Cinnamaldehyde Derivatives Inhibit Coxsackievirus B3-Induced Viral Myocarditis

Li, Xiaoqiang; Liu, Xiaoxiao; Xie, Youhua; Yang, Qian; Liu, Xinxin; Ding, Yuan-Yuan; Cao, Wei; Wang, Siwang

doi:10.4062/biomolther.2016.070

Cited by 12 publications

(5 citation statements)

References 36 publications

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“…The cardioprotection and related activity of cinnamaldehyde and its derivatives has also been studied. X.-Q Li et al [41] assessed the therapeutic effects of cinnamaldehyde and five derivatives on viral myocarditis (VMC). Here, synthetic derivatives α-bromo-4-methylcinnamaldehyde and α-bromo-4-chlorocinnamaldehyde (Fig.…”

Section: Cardioprotection Functionmentioning

confidence: 99%

A review of cinnamaldehyde and its derivatives as antibacterial agents

2019

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There is a continuing rise in the occurrence of multidrug-resistant bacterial infections. Antibiotic resistance to currently available antibiotics has become a global health issue leading to an urgent need for alternative antibacterial strategies. There has been a renewed interest in the development of antibacterial agents from natural sources, and trans-cinnamaldehyde is an example of a naturally occurring compound that has received significant attention in recent years. Trans-Cinnamaldehyde has been shown to possess substantial antimicrobial activity, as well as an array of other medicinal properties, and represents an intriguing hit compound from which a number of derivatives have been developed. In some cases, these derivatives have been shown to possess improved activity, not only compared to trans-cinnamaldehyde but also to commonly used antibiotics. Therefore, understanding the antibacterial mechanisms of action that these compounds elicit is imperative in order to facilitate their development and the development of new antibacterial agents that could exploit similar mechanistic approaches. The purpose of this review is to provide an overview of current knowledge on the antibacterial activity and mechanisms of action of cinnamaldehyde and its derivatives, and to highlight significant contributions made in this research area. It is hoped that the findings presented in this work will aid the future development of new antibacterial agents.

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Section: Cardioprotection Functionmentioning

confidence: 99%

A review of cinnamaldehyde and its derivatives as antibacterial agents

2019

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“…The neonatal mouse cardiomyocytes were obtained from neonatal WT, Trpc1 −/− , or Trpc6 −/− mice (2- to 3-d-old) as described previously 102 . In brief, the hearts were excised from neonatal mice under isoflurane anesthesia, minced, and dispersed with PBS.…”

Section: Methodsmentioning

confidence: 99%

TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and Ca2+ leakage

Tang

Tian

et al. 2022

Nat Commun

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Intracellular Ca2+ dysregulation is a key marker in septic cardiac dysfunction; however, regulation of the classic Ca2+ regulatory modules cannot successfully abolish this symptom. Here we show that the knockout of transient receptor potential canonical (TRPC) channel isoforms TRPC1 and TRPC6 can ameliorate LPS-challenged heart failure and prolong survival in mice. The LPS-triggered Ca2+ release from the endoplasmic reticulum both in cardiomyocytes and macrophages is significantly inhibited by Trpc1 or Trpc6 knockout. Meanwhile, TRPC’s molecular partner — calmodulin — is uncoupled during Trpc1 or Trpc6 deficiency and binds to TLR4’s Pococurante site and atypical isoleucine-glutamine-like motif to block the inflammation cascade. Blocking the C-terminal CaM/IP3R binding domain in TRPC with chemical inhibitor could obstruct the Ca2+ leak and TLR4-mediated inflammation burst, demonstrating a cardioprotective effect in endotoxemia and polymicrobial sepsis. Our findings provide insight into the pathogenesis of endotoxemic cardiac dysfunction and suggest a novel approach for its treatment.

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“…The MTT assay was performed as previously described ( Li et al ., 2017 ). LoVo cells were treated with Gomisin D, G, J, N and O each at a concentration of 0, 1, 5, and 10 μM, or with dimethyl sulfoxide (DMSO) as a control for 3 and 5 days.…”

Section: Methodsmentioning

confidence: 99%

Gomisin G Suppresses the Growth of Colon Cancer Cells by Attenuation of AKT Phosphorylation and Arrest of Cell Cycle Progression

et al. 2019

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Colorectal cancer is one of the leading causes of cancer related death due to a poor prognosis. In this study, we investigated the effect of Gomisin G on colon cancer growth and examined the underlying mechanism of action. We found that Gomisin G significantly suppressed the viability and colony formation of LoVo cells. Gomisin G reduced the phosphorylation level of AKT implying that Gomisin G suppressed the PI3K-AKT signaling pathway. Gomisin G also induced apoptosis shown by Annexin V staining and an increased level of cleaved poly-ADP ribose polymerase (PARP) and Caspase-3 proteins. Furthermore, Gomisin G remarkably triggered the accumulation of cells at the sub-G1 phase which represents apoptotic cells. In addition, the level of cyclin D1 and phosphorylated retinoblastoma tumor suppressor protein (Rb) was also reduced by the treatment with Gomisin G thus curtailing cell cycle progression. These findings show the suppressive effect of Gomisin G by inhibiting proliferation and inducing apoptosis in LoVo cells. Taken together, these results suggest Gomisin G could be developed as a potential therapeutic compound against colon cancer.

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Cinnamaldehyde Derivatives Inhibit Coxsackievirus B3-Induced Viral Myocarditis

Cited by 12 publications

References 36 publications

A review of cinnamaldehyde and its derivatives as antibacterial agents

A review of cinnamaldehyde and its derivatives as antibacterial agents

TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and Ca2+ leakage

Gomisin G Suppresses the Growth of Colon Cancer Cells by Attenuation of AKT Phosphorylation and Arrest of Cell Cycle Progression

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