Icariin exhibits protective effects on cisplatin-induced cardiotoxicity via ROS-mediated oxidative stress injury in vivo and in vitro

Xia, Juan; Hu, Jun‐Nan; Zhang, Ruobing; Liu, Wei; Zhang, Hao; Wang, Zi; Jiang, Shuang; Ying-ping, Wang; Li, Wei

doi:10.1016/j.phymed.2022.154331

Cited by 16 publications

(7 citation statements)

References 47 publications

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“…Zhao and colleagues [ 41 ] used a cell-free system to examine the anti-oxidant effects of Icariin, and they observed reduced DNA damage after Icariin treatment. Xia et al [ 42 ] reported that Icariin could inhibit oxidative stress, inflammation, and apoptosis in chemotherapy-induced cardiotoxicity. The myocardial injury was significantly reduced via activating PI3K/Akt, inhibiting the MAPKs signaling pathway, and downregulating the secretion of inflammatory factors in H9c2 cells and mice models after Icariin treatment [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

“…Xia et al [ 42 ] reported that Icariin could inhibit oxidative stress, inflammation, and apoptosis in chemotherapy-induced cardiotoxicity. The myocardial injury was significantly reduced via activating PI3K/Akt, inhibiting the MAPKs signaling pathway, and downregulating the secretion of inflammatory factors in H9c2 cells and mice models after Icariin treatment [ 42 ]. In addition, Icariin can inhibit ROS-induced JNK and p38 signaling pathways and thus protect cardiomyocytes from apoptosis [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

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Pharmacology-Based Prediction of the Targets and Mechanisms for Icariin against Myocardial Infarction

Wang

Silimu³

et al. 2023

Medicina

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Background and Objectives: This study aims to illustrate the mechanisms underlying the therapeutic effect of Icariin after myocardial infarction (MI). Materials and Methods: Based on the network pharmacology strategy, we predict the therapeutic targets of Icariin against MI and investigate the pharmacological molecular mechanisms. A topological network was created. Biological process and Kyoto Encyclopedia of Genes and Genomes pathway enrichment were also performed. We also conducted the molecular docking analysis to stimulate the component–target interaction further and validate the direct bind effect. Results: Network pharmacology analysis identified 61 candidate genes related to the therapeutic effect of Icariin against MI. EGFR, AKT1, TP53, JUN, ESR1, PTGS2, TNF, RELA, HSP90AA1, and BCL2L1 were identified as hub genes. The biological processes of the candidate targets were significantly involved in the reactive oxygen species metabolic process, response to hypoxia, response to decreased oxygen levels, response to oxidative stress, regulation of reactive oxygen species metabolic process, and so forth. Overall, biological process enrichment analysis indicated that the protective effect of Icariin against MI might be associated with oxidative stress. Moreover, the pathway analysis showed that the candidate targets were closely associated with lipid and atherosclerosis, AGE-RAGE signaling pathway in diabetic complications, HIF-1 signaling pathway, etc. We identified the conformation with the lowest affinity score as the docking conformation. The simulated molecular docking was displayed to illustrate the topical details of the binding sites between Icariin and TNF protein. Conclusions: This study provides an overview of the mechanisms underlying the protective effect of Icariin against MI.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Pharmacology-Based Prediction of the Targets and Mechanisms for Icariin against Myocardial Infarction

Wang

Silimu³

et al. 2023

Medicina

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“…As a native compound, ICA has antioxidant biological activity against ROS. Xia et al demonstrated that ROS triggered by cisplatin chemotherapy led to cardiac injury through oxidative stress and activation of MAPKs and NF-κB signaling pathways, and ICA could alleviate these adverse effects [ 28 ]. The application of ICA in bone tissue engineering has great prospects.…”

Section: Discussionmentioning

confidence: 99%

“…Cell experiments have shown that ICA could increase the osteoblast differentiation and mineralization of bone marrow mesenchymal stem cells (BMSCs) as well as inhibit the formation of osteoclasts and bone resorption [ 26 , 27 ]. In addition, ICA has attracted much attention due to ameliorating lipid metabolism disorders, inflammation, insulin resistance, and mitochondrial dysfunction [ 28 , 29 ]. Ding et al proposed that ICA could promote Sesn2-induced mitophagy to inhibit NLRP3 inflammasome activation in diabetic nephropathy SD rats [ 30 ].…”

Section: Introductionmentioning

confidence: 99%

Icariin Treatment Rescues Diabetes Induced Bone Loss via Scavenging ROS and Activating Primary Cilia/Gli2/Osteocalcin Signaling Pathway

Liu

Cheng

et al. 2022

Cells

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Diabetes-associated bone complications lead to fragile bone mechanical strength and osteoporosis, aggravating the disease burden of patients. Advanced evidence shows that chronic hyperglycemia and metabolic intermediates, such as inflammatory factor, reactive oxygen species (ROS), and advanced glycation end products (AGEs), are regarded as dominant hazardous factors of bone complications, whereas the pathophysiological mechanisms are complex and controversial. By establishing a diabetic Sprague-Dawley (SD) rat model and diabetic bone loss cell model in vitro, we confirmed that diabetes impaired primary cilia and led to bone loss, while adding Icariin (ICA) could relieve the inhibitions. Mechanistically, ICA could scavenge ROS to maintain the mitochondrial and primary cilia homeostasis of osteoblasts. Intact primary cilia acted as anchoring and modifying sites of Gli2, thereby activating the primary cilia/Gli2/osteocalcin signaling pathway to promote osteoblast differentiation. All results suggest that ICA has potential as a therapeutic drug targeting bone loss induced by diabetes.

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“…An additional CMN combination with piperine significantly increases anti-OS enzyme levels in the cardiac tissue of CP-treated rats ( 81 , 82 ). Icariin (ICA) and rutin, attenuated CP-induced myocardial injury by increasing anti-OS enzyme and decreasing lipid peroxidase product levels ( 83 , 84 ). QUE, salvianolic acid B (SalB), and luteolin (Lut) significantly reduced CP-induced OS by regulating Nrft2 signaling pathways ( 85 – 88 ).…”

Section: Molecular Mechanisms Of Chemoradiotherapy-related Cardiotoxi...mentioning

confidence: 99%

Role and molecular mechanism of traditional Chinese medicine in preventing cardiotoxicity associated with chemoradiotherapy

Wen

et al. 2022

Front. Cardiovasc. Med.

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Cardiotoxicity is a serious complication of cancer therapy. It is the second leading cause of morbidity and mortality in cancer survivors and is associated with a variety of factors, including oxidative stress, inflammation, apoptosis, autophagy, endoplasmic reticulum stress, and abnormal myocardial energy metabolism. A number of studies have shown that traditional Chinese medicine (TCM) can mitigate chemoradiotherapy-associated cardiotoxicity via these pathways. Therefore, this study reviews the effects and molecular mechanisms of TCM on chemoradiotherapy-related cardiotoxicity. In this study, we searched PubMed for basic studies on the anti-cardiotoxicity of TCM in the past 5 years and summarized their results. Angelica Sinensis, Astragalus membranaceus Bunge, Danshinone IIA sulfonate sodium (STS), Astragaloside (AS), Resveratrol, Ginsenoside, Quercetin, Danggui Buxue Decoction (DBD), Shengxian decoction (SXT), Compound Danshen Dripping Pill (CDDP), Qishen Huanwu Capsule (QSHWC), Angelica Sinensis and Astragalus membranaceus Bunge Ultrafiltration Extract (AS-AM),Shenmai injection (SMI), Xinmailong (XML), and nearly 60 other herbs, herbal monomers, herbal soups and herbal compound preparations were found to be effective as complementary or alternative treatments. These preparations reduced chemoradiotherapy-induced cardiotoxicity through various pathways such as anti-oxidative stress, anti-inflammation, alleviating endoplasmic reticulum stress, regulation of apoptosis and autophagy, and improvement of myocardial energy metabolism. However, few clinical trials have been conducted on these therapies, and these trials can provide stronger evidence-based support for TCM.

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Icariin exhibits protective effects on cisplatin-induced cardiotoxicity via ROS-mediated oxidative stress injury in vivo and in vitro

Cited by 16 publications

References 47 publications

Pharmacology-Based Prediction of the Targets and Mechanisms for Icariin against Myocardial Infarction

Pharmacology-Based Prediction of the Targets and Mechanisms for Icariin against Myocardial Infarction

Icariin Treatment Rescues Diabetes Induced Bone Loss via Scavenging ROS and Activating Primary Cilia/Gli2/Osteocalcin Signaling Pathway

Role and molecular mechanism of traditional Chinese medicine in preventing cardiotoxicity associated with chemoradiotherapy

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