Icariin attenuated oxidative stress induced-cardiac apoptosis by mitochondria protection and ERK activation

Song, Yinglin; Cai, Hui; Zhao, Zhenzhen; Chang, Wenjing; Gu, Ning; Cao, Shou-Pei; Wu, M. K.

doi:10.1016/j.biopha.2016.08.016

Cited by 62 publications

(40 citation statements)

References 23 publications

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“…27 In the past few decades, researchers have never stopped exploring the pathogenesis of ETEC K88-induced diarrhea in piglets. 29,30 In this study, ICA and pICA have an effective protective effect on ETEC-induced piglet diarrhea. pICA + K88: pICA (160 μg/mL) pretreated cells for 12 hours, then challenged with 6.5 × 10 7 cfu ETEC K88 for 3 hours recognized as biological process involved in the ETEC K88-induced diarrhea.…”

Section: Discussionmentioning

confidence: 70%

Icariin and its phosphorylated derivatives alleviate intestinal epithelial barrier disruption caused by enterotoxigenic Escherichia coli through modulate p38 MAPK in vivo and in vitro

Xiong

Huang

et al. 2019

The FASEB Journal

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. AbstractThe natural product icariin (ICA) and its phosphorylated derivatives (pICA) have been shown to have outstanding anti-inflammatory and antioxidant properties. This study was to explore the protective effects of ICA and pICA on the intestinal epithelium of enterotoxigenic Escherichia coli (ETEC)-induced piglet diarrhea and its underlying mechanisms in vivo and in vitro. ETEC K88 increased pro-inflammatory cytokine expression, activated oxidative stress and inhibited antioxidant enzyme activity, induced phosphorylated p38 MAPK gene and protein expression, disrupted intestinal barrier function, and led to diarrhea in piglets. Pretreatment with ICA and pICA effectively alleviated ETEC-induced intestinal barrier dysfunction in vivo and in vitro. Pretreatment with p38 MAPK inhibitor (SB203580) significantly rescued the IPEC-J2 cells barrier function damaged by ETEC challenge. However, pretreatment with p38 MAPK activator (anisomycin) did not alleviated the IPEC-J2 cells barrier function damaged by ETEC challenge. Our data demonstrated that ICA and pICA regulate the inflammatory response and oxidative stress of intestinal epithelial cells by inhibiting the expression of p38 MAPK, thereby alleviating ETEC K88-induced disruption of intestinal barrier function and intestinal permeability. These findings provide new insights into the prevention and treatment of intestinal barrier dysfunction induced by ETEC K88. K E Y W O R D S enterotoxigenic Escherichia coli K88, icariin, intestinal barrier function, p38 MAPK, phosphorylated icariin 1784 | XIONG et al.

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Section: Discussionmentioning

confidence: 70%

Icariin and its phosphorylated derivatives alleviate intestinal epithelial barrier disruption caused by enterotoxigenic Escherichia coli through modulate p38 MAPK in vivo and in vitro

Xiong

Huang

et al. 2019

The FASEB Journal

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“…Icariin (C 33 H 40 O 15 , ICA) is a flavonoid monomer isolated from the herb Epimedium, and it has garnered attention for its prospects in pharmacology, including its cardioprotective functions (Zhou et al, 2014;Meng et al, 2015). Icariin protects cardiomyocytes against oxidative stress by activating sirtuin-1 (Wu et al, 2018), thereby alleviating oxidative stress-induced cardiac apoptosis via mitochondrial protection (Song et al, 2016), and protects cardiomyocytes from apoptosis induced by hypertrophy via inhibition of ROS-dependent JNK (Zhou et al, 2014). However, the protective effect of icariin against DCM has not yet been reported.…”

Section: Introductionmentioning

confidence: 99%

Icariin Ameliorates Diabetic Cardiomyopathy Through Apelin/Sirt3 Signalling to Improve Mitochondrial Dysfunction

Lin

Huang

et al. 2020

Front. Pharmacol.

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Myocardial contractile dysfunction in diabetic cardiomyocytes is a significant promoter of heart failure. Herein, we investigated the effect of icariin, a flavonoid monomer isolated from Epimedium, on diabetic cardiomyopathy (DCM) and explored the mechanisms underlying its unique pharmacological cardioprotective functions. High glucose (HG) conditions were simulated in vitro using cardiomyocytes isolated from neonatal C57 mice, while DCM was stimulated in vivo in db/db mice. Mice and cardiomyocytes were treated with icariin, with or without overexpression or silencing of Apelin and Sirt3 via transfection with adenoviral vectors (Ad-RNA) and specific small hairpin RNAs (Ad-sh-RNA), respectively. Icariin markedly improved mitochondrial function both in vivo and in vitro, as evidenced by an increased level of mitochondrial-related proteins via western blot analysis (PGC-1a, Mfn2, and Cyt-b) and an increased mitochondrial membrane potential, as observed via JC-1 staining. Further, icariin treatment decreased cardiac fibrogenesis (Masson staining), and inhibited apoptosis (TUNEL staining). Together, these changes improved cardiac function, according to multiple transthoracic echocardiography parameters, including LVEF, LVSF, LVESD, and LVEDD. Moreover, icariin significantly activated Apelin and Sirt3, which were inhibited by HG and DCM. Importantly, when Ad-sh-Apelin and Ad-sh-Sirt3 were transfected in cardiomyocytes or injected into the heart of db/db mice, the cardioprotective effects of icariin were abolished and mitochondrial homeostasis was disrupted. Further, it was postulated that since Ad-Apelin

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“…MAPKs regulate various cellular responses to environmental stimuli, including cell survival, transformation and apoptosis, and serve important roles in cardiomyocyte apoptosis (29)(30)(31). ERK protects cardiomyocytes from apoptosis, whereas p38 MAPK is involved in the induction of cardiomyocyte apoptosis (32,33). Furthermore, JNK signaling exerts pro-and anti-apoptotic effects; however, the proapoptotic effects appear to be most dominant in the majority of experimental models (34,35).…”

Section: Discussionmentioning

confidence: 99%

Jujuboside A attenuates norepinephrine-induced apoptosis of H9c2 cardiomyocytes by modulating MAPK and AKT signaling pathways

Wan

Han

et al. 2017

Mol Med Report

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Cardiomyocyte apoptosis is closely associated with the pathogenesis of heart failure. Jujuboside A (JUA) is a type of saponin isolated from the seeds of Zizyphus jujuba. In traditional Chinese medicine, it is believed that JUA possesses multiple biological effects, including antianxiety, antioxidant and anti‑inflammatory activities. The present study aimed to evaluate the effects of JUA on norepinephrine (NE)‑induced apoptosis of H9c2 cells and to investigate its underlying mechanisms. Rat H9c2 cardiomyocytes were pretreated with JUA and were then exposed to NE as an in vitro model of myocardial apoptosis. A cell viability assay, scanning electron microscopy, transmission electron microscopy, flow cytometry assay, acridine orange/ethidium bromide staining, reverse transcription‑quantitative polymerase chain reaction and western blotting, all revealed that NE induced H9c2 cell apoptosis. The results demonstrated that NE inhibited cell viability, and enhanced cell damage and apoptosis of H9c2 cells. Conversely, pretreatment with JUA was able to reverse NE‑induced decreased cell viability and increased apoptosis. Furthermore, JUA suppressed upregulation of the B‑cell lymphoma 2 (Bcl‑2)‑associated X protein/Bcl‑2 ratio, and inhibited the increased protein expression levels of cleaved caspase‑3 and cleaved caspase‑9 following NE exposure. However, the protein expression levels of cleaved caspase‑12 and cleaved caspase‑8 were not significantly altered following exposure to NE or JUA pretreatment. In addition, in JUA‑pretreated cells, the protein expression levels of phosphorylated (p)‑p38 and p‑c‑Jun N‑terminal kinase were downregulated compared with in NE‑treated cells. Furthermore, JUA regulated the activation of extracellular signal‑regulated kinase (ERK) in NE‑treated cells and significantly increased the expression levels of p‑AKT. Taken together, these data suggested that JUA may protect against NE‑induced apoptosis of cardiomyocytes via modulation of the mitogen‑activated protein kinase and AKT signaling pathways. Therefore, JUA may be considered a potential therapeutic strategy for the treatment of heart disease.

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Icariin attenuated oxidative stress induced-cardiac apoptosis by mitochondria protection and ERK activation

Cited by 62 publications

References 23 publications

Icariin and its phosphorylated derivatives alleviate intestinal epithelial barrier disruption caused by enterotoxigenic Escherichia coli through modulate p38 MAPK in vivo and in vitro

Icariin and its phosphorylated derivatives alleviate intestinal epithelial barrier disruption caused by enterotoxigenic Escherichia coli through modulate p38 MAPK in vivo and in vitro

Icariin Ameliorates Diabetic Cardiomyopathy Through Apelin/Sirt3 Signalling to Improve Mitochondrial Dysfunction

Jujuboside A attenuates norepinephrine-induced apoptosis of H9c2 cardiomyocytes by modulating MAPK and AKT signaling pathways

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