Tid1‐S attenuates LPS‐induced cardiac hypertrophy and apoptosis through ER‐a mediated modulation of p‐PI3K/p‐Akt signaling cascade

Chao, Chun Nun; Lo, Jeng‐Fan; Badrealam, Khan Farheen; Day, Cecilia Hsuan; Lai, Chao Hung; Chen, Chia Hua; Chen, Ray Jade; Viswanadha, Vijaya Padma; Kuo, Chia‐Hua; Huang, Chih‐Yang

doi:10.1002/jcb.28928

Cited by 11 publications

(8 citation statements)

References 40 publications

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“…The binding of E2 and ERα exists in the cell membrane and nucleus, 56 which can be divided into genomic oestrogen signalling pathways and non‐genomic oestrogen signalling pathways. E2 diffuses through the cell membrane, and when it encounters palmitoylated‐ERα binding on the cell membrane, the ligand (E2) binds to the receptor (ERα), which can activate various cytoplasmic enzymes through non‐genomic interactions, including mediating the PI3K‐Akt pathway to regulate cell proliferation and survival 56–58 . In addition, the MAPK/ERK1/2 signal transduction pathway can also be activated to regulate tumour growth and progression 56,59,60 .…”

Section: Discussionmentioning

confidence: 99%

Integrated multicomponent analysis based on UHPLC‐Q‐Exactive Orbitrap‐MS and network pharmacology to elucidate the potential mechanism of Baoyuan decoction against idiopathic pulmonary fibrosis

Zhang

Gao

et al. 2022

Phytochemical Analysis

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Introduction: Idiopathic pulmonary fibrosis (IPF) is a serious lung disease with a high mortality rate. Baoyuan decoction (BYD), a classic medicinal food homology recipe, has anti-apoptotic effects, enhances immune function, and alleviates fibrosis, suggesting that it may be a potential therapeutic drug for IPF.Objectives: We aimed to identify the main active ingredients of BYD, determine the basis of its efficacy, prove its anti-IPF effects, and explore the mechanisms underlying its anti-IPF effects. Materials and methods:In this study, the active components of BYD were detected and analysed by ultra-high-performance liquid chromatography coupled with hybrid quadrupole Orbitrap mass spectrometry (UHPLC-Q-Exactive Orbitrap-MS). A network pharmacology analysis was performed to determine the potential targets and relevant pathways of BYD in treating IPF. Western blotting and quantitative realtime polymerase chain reaction (qPCR) were conducted to verify the efficacy of BYD against IPF. Finally, molecular docking and qPCR were performed to identify the central targets of BYD.Results: A total of 39 components of BYD were identified. After performing the network pharmacology analysis, 35 active components and eight presumptive targets of BYD were found to play a central role in its anti-IPF effects. The molecular docking results indicated that most of the active components of BYD exhibited good binding activity with these eight central target proteins. In addition, the expression of collagen, α-SMA, and these eight targets in human pulmonary fibroblast (HPF) cells was suppressed from treatment with BYD. Conclusion:This study determined the efficacy of BYD against IPF and clarified its multiple-target and multiple-pathway mechanisms. Furthermore, the study also provides a new method for exploring the chemical and pharmacological bases of other traditional Chinese medicine (TCM).

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Section: Discussionmentioning

confidence: 99%

Integrated multicomponent analysis based on UHPLC‐Q‐Exactive Orbitrap‐MS and network pharmacology to elucidate the potential mechanism of Baoyuan decoction against idiopathic pulmonary fibrosis

Zhang

Gao

et al. 2022

Phytochemical Analysis

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“…When LPS stimulates H9C2 cells (rat embryonic cardiomyoblasts), the overexpression of miR-146a suppresses apoptosis and helps attenuate myocardial depression ( An et al, 2018 ). Chao et al found that the overexpression of Tid1-S can enhance ER-α to activate p-PI3K/p-Akt, attenuating LPS-induced apoptosis in H9C2 cells ( Chao et al, 2019 ). In recent years, as the understanding of m 6 A modification has gradually deepened, studies have found that m 6 A modification plays an important role in the process of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide Alters the m6A Epitranscriptomic Tagging of RNAs in Cardiac Tissue

Yao

Xie

et al. 2021

Front. Mol. Biosci.

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N6-methyladenosine (m6A) modification plays important roles in the pathology of a variety of diseases. However, the roles of m6A modification in sepsis-induced myocardial dysfunction are not well defined. Rats were divided into control and lipopolysaccharide (LPS)-induced sepsis group. Global m6A levels of left ventricle tissue were measured by LC-MS/MS, and transcriptome-wide m6A modifications were profiled using epitranscriptomic microarrays (mRNAs and lncRNAs). Bioinformatics analysis was conducted to understand the functional implications of m6A modifications during sepsis. Methylated lncRNAs and mRNAs were measured by m6A single-base site qPCR. The global m6A levels in left ventricle tissue were significantly decreased in the LPS group. While 27 transcripts (23 mRNAs and four lncRNAs) were hypermethylated, 46 transcripts (39 mRNAs and 7 lncRNAs) were hypomethylated in the LPS group. The mRNA expression of writers and readers was significantly decreased in the LPS group. The m6A modification of Clec1b, Stk38l and Tnfrsf26 was associated with platelet activation and apoptotic pathways. Moreover, the decrease in m6A modification of lncRNA XR_346,771 may be related to cation import in cardiac tissue. Our data provide novel information regarding changes to m6A modifications in cardiac tissue during sepsis, and m6A modifications might be promising therapeutic targets.

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“…Studies have shown that cardiac complications induced LPS by are associated with cardiac apoptosis (11), as well as with the overexpression of pro-inflammatory cytokines (12). In addition, furthermore, the pro-inflammatory cytokinin activation induced by LPS is triggered by the nuclear factor-κB (NF-κB), which can stimulate the overexpression of multiple pro-inflammatory cytokines, thereby affecting myocardial function (13).…”

Section: Original Articlementioning

confidence: 99%

Paeoniflorin improves myocardial injury via p38 MAPK/NF-KB p65 inhibition in lipopolysaccharide-induced mouse

Wang¹,

Dong²,

Lu³

et al. 2021

Ann Transl Med

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Background: Paeoniflorin (Pae) is an active compound with a variety of pharmacological effects. This aim was to investigate how Pae protects against myocardial injury and to explore its potential mechanism. Methods:We established a BALB/c mouse model that was intraperitoneal injection (i.p.) of RvE1 (25 µg/kg) or Pae (20 mg/kg) for 3 days, and then treated with lipopolysaccharide (LPS, 10 mg/kg, i.p.).The mice were randomly divided into the sham group, the LPS group, the LPS + RvE1 group, the LPS + Pae group (n=8). Cardiac dysfunction was detected by HE staining and ELISA assay. The oxidative stress, mitochondrial membrane potential (MMP), mitochondrial permeability transition pore (mPTP) and apoptosis were assessed. Furthermore, western blotting (WB) assay were employed to analyze the protective mechanisms. Results: Pae improved LPS-induced cardiac function and impeded apoptosis. Pae significantly reduced the release of inflammatory cytokines such as interleukin (IL)-6, tumor necrosis factor-α (TNF-α), and IL-1β. Furthermore, Pae decreased malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS), and increased superoxide dismutase (SOD). In addition, Pae attenuated the mPTP opening and MMP depolarization. Notably, Pae treatment inhibited the activation of p38 MAPK and NF-κB p65. Conclusions: It was confirmed that Pae alleviated LPS-induced myocardial injury. Pae might be as a new drug candidate for myocardial ischaemic complications.

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Tid1‐S attenuates LPS‐induced cardiac hypertrophy and apoptosis through ER‐a mediated modulation of p‐PI3K/p‐Akt signaling cascade

Cited by 11 publications

References 40 publications

Integrated multicomponent analysis based on UHPLC‐Q‐Exactive Orbitrap‐MS and network pharmacology to elucidate the potential mechanism of Baoyuan decoction against idiopathic pulmonary fibrosis

Integrated multicomponent analysis based on UHPLC‐Q‐Exactive Orbitrap‐MS and network pharmacology to elucidate the potential mechanism of Baoyuan decoction against idiopathic pulmonary fibrosis

Lipopolysaccharide Alters the m6A Epitranscriptomic Tagging of RNAs in Cardiac Tissue

Paeoniflorin improves myocardial injury via p38 MAPK/NF-KB p65 inhibition in lipopolysaccharide-induced mouse

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