TLR4 participates in sympathetic hyperactivity Post-MI in the PVN by regulating NF-κB pathway and ROS production

Wang, Yu; Hu, Hesheng; Yin, Jing; Shi, Yugen; Tan, Jieqiong; Zheng, Lu; Wang, Cailing; Li, Xiaolu; Xue, Mei; Ju, Liu; Wang, Ye; Li, Yan; Li, Xinran; Liu, Fuhong; Liu, Qiang; Yan, Shi Fang

doi:10.1016/j.redox.2019.101186

Cited by 83 publications

(57 citation statements)

References 57 publications

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“…For instance, under anaerobic conditions, mitochondrial fission and apoptosis-related circRNA (MFACR) suppresses the uninterrupted expression of miR-652-3p and MTP18 proteins, which leads to the imbalance of ROS, triggers the accumulation of mitochondrial fragments, and then results in apoptotic cell death [100]. ROS is involved in the toll-like receptor 4 (TLR4) and its downstream molecular pathway in mediating sympathetic activity post-MI within the paraventricular nucleus (PVN) [101]. The activation of TLR4 enhances the sympathetic activity after myocardial infarction by activating the microglia NF-κB and ROS in the paraventricular nucleus of the hypothalamus.…”

Section: Myocardial Infarction (Mi)mentioning

confidence: 99%

Effects of REDOX in Regulating and Treatment of Metabolic and Inflammatory Cardiovascular Diseases

Wang

Dong

Liu

et al. 2020

Oxidative Medicine and Cellular Longevity

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Reduction oxidation (REDOX) reaction is crucial in life activities, and its dynamic balance is regulated by ROS. Reactive oxygen species (ROS) is associated with a variety of metabolic diseases involving in multiple cellular signalling in pathologic and physiological signal transduction. ROS are the by-products of numerous enzymatic reactions in various cell compartments, including the cytoplasm, cell membrane, endoplasmic reticulum (ER), mitochondria, and peroxisome. ROS signalling is not only involved in normal physiological processes but also causes metabolic dysfunction and maladaptive responses to inflammatory signals, which depends on the cell type or tissue environment. Excess oxidants are able to alter the normal structure and function of DNA, lipids, and proteins, leading to mutations or oxidative damage. Therefore, excessive oxidative stress is usually regarded as the cause of various pathological conditions, such as cancer, neurodegeneration, cardiovascular diseases (CVDs), diabetes, and kidney diseases. Currently, it has been possible to detect diabetes and other cardiac diseases by detecting derivatives accompanied by oxidative stress in vivo as biomarkers, but there is no effective method to treat these diseases. In consequence, it is essential for us to seek new therapy targeting these diseases through understanding the role of ROS signalling in regulating metabolic activity, inflammatory activation, and cardiac diseases related to metabolic dysfunction. In this review, we summarize the current literature on REDOX and its role in the regulation of cardiac metabolism and inflammation, focusing on ROS, local REDOX signalling pathways, and other mechanisms.

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Section: Myocardial Infarction (Mi)mentioning

confidence: 99%

Effects of REDOX in Regulating and Treatment of Metabolic and Inflammatory Cardiovascular Diseases

Wang

Dong

Liu

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Sepsis-induced myocardial injury is characterized by neutrophil infiltration which triggers inflammatory response and edema [13]. The protein expressions of toll-like receptor 4 (TLR-4) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) have been shown to be upregulated in myocardial tissues of myocardial injury rats [14]. The results of this study suggest that inflammation in myocardial injury rats may have been due to increased release of inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 73%

Trigonoside II mitigates sepsis-induced myocardial injury via reduction in oxidative stress and regulation of TLR- 4/NF-kB inflammatory pathway

Wang¹,

Wu²,

Liang³

2020

Trop. J. Pharm Res

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Purpose: To investigate the protective effect of trigonoside II against sepsis-induced myocardial injury in rats, and the mechanism involved. Methods: Adult male Sprague Dawley rats (n = 30) weighing 200 - 230 g (mean weight = 215 ± 15 g) were used for this study. The rats were randomly assigned to 3 groups (10 rats/group): sham, cecal ligation puncture (CLP), and trigonoside II. Rats in the treatment group received trigonoside II at a dose of 2 mg/kg intraperitoneally (i.p.) at 3, 12 and 24 h post-surgery. Sepsis was induced using CLP method. Lactate dehydrogenase (LDH) and creatine kinase (CK-MB) activities, and hemodynamic functions were determined in the rats. The levels of interleukin (IL)-1β and IL-6, and tumor necrosis factor α (TNF-α) were assayed in rat serum. Oxidative stress and myocardial cell apoptosis were determined by measuring malondialdehyde (MDA) levels, while activities of glutathione peroxidase (GPx), superoxide dismutase (SOD) and myeloperoxidase (MPO), as well as levels of expression of bax, bcl-2 and caspase-3 were also assessed. Results: Treatment of myocardial injury rats with trigonoside II led to significant reductions in the activities of LDH, CK-MB and MPO, and decreases in levels of IL-1β, IL-6 and TNF-α (p < 0.05). It also significantly reversed the effects of sepsis on rat hemodynamic functions (p < 0.05). Trigonoside IItreatment significantly reduced MDA levels in rat myocardial tissues, but significantly increased SOD and GPx activities (p < 0.05). It significantly down-regulated protein expressions of NF-kB and TLR-4 in myocardial tissues (p < 0.05). The number of apoptotic cells and activity of caspase-3 were significant increased in myocardial tissues of rats in CLP group, when compared with sham group, but were reduced significantly in myocardial tissues of trigonoside II-treated rats (p < 0.05). Similarly, trigonoside II treatment down-regulated the protein expressions of caspase-3 and bax, but upregulated bcl-2 protein expression in the rat myocardial tissues (p < 0.05). Conclusion: The results of this study indicate that trigonoside II confers protection on sepsis-induced myocardial injury via reduction in oxidative stress and regulation of TLR-4/NF-kB inflammatory pathway. Keywords: Cecal ligation puncture, Myocardial injury, Oxidative stress, Sepsis, Trigonoside II

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“…Among these candidate signaling pathways, the toll-like receptor (TLR) signaling pathway was identified as the relatively most significantly pathway. Previous studies reported that TLR4/NF-κB signaling cascades contributes to VA under myocardial ischemia condition ( Jiang et al., 2019 ; Wang et al., 2019 ). Our former work demonstrated that TLR4/MyD88/CaMKII signaling pathway contributed to obesity-induced ventricular electrical remodeling ( Shuai et al., 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Shensong Yangxin Protects Against Metabolic Syndrome-Induced Ventricular Arrhythmias by Inhibiting Electrical Remodeling

et al. 2020

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Shensong Yangxin (SSYX) is a traditional Chinese medicine, which has been proven to improve the clinical symptoms of arrhythmia. However, the role of SSYX in metabolic syndrome (MetS)-induced electrical remodeling remains to be fully elucidated. Here, we sought to clarify whether SSYX can alter the electrophysiological remodeling of cardiac myocytes from MetS rats by regulating transient outward potassium current ( I to ) and calcium current ( I Ca-L ). Male Wistar rats were subjected to 16 weeks of high-carbohydrate, high-fat to produce a MetS model group. SSYX (0.4 g/kg) was administrated by daily gavage 8 weeks following high-carbohydrate, high-fat for 8 weeks. In vivo electrophysiological study was performed to evaluated ventricular arrhythmias (VA) vulnerability and electrophysiological properties. The potential electrical mechanisms were estimated by whole-cell patch-clamp and molecular analysis. The H9C2 cells were used to verify the protective role of SSYX in vitro . After 16-week high-carbohydrate, high-fat feeding, MetS model rats showed increased body weight (BW), blood pressure (BP), blood sugar (BS), heart rate (HR) and heart weights to tibia length (HW/TL) ratio. Furthermore, MetS rats depicted increased VA inducibility, shortened effective refractory period (ERP) and prolonged action potential duration (APD). Lower I Ca-L and I to current densities were observed in MetS rats than CTL rats. Additionally, MetS rats exhibited significantly increased cardiac fibrosis, decreased Cx43 expression and protein levels of Cav1.2, Kv4.2, Kv4.3 than CTL group. As expected, these MetS-induced effects above were reversed when SSYX was administrated. Mechanistically, SSYX administrated significantly down-regulated the TLR4/MyD88/CaMKII signaling pathway both in vivo and in vitro . Collectively, our data indicated that the electrical remodeling induced by MetS contributed to the increased VA susceptibility. SSYX protects against MetS-induced VA by inhibiting electrical remodeling through TLR4/MyD88/CaMKII signaling pathway.

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TLR4 participates in sympathetic hyperactivity Post-MI in the PVN by regulating NF-κB pathway and ROS production

Cited by 83 publications

References 57 publications

Effects of REDOX in Regulating and Treatment of Metabolic and Inflammatory Cardiovascular Diseases

Effects of REDOX in Regulating and Treatment of Metabolic and Inflammatory Cardiovascular Diseases

Trigonoside II mitigates sepsis-induced myocardial injury via reduction in oxidative stress and regulation of TLR- 4/NF-kB inflammatory pathway

Shensong Yangxin Protects Against Metabolic Syndrome-Induced Ventricular Arrhythmias by Inhibiting Electrical Remodeling

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