Calycosin inhibits oxidative stress-induced cardiomyocyte apoptosis via activating estrogen receptor-α/β

Liu, Bin; Zhang, Jingzhi; Liu, Weihua; Liu, Ningning; Fu, Xiu‐Qiong; Kwan, Hiu Yee; Liu, Shaojun; Liu, Benrong; Zhang, Shuangwei; Yu, Zujiang

doi:10.1016/j.bmcl.2015.11.005

Cited by 45 publications

(33 citation statements)

References 19 publications

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“…Data are expressed as means ± standard error of the mean; one-way analysis of variance (ANOVA) followed by Tukey test was used for pairwise comparisons among groups. ** p < .01 versus control group, *** p < .001 versus control group, # p < .05 versus DOX group, ## p < .01 versus DOX group, ### p < .001 versus DOX group stress and reduce ROS accumulation (Liu & Zhang, 2016a). In the present study, we observed that CA could decrease the generation of ROS induced by both DOX and H 2 O 2 (Figure 3).…”

Section: Discussionsupporting

confidence: 65%

“…These two important functions are related to treatment of cardiotoxicity induced by DOX. Furthermore, previous studies demonstrated that CA attenuated cardiomyocyte apoptosis induced by oxidative stress in H9c2 cells (Liu & Zhang, 2016a). Therefore, we investigated whether CA could suppress DOX-induced cardiotoxicity and explored the protective mechanism.…”

Section: Discussionmentioning

confidence: 97%

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Calycosin ameliorates doxorubicin‐induced cardiotoxicity by suppressing oxidative stress and inflammation via the sirtuin 1–NOD‐like receptor protein 3 pathway

Zhai

Tao

Zhang

et al. 2019

Phytotherapy Research

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The limitation of doxorubicin (DOX), which is widely used for the treatment of solid tumors and hematologic malignancies, is a vital problem in clinical application. The most serious of limit factors is cardiotoxicity. Calycosin (CA), an isoflavonoid that is the major active component in Radix astragali, has been reported in many bioactivities including antitumor, anti‐inflammatory, and cardioprotection. The aim of the study was to investigate the effects and mechanisms of CA on DOX‐induced cardiotoxicity in vitro and in vivo. CA increased H9c2 cell viability and reduced apoptosis induced by DOX via Bcl‐2, Bax, and the PI3K‐Akt signaling pathway. Moreover, CA prevented DOX‐induced oxidative stress in cells by decreasing the generation of reactive oxygen species. Similarly, oxidative stress was inhibited by CA through the increased activities of antioxidant enzymes such as glutathione peroxidase, catalase, and superoxide dismutase and decreased the levels of aspartate aminotransferase, lactate dehydrogenase, and malondialdehyde in vivo. Furthermore, the levels of sirtuin 1 (Sirt1)–NOD‐like receptor protein 3 (NLRP3) and related proteins were ameliorated by CA in cells and in mice hearts. When H9c2 cells were treated by Ex527 (Sirt1 inhibitor), the effect of CA on expressions of NLRP3 and thioredoxin‐interacting protein was suppressed. In conclusion, the results suggested that CA might be a cotreatment with DOX to ameliorate cardiotoxicity by Sirt1–NLRP3 pathway.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 97%

Calycosin ameliorates doxorubicin‐induced cardiotoxicity by suppressing oxidative stress and inflammation via the sirtuin 1–NOD‐like receptor protein 3 pathway

Zhai

Tao

Zhang

et al. 2019

Phytotherapy Research

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“…Oxidative stress is important in the development and progression of diverse cardiac disorders, including cardiac fibrosis (14), hypertrophy (22), apoptosis (23), inflammation (24) and resultant heart failure (25,26). It has previously been demonstrated that ROS may modulate ECM remodeling by mediating CF function and stimulating collagen turnover (26).…”

Section: Discussionmentioning

confidence: 99%

Astragaloside IV inhibits isoprenaline-induced cardiac fibrosis by targeting the reactive oxygen species/mitogen-activated protein kinase signaling axis

Dai

Jia

Lü

et al. 2017

Molecular Medicine Reports

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Cardiac fibrosis is considered an important pathological mechanism in the progression of cardiac remodeling and heart failure. Astragaloside IV (AsIV) is a major active ingredient in Astragalus membranaceus. In a preliminary experiment, it was demonstrated that this naturally occurring substance exhibited cardioprotective effects via preventing cardiomyocyte hypertrophy and apoptosis. The present study aimed to investigate the effects of AsIV on β‑adrenergic receptor (β‑AR)‑mediated cardiac fibrosis, and the associated mechanism. Cell Counting Kit‑8 (CCK‑8) assay was used to examine the proliferation of rat cardiac fibroblast (CF) cultures. Collagen I secretion was detected by ELISA. Dihydroethidium was used to determine intracellular ROS levels. Western blotting was used to examine the expression level of total and phosphorylated mitogen‑activated protein kinases (MAPKs). In the present study, the effects of AsIV on β‑adrenergic receptor (β‑AR) ‑mediated cardiac fibrosis were investigated, and the associated mechanism was revealed. Isoprenaline (ISO) is a selective β‑AR agonist, and treatment with AsIV significantly inhibited (ISO)‑triggered cardiac fibroblast proliferation and type I collagen synthesis. In addition, ISO resulted in a significant elevation of reactive oxygen species (ROS) levels and phosphorylation of the three profibrotic MAPKs, namely extracellular signal‑regulated kinase, p38MAPK and c‑Jun N‑terminal kinase. AsIV effectively reversed the aforementioned ISO‑induced alterations. In addition, N‑acetylcysteine, a typical ROS scavenger, mimicked the inhibitory effects of AsIV on MAPK activation. The present study demonstrated that AsIV may inhibit ISO‑induced cardiac fibrosis by suppressing ROS‑mediated MAPK activation.

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“…It has been found that pretreatment with calycosin (5, 10, 20 µM) enhanced the expression and activation of ERα/β and Akt phosphorylation and inhibited H 2 O 2 -induced cell injury and apoptosis [91]. …”

Section: In Vitro Effects Of Polyphenols Against Oxidative Stress-mentioning

confidence: 99%

Effects of Polyphenols on Oxidative Stress-Mediated Injury in Cardiomyocytes

et al. 2017

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Cardiovascular diseases are the main cause of mortality and morbidity in the world. Hypertension, ischemia/reperfusion, diabetes and anti-cancer drugs contribute to heart failure through oxidative and nitrosative stresses which cause cardiomyocytes nuclear and mitochondrial DNA damage, denaturation of intracellular proteins, lipid peroxidation and inflammation. Oxidative or nitrosative stress-mediated injury lead to cardiomyocytes apoptosis or necrosis. The reactive oxygen (ROS) and nitrogen species (RNS) concentration is dependent on their production and on the expression and activity of anti-oxidant enzymes. Polyphenols are a large group of natural compounds ubiquitously expressed in plants, and epidemiological studies have shown associations between a diet rich in polyphenols and the prevention of various ROS-mediated human diseases. Polyphenols reduce cardiomyocytes damage, necrosis, apoptosis, infarct size and improve cardiac function by decreasing oxidative stress-induced production of ROS or RNS. These effects are achieved by the ability of polyphenols to modulate the expression and activity of anti-oxidant enzymes and several signaling pathways involved in cells survival. This report reviews current knowledge on the potential anti-oxidative effects of polyphenols to control the cardiotoxicity induced by ROS and RNS stress.

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Calycosin inhibits oxidative stress-induced cardiomyocyte apoptosis via activating estrogen receptor-α/β

Cited by 45 publications

References 19 publications

Calycosin ameliorates doxorubicin‐induced cardiotoxicity by suppressing oxidative stress and inflammation via the sirtuin 1–NOD‐like receptor protein 3 pathway

Calycosin ameliorates doxorubicin‐induced cardiotoxicity by suppressing oxidative stress and inflammation via the sirtuin 1–NOD‐like receptor protein 3 pathway

Astragaloside IV inhibits isoprenaline-induced cardiac fibrosis by targeting the reactive oxygen species/mitogen-activated protein kinase signaling axis

Effects of Polyphenols on Oxidative Stress-Mediated Injury in Cardiomyocytes

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