulum Calcium-Transporting ATPases ; Signal Transduction
Chemical Substances	Drugs, Chinese Herbal ; Membrane Proteins ; Muscle Proteins ; junctophilin-2 protein, mouse ; xin-ji-er-kang ; Calpain (EC 3.4.22.-) ; Capn1 protein, mouse (EC 3.4.22.52) ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8) ; Atp2a2 protein, mouse (EC 7.2.2.10)
Language	English
Publishing date	2021-07-18
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2021.153675
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Xin-Ji-Er-Kang Alleviates Myocardial Infarction-Induced Cardiovascular Remodeling in Rats by Inhibiting Endothelial Dysfunction.

Cheng, Pan / Lian, Feng-Zhen / Wang, Xiao-Yun / Cai, Guo-Wei / Huang, Guang-Yao / Chen, Mei-Ling / Shen, Ai-Zong / Gao, Shan

BioMed research international

2019 Volume 2019, Page(s) 4794082

Abstract: The present study was designed to elucidate the beneficial effects of XJEK on myocardial infarction (MI) in rats, especially through the amelioration of endothelial dysfunction (ED). 136 Sprague-Dawley rats were randomized into 13 groups: control group ... ...

Abstract	The present study was designed to elucidate the beneficial effects of XJEK on myocardial infarction (MI) in rats, especially through the amelioration of endothelial dysfunction (ED). 136 Sprague-Dawley rats were randomized into 13 groups: control group for 0wk (
MeSH term(s)	Animals ; Drugs, Chinese Herbal/pharmacology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Endothelium, Vascular/physiopathology ; Male ; Myocardial Infarction/drug therapy ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Myocardial Infarction/physiopathology ; Rats ; Rats, Sprague-Dawley ; Vascular Remodeling/drug effects ; Ventricular Remodeling/drug effects
Chemical Substances	Drugs, Chinese Herbal ; xin-ji-er-kang
Language	English
Publishing date	2019-06-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2019/4794082
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Xin-Ji-Er-Kang protects myocardial and renal injury in hypertensive heart failure in mice

Ling, Xin-xin / Chen, Hua / Fu, Bei-bei / Ruan, Cheng-shao / Pana, Ming / Zhou, Kai / Fang, Zhi-rui / Shao, Jun-tang / Zhu, Feng-qin / Gao, Shan

Phytomedicine. 2021 Oct., v. 91

2021

Abstract: Xin-Ji-Er-Kang (XJEK) as a herbal formula of traditional Chinese medicine (TCM) has shown ...

Abstract	Xin-Ji-Er-Kang (XJEK) as a herbal formula of traditional Chinese medicine (TCM) has shown the protective effects on myocardial function as well as renal function in mouse models of myocardial infarction.We investigated the effects of XJEK on cardiovascular- and renal-function in a heart failure mouse model induced by high salt (HS) and the associated mechanisms.For the purpose of assessing the effects of XJEK on a hypertensive heart failure model, mice were fed with 8% high salt diet. XJEK was administered by oral gavage for 8 weeks. Cardiovascular function parameters, renal function associated biomarkers and XJEK's impact on renin-angiotensin–aldosterone system (RAAS) activation were assessed. To determine the underlying mechanism, the calpain1/junctophilin-2 (JP2)/sarcoplasmic reticulum Ca²⁺ ATPase (SERCA2a) pathway was further studied in AC16 cells after angiotensin II-challenge or after calpastatin small interfering RNA (siRNA) transfection.Mice on HS-diet exhibited hypertensive heart failure along with progressive kidney injury. Similar to fosinopril, XJEK ameliorated hypertension, cardiovascular-and renal- dysfunction in mice of HS-diet group. XJEK inhibited HS-induced activation of RAAS and reversed the abnormal expression pattern of calpain1and JP2 protein in heart tissues. XJEK significantly improved cell viability of angiotensin II-challenged AC16 cells. Moreover, XJEK's impact on calpain1/JP2 pathway was partly diminished in AC16 cells transfected with calpastatin siRNA.XJEK was found to exert cardiovascular- and renal protection in HS-diet induced heart failure mouse model. XJEK inhibited HS-diet induced RAAS activation by inhibiting the activity and expression of calpain1 and protected the junctional membrane complex (JMC) in cardiomyocytes.
Keywords	Oriental traditional medicine ; adenosinetriphosphatase ; biomarkers ; calcium ; calpastatin ; cardiomyocytes ; cell viability ; diet ; heart failure ; hypertension ; kidneys ; mice ; renal function ; renoprotective effect ; reticulum
Language	English
Dates of publication	2021-10
Publishing place	Elsevier GmbH
Document type	Article
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2021.153675
Database	NAL-Catalogue (AGRICOLA)

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Article: Protective effect of Xin-Ji-Er-Kang on cardiovascular remodeling in high salt-induced hypertensive mice.

Huang, Guangyao / Cheng, Pan / Ding, Ling / Wang, Li / Hu, Juan / Zhang, Yongxue / Cai, Guowei / Chen, Meiling / Shen, Aizong / Gao, Shan

Experimental and therapeutic medicine

2018 Volume 17, Issue 3, Page(s) 1551–1562

Abstract: The aim of the present study was to investigate the effects of Xin-Ji-Er-Kang (XJEK) on high salt ...

Abstract	The aim of the present study was to investigate the effects of Xin-Ji-Er-Kang (XJEK) on high salt-induced hypertensive mice. Mice with high-salt diet-induced hypertension were divided into four groups: Control (standard diet alone for 8 weeks), model (diet containing 8% NaCl for 8 weeks and intragastric administration of distilled water for the last 4 weeks), XJEK + high-salt-treated (diet containing 8% NaCl for 8 weeks and intragastric administration of XJEK for the last 4 weeks) and irbesartan + high-salt-treated (diet containing 8% NaCl for 8 weeks with intragastric administration of irbesartan for the last 4 weeks). The hemodynamic index and cardiac pathological changes in the hypertensive mice were then examined. An aortic ring apparatus was used to detect acetylcholine-dependent endothelium relaxation function. Colorimetric analysis was applied to determine serum nitric oxide (NO), superoxide dismutase activity and malondialdehyde content; ELISA was employed to measure brain natriuretic peptide, serum angiotensin II (Ang II), endothelin-1 content and aldosterone; and immunohistochemistry was used to detect the expression of endothelial nitric oxide synthase (eNOS), interleukin (IL)-1β, IL-10 and tumor necrosis factor (TNF)-α in cardiac tissues. XJEK improved the heart systolic and diastolic function, ameliorated hemodynamic parameters and cardiovascular remodeling indices, blunted the cardiac pathological changes and improved endothelial dysfunction (ED) via boosting eNOS activity, promoting NO bioavailability and decreasing serum Ang II content. Furthermore, treatment with XJEK inhibited the increase of IL-1β and TNF-α expression and the decrease of IL-10 expression in cardiac tissues, and ameliorated oxidative stress status. Therefore, XJEK exerted protective effects against high salt-induced hypertension and cardiovascular remodeling in mice via improving ED, restoring pro- and anti-inflammatory factor balance and decreasing oxidative stress.
Language	English
Publishing date	2018-12-17
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2683844-8
ISSN	1792-1015 ; 1792-0981
ISSN (online)	1792-1015
ISSN	1792-0981
DOI	10.3892/etm.2018.7105
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Xin-Ji-Er-Kang ameliorates kidney injury following myocardial infarction by inhibiting oxidative stress via Nrf2/HO-1 pathway in rats.

Lian, Feng-Zhen / Cheng, Pan / Ruan, Cheng-Shao / Ling, Xin-Xin / Wang, Xiao-Yun / Pan, Ming / Chen, Mei-Ling / Shen, Ai-Zong / Gao, Shan

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2019 Volume 117, Page(s) 109124

Abstract: ... to investigate the effects of Xin-Ji-Er-Kang (XJEK) on kidney injury and renal oxidative stress. In addition ...

Abstract	Aim: Cardiovascular diseases, such as coronary heart disease and myocardial infarction (MI) are currently considered as the leading causes of death and disability. The aim of the present study is to investigate the effects of Xin-Ji-Er-Kang (XJEK) on kidney injury and renal oxidative stress. In addition, the associated mechanism involved in these processes was examined in an MI model, and particularly focused on the nuclear factor erythroid 2-related factor (NRF2)/heme oxygenase-1 (HO-1) pathway. Materials and methods: A total of 138 Sprague-Dawley rats were used in the present study. The control group was designated as 0 wk (n = 8). A total of 3 phases (2, 4, 6 wk) of administration were used in the sham-operated groups (sham, n = 10), MI groups (MI, n = 10), MI + XJEK groups (XJEK, n = 10) and MI + fosinopril groups (fosinopril, n = 10). Additional 10 rats were used to evaluate the infarct area. At 2, 4 or 6 wk post-MI, the hemodynamic parameters were monitored, the rats were sacrificed, then blood, heart and renal tissues were collected for furtherly analysis. Results: The results indicated that XJEK administration continuously ameliorated renal hypertrophy index, blood urea nitrogen and cystatin C concentrations. XJEK further improved post-MI cardiac function by limiting scar formation and caused a downregulation in the hemodynamic parameters at the end of 2 and 4 wk. The hemodynamic parameters were upregulated after 6 wk treatment with XJEKcompared with those noted in the MI groups. Similarly, XJEK treatment for 2 wk potentiated Nrf2 nuclear translocation and HO-1 expression and inhibited the deficiency of nuclear Nrf2 and HO-1 at 6 wk post-MI compared with that of the MI groups, indicating the attenuation of the renal oxidative stress condition. The levels of malondialdehyde and angiotensin II (Ang II) in plasma and renal tissues, as well as the levels of aldosterone, 8-hydroxydeoxyguanosine, angiotensin II type 1 receptor and NADPH Oxidase-4 in the kidney tissue significantly decreased following XJEK treatment for 6 wk. In addition, the XJEK treatment groups revealed a significant upregulation in the activity of superoxide dismutase and in the total antioxidant capacity activity compared with those noted in the corresponding MI groups. Conclusion: These results demonstrated that progressive nephropathy in MI rats was associated with intrarenal activation of the renin-angiotensin-aldosterone system. Concomitantly, this process was associated with oxidative stress and impaired Nrf2 activation. The improvement in the severity of nephropathy by XJEK in this model may be associated with the reversal of these abnormalities.
MeSH term(s)	Angiotensin II/metabolism ; Animals ; Blood Urea Nitrogen ; Cystatin C/metabolism ; DNA Damage ; Down-Regulation/drug effects ; Drugs, Chinese Herbal/pharmacology ; Heme Oxygenase-1/metabolism ; Hemodynamics/drug effects ; Kidney/drug effects ; Kidney/injuries ; Kidney/pathology ; Kidney/physiopathology ; Myocardial Infarction/blood ; Myocardial Infarction/complications ; Myocardial Infarction/physiopathology ; NADPH Oxidase 4/metabolism ; NF-E2-Related Factor 2/metabolism ; Organ Size/drug effects ; Oxidative Stress/drug effects ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1/metabolism ; Signal Transduction/drug effects
Chemical Substances	Cystatin C ; Drugs, Chinese Herbal ; NF-E2-Related Factor 2 ; Receptor, Angiotensin, Type 1 ; xin-ji-er-kang ; Angiotensin II (11128-99-7) ; Heme Oxygenase-1 (EC 1.14.14.18) ; NADPH Oxidase 4 (EC 1.6.3.-) ; Nox4 protein, rat (EC 1.6.3.-)
Language	English
Publishing date	2019-06-19
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2019.109124
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Article ; Online: Protective effect of Xin-Ji-Er-Kang on cardiovascular remodeling in high-salt induced hypertensive mice: Role ofoxidative stress and endothelial dysfunction.

Wang, Xiao-Yun / Huang, Guang-Yao / Lian, Feng-Zhen / Pan, Ming / Ruan, Cheng-Shao / Ling, Xin-Xin / Chen, Mei-Ling / Shen, Ai-Zong / Gao, Shan

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2019 Volume 115, Page(s) 108937

Abstract: Background: Xin-Ji-Er-Kang (XJEK) is a Chinese herbal formula that has beenreported to exert ...

Abstract	Background: Xin-Ji-Er-Kang (XJEK) is a Chinese herbal formula that has beenreported to exert effective protection against cardiovascular diseases, such as hypertension and myocarditis. Objective: The aim of the present study was to investigate the effect of XJEK on high-salt-induced hypertensive mice and its possible mechanism. Methods: The model of hypertension was established through a high-salt diet. Sixty male Kunming mice were randomized into six groups, namely the Control, Model, Low-dose XJEK, Middle-dose XJEK, High-dose XJEK and Fosinopril groups (n=10 per group). Different steady interventions were given to each group: 0.9% Sodium chloride was added to the diet of the Control group and 8% sodium chloride to the diet of the other five groups from the very beginning. An additional 4, 8 and 12 g/kg/day XJEK were intragastrically administered to the Low-dose, Middle-dose and High-dose XJEK groups, respectively, and 2 mg/kg/day fosinopril to the fosinopril group, from the start of week 5. Systolic blood pressure (SBP) was measured weekly from weeks 1 to 8 using the tail-cuff method. At the end of week 8, left ventricular (LV) systolic pressure, LV end-diastolic pressure and rate of rise of LV pressure were examined using a TransonicScisense catheter (Transonic Systems Inc,Ithaca, NY,USA). Endothelium-dependent relaxations induced by acetylcholine were observed in an isolated thoracic aorta ring. Serum and heartsweresampled for the measurement of the following indexes:Serum nitric oxide (NO), superoxide dismutase (SOD) activity and malondialdehyde (MDA) content (determined by colorimetricanalysis); serum angiotensin II(Ang II), endothelin-1, endothelial NO synthase (eNOS), asymmetric dimethylarginine (ADMA), tetrahydrobiopterin (BH Results: Statistical data showed that the HW/BW ratio was significantly decreased in the drug treatment group. XJEK treatment could improve the heart systolic and diastolic function and ameliorate hemodynamic parameters and vascular remodeling indexes. Colorimetric results showed that, compared with the model group, XJEK increased serum SOD, NOlevels, and decreased those of serum MDA and Ang II. XJEK reverted changes in cardiac pathology, decreased the myocardial cross-sectional area, collagen volume fraction and perivascular collagen area and improved endothelial dysfunction (ED) by promoting eNOS activity, enhancing NO bioavailability, increasing the expression of BH Conclusion: In conclusion, XJEK mitigates cardiac remodeling in high-salt-induced hypertensive mice. The potential mechanism involves improved oxidative stress and endothelial dysfunction, independently of ameliorating BP.
MeSH term(s)	Animals ; Blood Pressure/drug effects ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal/therapeutic use ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/physiopathology ; Hypertension/drug therapy ; Hypertension/etiology ; Hypertension/physiopathology ; Male ; Mice, Inbred Strains ; Oxidative Stress/drug effects ; Sodium Chloride, Dietary/adverse effects ; Vascular Remodeling/drug effects ; Ventricular Remodeling/drug effects
Chemical Substances	Drugs, Chinese Herbal ; Sodium Chloride, Dietary ; xin-ji-er-kang
Language	English
Publishing date	2019-05-09
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2019.108937
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Effects of Xin-Ji-Er-Kang on heart failure induced by myocardial infarction: Role of inflammation, oxidative stress and endothelial dysfunction.

Hu, Juan / Cheng, Pan / Huang, Guang-Yao / Cai, Guo-Wei / Lian, Feng-Zhen / Wang, Xiao-Yun / Gao, Shan

Phytomedicine : international journal of phytotherapy and phytopharmacology

2018 Volume 42, Page(s) 245–257

Abstract: Background: Xin-Ji-Er-Kang (XJEK) is a Chinese herbal formula, which has been reported to exert ...

Abstract	Background: Xin-Ji-Er-Kang (XJEK) is a Chinese herbal formula, which has been reported to exert effective protection on cardiovascular diseases like hypertension and myocarditis. Purpose: To elucidate the protective effects of XJEK on heart failure (HF) induced by myocardial infarction (MI) through the amelioration of inflammation, oxidative stress (OS) and endothelial dysfunction(ED). Materials and methods: Fifty-seven male KM mice were randomized into the following six groups (n = 9-10 for each): control group, model group, MI+XJEK low dose group(XJEKL) group, MI+XJEK middle dose group(XJEKM), MI+XJEK high dose group(XJEKH), and MI+fosinopril group (positive control group). After treatment for four weeks, electrocardiography (ECG) and haemodynamics were recorded. Serum and tissues were collected for further analysis. Endothelium-dependent relaxation induced by acetylcholine was assessed in isolated thoracic aorta ring experiment. Hematoxylin and eosin (HE) and Van Gieson (VG) staining were used to detect the pathological changes of heart and thoracic aorta. Colorimetric analysis was employed to determine serum nitric oxide level (NO), malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity. ELISA was used to detect serum B-type natriuretic peptide (BNP) and serum inflammatory cytokines, as well as endothelial NO synthetase (eNOS), angiotensinII (Ang II) and endothelin-1(ET-1) concentration in both serum and cardiac tissues. Immunohistochemistry and Western blotting (WB) were employed to detect eNOS and inflammatory cytokine expressions in cardiac tissues. Results: XJEK administration markedly ameliorated cardiac dysfunction and abnormal ECG manifested by decreased weight/body weight (HW/BW) ratio, BNP and remedied hypertrophy of cardiomyocytes and deposition of collagen, which might be in part attributed to the increased SOD and decreased MDA in serum. Furthermore, XJEK administration improved ED with boosted eNOS activities in serum and cardiac tissues, as well as up-regulated NO levels in serum, down-regulated Ang II and ET-1 content in serum and cardiac tissues. Lastly, protein expression of pro-inflammation cytokines significantly decreased, and anti-inflammatory cytokine was significantly enhanced in serum and cardiac tissues compared to model group. Conclusion: XJEK may exert beneficial effects on HF induced by MI in mice, and the underlying mechanism may be attributable to the amelioration of ED, anti-OS and anti-inflammation effects.
MeSH term(s)	Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Cardiotonic Agents/pharmacology ; Drugs, Chinese Herbal/administration & dosage ; Drugs, Chinese Herbal/pharmacology ; Electrocardiography ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/physiopathology ; Heart/drug effects ; Heart Failure/etiology ; Heart Failure/prevention & control ; Male ; Malondialdehyde/metabolism ; Mice ; Myocardial Infarction/complications ; Myocardial Infarction/metabolism ; Myocardial Infarction/mortality ; Myocarditis/drug therapy ; Myocarditis/physiopathology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type III/metabolism ; Oxidative Stress/drug effects
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Cardiotonic Agents ; Drugs, Chinese Herbal ; xin-ji-er-kang ; Nitric Oxide (31C4KY9ESH) ; Malondialdehyde (4Y8F71G49Q) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos3 protein, mouse (EC 1.14.13.39)
Language	English
Publishing date	2018-03-19
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2018.03.036
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Xin-Ji-Er-Kang Alleviates Myocardial Infarction-Induced Cardiovascular Remodeling in Rats by Inhibiting Endothelial Dysfunction

Pan Cheng / Feng-zhen Lian / Xiao-yun Wang / Guo-wei Cai / Guang-yao Huang / Mei-ling Chen / Ai-zong Shen / Shan Gao

BioMed Research International, Vol

2019 Volume 2019

Abstract	The present study was designed to elucidate the beneficial effects of XJEK on myocardial infarction (MI) in rats, especially through the amelioration of endothelial dysfunction (ED). 136 Sprague-Dawley rats were randomized into 13 groups: control group for 0wk (n = 8); sham groups for 2, 4, and 6 weeks (wk); MI groups for 2, 4, and 6 wk; MI+XJEK groups for 2, 4, and 6w k; MI+Fosinopril groups for 2, 4, and 6 wk (n = 8~10). In addition, 8 rats were treated for Evans blue staining and Tetrazolium chloride (TTC) staining to determine the infarct size. Cardiac function, ECG, and cardiac morphological changes were examined. Colorimetric analysis was employed to detect nitric oxide (NO), and enzyme-linked immunosorbent assay (ELISA) was applied to determine N-terminal probrain natriuretic peptide (NT-ProBNP), endothelin-1 (ET-1), angiotensin II (Ang II), asymmetric dimethylarginine (ADMA), tetrahydrobiopterin (BH4), and endothelial NO synthase (eNOS) content. The total eNOS and eNOS dimer/(dimer+monomer) ratios in cardiac tissues were detected by Western blot. We found that administration of XJEK markedly ameliorated cardiovascular remodeling (CR), which was manifested by decreased HW/BW ratio, CSA, and less collagen deposition after MI. XJEK administration also improved cardiac function by significant inhibition of the increased hemodynamic parameters in the early stage and by suppression of the decreased hemodynamic parameters later on. XJEK also continuously suppressed the increased NT-ProBNP content in the serum of MI rats. XJEK improved ED with stimulated eNOS activities, as well as upregulated NO levels, BH4 content, and eNOS dimer/(dimer+monomer) ratio in the cardiac tissues. XJEK downregulated ET-1, Ang II, and ADMA content obviously compared to sham group. In conclusion, XJEK may exert the protective effects on MI rats and could continuously ameliorate ED and reverse CR with the progression of MI over time.
Keywords	Medicine ; R
Subject code	630
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The protective effects of polysaccharide extract from Xin-Ji-Er-Kang formula on Ang II-induced HUVECs injury, L-NAME-induced hypertension and cardiovascular remodeling in mice.

Ding, Ling / Cheng, Pan / Wang, Li / Hu, Juan / Zhang, Yong-Xue / Cai, Guo-Wei / Huang, Guang-Yao / Gao, Shan

BMC complementary and alternative medicine

2019 Volume 19, Issue 1, Page(s) 127

Abstract: Background: Xin-Ji-Er-Kang (XJEK) is a Chinese herbal formula, which has been reported to exert ...

Abstract	Background: Xin-Ji-Er-Kang (XJEK) is a Chinese herbal formula, which has been reported to exert effective protection against cardiovascular diseases, including hypertension and myocarditis. Methods: Cultured human umbilical vascular endothelial cells (HUVECs) were treated with angiotensin II (Ang II) and different concentrations of aqueous layer extracts (AqE). Subsequently nitric oxide (NO) and endothelial nitric oxide synthase (eNOS) expression levels were detected. In addition, fifty Kunming mice were randomized into control, Nω-nitro-L-arginine methyl ester (L-NAME), L-NAME+AqE, L-NAME+XJEK and L-NAME+fosinopril treatment groups. Following 8 weeks of treatment, the cardiac hemodynamic index was measured, relaxation of the aorta was examined and pathological changes were observed. Colorimetric analysis and enzyme linked immunosorbent assay (ELISA) were applied to determine the relevant indicators in plasma and cardiac tissues. Results: The in vitro study results demonstrated that AqE could preserve endothelial function (NO, 21.05 ± 2.03 vs. 8.64 ± 0.59; eNOS, 1.08 ± 0.17 vs.0.73 ± 0.06). In addition, the in vivo results demonstrated that compared with the control group, treatment with AqE could enhance a high hemodynamic state (left ventricular systolic pressure, 116.76 ± 9.96 vs.114.5 ± 15.16), improve endothelial function (NO, 7.98 ± 9.64 vs. 1.66 ± 3.11; eNOS, 19.78 ± 3.18 vs.19.38 ± 3.85), suppress oxidative stress (OS) (superoxide dismutase, 178.17 ± 13.78 vs. 159.38 ± 18.86; malondialdehyde, 0.77 ± 0.13 vs.1.25 ± 0.36) and reverse cardiovascular remodeling. Conclusion: Polysaccharide from XJEK exerts protective effects against Ang II-induced injury in HUVECs and L-NAME-induced hypertension in mice and the underlying mechanism may be attributed to improving endothelial dysfunction, OS and the inflammation status in mice.
MeSH term(s)	Angiotensin II ; Animals ; Aorta/drug effects ; Arginine/analogs & derivatives ; Arginine/blood ; Blood Pressure/drug effects ; Cytokines/metabolism ; Drug Evaluation, Preclinical ; Drugs, Chinese Herbal/pharmacology ; Drugs, Chinese Herbal/therapeutic use ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Endothelium, Vascular/drug effects ; Human Umbilical Vein Endothelial Cells ; Humans ; Hypertension/chemically induced ; Hypertension/drug therapy ; Inflammation/drug therapy ; Male ; Malondialdehyde/blood ; Mice ; Myocardium/metabolism ; NG-Nitroarginine Methyl Ester ; Nitric Oxide/blood ; Nitric Oxide Synthase Type III/metabolism ; Oxidative Stress/drug effects ; Phytotherapy ; Superoxide Dismutase/blood ; Vascular Remodeling/drug effects
Chemical Substances	Cytokines ; Drugs, Chinese Herbal ; xin-ji-er-kang ; Angiotensin II (11128-99-7) ; Nitric Oxide (31C4KY9ESH) ; Malondialdehyde (4Y8F71G49Q) ; N,N-dimethylarginine (63CV1GEK3Y) ; Arginine (94ZLA3W45F) ; NOS3 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Superoxide Dismutase (EC 1.15.1.1) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
Language	English
Publishing date	2019-06-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2050429-9
ISSN	1472-6882 ; 1472-6882
ISSN (online)	1472-6882
ISSN	1472-6882
DOI	10.1186/s12906-019-2539-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

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