Effect of the Miaoyao Fanggan sachet-derived isorhamnetin on TLR2/4 and NKp46 expression in mice

Wang, Hui; Zhang, Quan; Cheng, Ming; Ma, Li; Meng, Qing Zhi; Duan, Liang; Chen, Yun; Tan, Jia Wu; Chen, Man; Liang, Tiantian; Li, Guo Jun; Li, Jun Li

doi:10.1016/j.jep.2012.08.040

Cited by 12 publications

(9 citation statements)

References 32 publications

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“…Classically, during Th2 responses, DCs play a very important role by activating allergen-specific Th2 cells and inducing their proliferation, leading to the release of a particular set of cytokines, emergence of helper functions and generation of memory cells. Regardless of site, neutrophilic inflammation tends to show a direct relationship with lipopolysaccharides (LPS) exposure, a major component of the outer cell wall of Gram-negative bacteria, by activation of the Th17 response with the assistance of DCs (McAleer, et al, 2010; L. Wang, et al, 2012; Wilson, et al, 2009).…”

Section: Tlrs and Nf-κb In Allergic Asthma: Effects On Epithelial mentioning

confidence: 99%

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Oxidative stress and cellular pathways of asthma and inflammation: Therapeutic strategies and pharmacological targets

Mishra

Banga

Silveyra

2018

Pharmacology & Therapeutics

220

127

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Asthma is a complex inflammatory disease characterized by airway inflammation and hyperresponsiveness. The mechanisms associated with the development and progression of asthma have been widely studied in multiple populations and animal models, and these have revealed involvement of various cell types and activation of intracellular signaling pathways that result in activation of inflammatory genes. Significant contributions of Toll-like-receptors (TLRs) and transcription factors such as NF-кB, have been reported as major contributors to inflammatory pathways. These have also recently been associated with mechanisms of oxidative biology. This is of important clinical significance as the observed inefficacy of current available treatments for severe asthma is widely attributed to oxidative stress. Therefore, targeting oxidizing molecules in conjunction with inflammatory mediators and transcription factors may present a novel therapeutic strategy for asthma. In this review, we summarize TLRs and NF-кB pathways in the context of exacerbation of asthma pathogenesis and oxidative biology, and we discuss the potential use of polyphenolic flavonoid compounds, known to target these pathways and possess antioxidant activity, as potential therapeutic agents for asthma.

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Section: Tlrs and Nf-κb In Allergic Asthma: Effects On Epithelial mentioning

confidence: 99%

“…Li, et al, 2015; Shishodia, Majumdar, Banerjee, & Aggarwal, 2003). Isorhamnetin also modulated TLR activity and offered protection against oxidative stress in an animal model of influenza infection, where it increased TLR2/4 expression in a dose-dependent manner (H. Wang, et al, 2012).…”

Section: Pharmacological Approaches Targeting Tlr/nf-κb and Oxidatmentioning

confidence: 99%

Oxidative stress and cellular pathways of asthma and inflammation: Therapeutic strategies and pharmacological targets

Mishra

Banga

Silveyra

2018

Pharmacology & Therapeutics

220

127

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“…Bao and colleagues found that Iso had protective effects on ox-LDL-induced endothelial cell injuries by increasing antioxidant activity and activating p38MAPK signaling pathway [ 17 ]. Anti-tumor [ 18 ], antiviral [ 19 ], and anti-inflammatory properties [ 20 ] and neurodegenerative injury protection [ 21 ] have also been reported. These studies highlight the potential function of Iso in the prevention and treatment of cardiovascular and cancer diseases.…”

Section: Introductionmentioning

confidence: 99%

Isorhamnetin Attenuates Atherosclerosis by Inhibiting Macrophage Apoptosis via PI3K/AKT Activation and HO-1 Induction

Luo

Sun

et al. 2015

PLoS ONE

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Background and PurposeIsorhamnetin (Iso) is a flavonoid compound extracted from the Chinese herb Hippophae rhamnoides L. Previous studies have revealed its anti-cancer, anti-inflammatory, and anti-oxidant activities. This study investigated the ability of Iso to inhibit oxidized low-density lipoprotein (ox-LDL)-induced cell apoptosis in THP-1-derived macrophages. The effects of Iso on atherosclerosis in vivo were also evaluated in apolipoprotein E knockout (ApoE-/-) mice fed a high fat diet.Methods and ResultsIso showed significant inhibitory effects on ox-LDL-induced THP-1-derived macrophage injuries via decreasing reactive oxygen species levels, lipid deposition, and caspase-3 activation, restoring mitochondrial membrane potential, reducing the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells, and regulating apoptosis-related proteins. We also determined the protective effects of Iso by PI3K/AKT activation and HO-1 induction. Iso reduced the atherosclerotic plaque size in vivo in ApoE-/- mice as assessed by oil red O, Sudan IV staining, and CD68-positive cells, and reduced macrophage apoptosis as assessed by caspase-3 and TUNEL assays in lesions.ConclusionIn conclusion, our results show that Iso inhibited atherosclerotic plaque development in ApoE-/- mice by PI3K/AKT activation and HO-1 induction.

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“…The expression levels of TLR2 and SIgA in the mice which continuously inhaled the sachet odor are signi cantly up-regulated compared with those in the mice that inhaled sachets intermittently. Nevertheless, the results of mice inhaled sachets continuously for 4 weeks are similar to those of mice inhaled for 6 weeks [20]. Based on these preliminary experimental results, our research team optimized and modi ed the previous experimental conditions by establishing a hypoimmunity model under cold stimulation.…”

Section: Discussionmentioning

confidence: 84%

Mechanism underlying the role of Miaoyao Fanggan sachet in up-regulating respiratory tract immunity through TLR-MyD88-NFκB signaling pathway

Zhu

Zhang

et al. 2020

Preprint

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Background To elucidate the mechanism underlying the role of Miaoyao Fanggan sachet (MFS) in improving respiratory immunity through the TLR-MyD88-NFκB signaling pathway in MyD88 knockout mouse models and human normal lung epithelial cell line (BEAS-2B).Methods Sixteen male C57BL/6J mice (SPF grade) were randomly divided into the control (n = 8) and MFS groups (n = 8) and 16 male MyD88 knockout mice were randomly assigned into the MyD88 knockout (MyD88-KO group, n = 8) and MyD88 KO + MFS groups (n = 8). Mice in the MFS intervention group were continuously treated with MFS inhalation from 8:00 am to 8:00 pm for 30 d and the sachets were replaced every 6 d. Hematoxylin-eosin (H.E.) staining was used to observe the pathological changes of lung tissues. The expression levels of TAK1, NFκB p65, IκB and IL6 in mouse lung tissues were detected by immunohistochemical staining, immunofluorescent staining, Western blot and qRT-PCR, respectively.Results Mikawa’s lung injury score did not significantly differ between the control and MFS groups (both P > 0.05). The parameters related to liver and kidney function did not significantly differ among four groups (all P > 0.05). The TAK1, NFκB p65, IκB and IL6 mRNA and protein in the MFS group were significantly up-regulated than those in the other groups (all P < 0.05). Compared with the MyD88-KO group, they were significantly up-regulated in the MyD88-KO + MFS group (P < 0.05).Conclusion HFS can improve the respiratory immunity probably by up-regulating the expression level of MyD88, activating the TLR-MyD88-NFκB signaling pathway and stimulating the release of cytokines in the downstream pathway.

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Effect of the Miaoyao Fanggan sachet-derived isorhamnetin on TLR2/4 and NKp46 expression in mice

Cited by 12 publications

References 32 publications

Oxidative stress and cellular pathways of asthma and inflammation: Therapeutic strategies and pharmacological targets

Oxidative stress and cellular pathways of asthma and inflammation: Therapeutic strategies and pharmacological targets

Isorhamnetin Attenuates Atherosclerosis by Inhibiting Macrophage Apoptosis via PI3K/AKT Activation and HO-1 Induction

Mechanism underlying the role of Miaoyao Fanggan sachet in up-regulating respiratory tract immunity through TLR-MyD88-NFκB signaling pathway

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