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

Ling, Xin-xin; Chen, Hua; Fu, Binying; Ruan, Cheng-shao; Pana, Ming; Zhou, Kai; Fang, Zhirui; Shao, Juntang; Zhu, Feng-qin; Gao, Shan

doi:10.1016/j.phymed.2021.153675

Cited by 5 publications

(2 citation statements)

References 38 publications

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“…Human cardiomyocyte‐like cells AC16 purchased from BeNa Culture Collection (BNCC339980) were cultured in DMEM (Gibco; Thermo Fisher Scientific) containing 10% fetal bovine serum (Gibco; Thermo Fisher Scientific) in 5% CO 2 at 37°C. The effect of Ang II on AC16 cells was assessed with 0.1, 0.5, and 1 μM human Ang II (HY‐13948; MedChem Express) for 24 h. 13 …”

Section: Methodsmentioning

confidence: 99%

PON2 ameliorates Ang II‐induced cardiomyocyte injury by targeting the CANX/NOX4 signaling pathway

Zhang

Guo

et al. 2023

Immunity Inflam & Disease

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Background The incidence of heart failure (HF) presents an escalating trend annually, second only to cancer. Few literatures are available regarding on the role of paraoxonase 2 ( PON2 ) in HF so far despite the protective role of PON2 in cardiovascular diseases. Methods PON2 expression in AC16 cells was examined with reverse transcriptase‐quantitative polymerase chain reaction and western blot following angiotensin II (Ang II) challenging. After PON2 elevation, 2, 7‐dichlorofluorescein diacetate assay estimated reactive oxygen species content, related kits appraised oxidative stress, enzyme‐linked immunosorbent assay evaluated inflammatory levels, and Western blot was applied to the analysis of apoptosis levels. Research on cytoskeleton was conducted by immunofluorescence (IF), and Western blot analysis of the expressions of hypertrophy‐related proteins was performed. BioGRID and GeneMania databases were used to analyze the relationship between PON2 and Calnexin ( CANX ), which was corroborated by co‐immunoprecipitation experiment. Subsequently, PON2 and CANX were simultaneously overexpressed in AC16 cells induced by Ang II to further figure out the mechanism. Results PON2 expression was depleted in Ang II‐induced AC16 cells. PON2 might mediate CANX/NOX4 signaling to inhibit oxidation, inflammatory, hypertrophy, and damage in Ang II‐induced AC16 cells. Conclusion PON2 can ease Ang II‐induced cardiomyocyte injury via targeting CANX/NOX4 signaling.

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Section: Methodsmentioning

confidence: 99%

PON2 ameliorates Ang II‐induced cardiomyocyte injury by targeting the CANX/NOX4 signaling pathway

Zhang

Guo

et al. 2023

Immunity Inflam & Disease

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“…Ker-Gawl, and so on (Table 1). Clinical and experimental data indicate that XJEK is an effective treatment for hypertension, viral myocarditis, myocardial infarction, and cardiovascular remodeling [15][16][17][18]. We have previously shown the protective effect of XJEK on ISO-induced ventricular remodeling in mice, which may be related to its actions in reducing oxidative stress and improving the antioxidant activity in the body [19].…”

Section: Introductionmentioning

confidence: 99%

Xin-Ji-Er-Kang Alleviates Isoproterenol-Induced Myocardial Hypertrophy in Mice through the Nrf2/HO-1 Signaling Pathway

Sun

Chen

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Xin-Ji-Er-Kang (XJEK) inhibited cardiovascular remodeling in hypertensive mice in our previous studies. We hypothesized that XJEK may prevent isoproterenol (ISO)-induced myocardial hypertrophy (MH) in mice by ameliorating oxidative stress (OS) through a mechanism that may be related to the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1(HO-1) pathways. Forty SPF male Kunming mice were randomized into 5 groups (n = 8 mice per group): control group, MH group, MH + different doses of XJEK (7.5 g/kg/day and 10 g/kg/day), and MH + metoprolol (60 mg/kg/day). On the eighth day after drug treatment, electrocardiogram (ECG) and echocardiography were performed, the mice were sacrificed, and blood and heart tissues were collected for further analysis. XJEK administration markedly ameliorated cardiovascular remodeling (CR), as manifested by a decreased HW/BW ratio and CSA and less collagen deposition after MH. XJEK administration also improved MH, as evidenced by decreased atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and β-myosin heavy chain (β-MHC) levels. XJEK also suppressed the decreased superoxide dismutase (SOD) and catalase (CAT) activities and increased malondialdehyde (MDA) levels in serum of mice with MH. XJEK-induced oxidative stress may be related to potentiating Nrf2 nuclear translocation and HO-1 expression compared with the MH groups. XJEK ameliorates MH by activating the Nrf2/HO-1 signaling pathway, suggesting that XJEK is a potential treatment for MH.

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Targeted pharmacokinetics and bioinformatics screening strategy reveals JAK2 as the main target for Xin-Ji-Er-Kang in treatment of MIR injury

Zhou¹,

Chen²,

Wang³

et al. 2022

Biomedicine & Pharmacotherapy

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

Cited by 5 publications

References 38 publications

PON2 ameliorates Ang II‐induced cardiomyocyte injury by targeting the CANX/NOX4 signaling pathway

PON2 ameliorates Ang II‐induced cardiomyocyte injury by targeting the CANX/NOX4 signaling pathway

Xin-Ji-Er-Kang Alleviates Isoproterenol-Induced Myocardial Hypertrophy in Mice through the Nrf2/HO-1 Signaling Pathway

Targeted pharmacokinetics and bioinformatics screening strategy reveals JAK2 as the main target for Xin-Ji-Er-Kang in treatment of MIR injury

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