scholarly journals Anti-Inflammatory Properties of Irisin, Mediator of Physical Activity, Are Connected with TLR4/MyD88 Signaling Pathway Activation

2017 ◽  
Vol 18 (4) ◽  
pp. 701 ◽  
Author(s):  
Agnieszka Irena Mazur-Bialy ◽  
Ewa Pocheć ◽  
Marcin Zarawski
Keyword(s):  
Physical Activity ◽  
Signaling Pathway ◽  
Pathway Activation ◽  
Anti Inflammatory ◽  
Myd88 Signaling

scholarly journals Baicalin inhibits TLR7/MYD88 signaling pathway activation to suppress lung inflammation in mice infected with influenza A virus

2014 ◽  
Vol 2 (3) ◽  
pp. 437-441 ◽  
Author(s):  
QIAOFENG WAN ◽  
HAO WANG ◽  
XUEBO HAN ◽  
YUAN LIN ◽  
YANHUI YANG ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Influenza A Virus ◽  
Lung Inflammation ◽  
Influenza A ◽  
Pathway Activation ◽  
Myd88 Signaling

scholarly journals Anemoside B4 protects against Klebsiella pneumoniae- and influenza virus FM1-induced pneumonia via the TLR4/Myd88 signaling pathway in mice

2020 ◽  
Author(s):  
Jia He ◽  
Renyikun Yuan ◽  
Xiaolan Cui ◽  
Yushun Cui ◽  
Shan Han ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Molecular Docking ◽  
Signaling Pathway ◽  
Therapeutic Effect ◽  
Inflammatory Cytokines ◽  
Inflammatory Activity ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Myd88 Signaling ◽  
Pro Inflammatory Cytokines

Abstract Background: Pneumonia refers to the inflammation of the terminal airway, alveoli and pulmonary interstitium, which can be caused by pathogenic microorganisms, physical and chemical factors, immune damage, and drugs. Anemoside B4, the major ingredient of Pulsatilla chinensis (Bunge) Regel, exhibited anti-inflammatory activity. However, the therapeutic effect of anemoside B4 on pneumonia has not been unraveled. This study aims to investigate that anemoside B4 attenuates the inflammatory responses in Klebsiella pneumonia (KP)- and influenza virus FM1 (FM1)-induced pneumonia mice model.Methods: The network pharmacology and molecular docking assays were employed to predict the targets of anemoside B4’s treatment of pneumonia. Two models (bacterial KP-infected mice and virus FM1-infected mice) were employed in our study. BALB/c mice were divided into six groups: control, model group (KP- induced pneumonia or FM1-induced pneumonia), anemoside B4 (B4)-treated group (2.5, 5, 10 mg/kg), and positive drug group (Ribavirin or Ceftriaxone Sodium Injection). Blood samples were collected for hematology analysis. The effects of B4 on inflammation-associated mediators were investigated by Enzyme-linked immunosorbent assay (ELISA) and hematoxylin and eosin staining (HE) staining. Proteins expression was quantified by western blotting.Results: The network results indicated that many pro-inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) participated in anemoside B4’s anti-inflammatory activity. The counts of neutrophil (NEU) and white blood cell (WBC), the level of myeloperoxidase (MPO), and the release of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 increased by KP or FM1 infection, which were reversed by anemoside B4. In addition, anemoside B4 significantly suppressed the FM1-induced expression of Toll-like receptor 4 (TLR4), myeloid differential protein-88 (MyD88), and myeloid differentiation protein-2 (MD-2), which were further validated by molecular docking data that anemoside B4 bound to bioactive sites of TLR4. Therefore, anemoside B4 exhibited a significant therapeutic effect on pneumonia via the TLR4/MyD88 pathway.Conclusion: Our findings demonstrated that anemoside B4 attenuates pneumonia via the TLR4/Myd88 signaling pathway, suggesting that anemoside B4 is a promising therapeutic candidate for bacterial-infected or viral-infected pneumonia.

Neuroprotective and anti-inflammatory effects of isoliquiritigenin in kainic acid-induced epileptic rats via the TLR4/MYD88 signaling pathway

2019 ◽  
Vol 27 (6) ◽  
pp. 1143-1153 ◽  
Author(s):  
Xiaobo Zhu ◽  
Jiankun Liu ◽  
Ou Chen ◽  
Jiang Xue ◽  
Shanying Huang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Kainic Acid ◽  
Anti Inflammatory ◽  
Myd88 Signaling

scholarly journals Gut Microbiota Disorders Promote Inflammation and Aggravate Spinal Cord Injury Through the TLR4/MyD88 Signaling Pathway

2021 ◽  
Vol 8 ◽  
Author(s):  
Zijie Rong ◽  
Yuliang Huang ◽  
Honghua Cai ◽  
Min Chen ◽  
Hao Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Gut Microbiota ◽  
Signaling Pathway ◽  
Nerve Cells ◽  
Inflammatory Factors ◽  
Arginase 1 ◽  
Cord Injury ◽  
Anti Inflammatory ◽  
Myd88 Signaling

Background: In spinal cord injury (SCI), systemic inflammation and the death of nerve cells in the spinal cord are life threatening. The connection between gut microbiota and signaling pathways has been a hot research topic in recent years. The Toll-like receptor 4/Myeloid differentiation factor 88 (TLR4/MyD88) signaling pathway is closely related to the inflammatory response. This study explored whether the gut microbiota imbalance could affect the TLR4/MyD88 signaling pathway to regulate SCI to provide a new basis for SCI research and treatment.Methods: An SCI model was constructed to study the influence on the injury of gut microbiota. 16S amplicon sequencing was used to identify the diversity and abundance of gut microbes. Fecal microbiota transplantation was performed in mice with SCI. ELISA was used to detect the serum levels of pro-inflammatory and anti-inflammatory factors in mice. Hematoxylin and eosin staining was used to observe SCI in mice. Immunofluorescence was used to detect the rates of loss glial fibrillary acidic protein (GFAP), neuronal nuclear protein (NeuN), and ionized calcium-binding adapter molecule 1 (IBA1) in the spinal cord as indicators of apoptosis. The expression of the TLR4/MyD88 signaling pathway was detected by qRT-PCR and western blotting.Results: Significant differences were observed in the gut microbiota of SCI mice and normal mice. The gut microbiota of SCI mice was imbalanced. The levels of pro-inflammatory cytokines tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 in SCI mice were increased, as was the level of the toxic induced nitric oxide synthase. The levels of anti-inflammatory factors IL-4, transforming growth factor-β, and IL-10 were decreased, as was the level of arginase-1. The apoptosis rates of GFAP, NeuN, and IBA1 were increased. The TLR4/MyD88 signaling pathway was activated. In the SCI group, inflammation increased after fecal transplantation, apoptosis of GFAP, NeuN, and IBA1 increased, and SCI was more serious.Conclusion: The TLR4/MyD88 signaling pathway promotes the death of nerve cells by inducing inflammation. Gut microbiota dysregulation can lead to aggravated SCI by activating the TLR4/MyD88 signaling pathway.

scholarly journals Anemoside B4 protects against Klebsiella pneumoniae- and influenza virus FM1-induced pneumonia via the TLR4/Myd88 signaling pathway in mice

2020 ◽  
Author(s):  
Jia He ◽  
Renyikun Yuan ◽  
Xiaolan Cui ◽  
Yushun Cui ◽  
Shan Han ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Molecular Docking ◽  
Signaling Pathway ◽  
Therapeutic Effect ◽  
Inflammatory Cytokines ◽  
Inflammatory Activity ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Myd88 Signaling ◽  
Pro Inflammatory Cytokines

Abstract Background Pneumonia refers to the inflammation of the terminal airway, alveoli and pulmonary interstitium, which can be caused by pathogenic microorganisms, physical and chemical factors, immune damage, and drugs. Anemoside B4, the major ingredient of Pulsatilla chinensis (Bunge) Regel, exhibited anti-inflammatory activity. However, the therapeutic effect of anemoside B4 on pneumonia has not been unraveled. This study aims to investigate that anemoside B4 attenuates the inflammatory responses in Klebsiella pneumonia (KP)- and influenza virus FM1 (FM1)-induced pneumonia mice model.Methods The network pharmacology and molecular docking assays were employed to predict the targets of anemoside B4’s treatment of pneumonia. Two models (bacterial KP-infected mice and virus FM1-infected mice) were employed in our study. BALB/c mice were divided into six groups: control, model group (KP- induced pneumonia or FM1-induced pneumonia), anemoside B4 (B4)-treated group (2.5, 5, 10 mg/kg), and positive drug group (Ribavirin or Ceftriaxone Sodium Injection). Blood samples were collected for hematology analysis. The effects of B4 on inflammation-associated mediators were investigated by Enzyme-linked immunosorbent assay (ELISA). Proteins expression was quantified by western blotting.Results The network results indicated that many pro-inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) participated in anemoside B4’s anti-inflammatory activity. The counts of neutrophil (NEU) and white blood cell (WBC), the level of myeloperoxidase (MPO), and the release of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 increased by KP or FM1 infection, which were reversed by anemoside B4. In addition, anemoside B4 significantly suppressed the FM1-induced expression of Toll-like receptor 4 (TLR4), myeloid differential protein-88 (MyD88), and myeloid differentiation protein-2 (MD-2), which were further validated by molecular docking data that anemoside B4 bound to bioactive sites of TLR4. Therefore, anemoside B4 exhibited a significant therapeutic effect on pneumonia via the TLR4/MyD88 pathway.Conclusion Our findings demonstrated that anemoside B4 attenuates pneumonia via the TLR4/Myd88 signaling pathway, suggesting that anemoside B4 is a promising therapeutic candidate for bacterial-infected or viral-infected pneumonia.

Role of Daphnetin in Rat Severe Acute Pancreatitis Through the Regulation of TLR4/NF-κB Signaling Pathway Activation

2016 ◽  
Vol 44 (01) ◽  
pp. 149-163 ◽  
Author(s):  
Zhiyong Liu ◽  
Jiao Liu ◽  
Kailiang Zhao ◽  
Qiao Shi ◽  
Teng Zuo ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Severe Acute Pancreatitis ◽  
Sodium Taurocholate ◽  
Neutrophil Infiltration ◽  
Sod Activity ◽  
Molecular Analyses ◽  
Pathway Activation ◽  
Anti Inflammatory

Severe acute pancreatitis (SAP) often results in multiple-organ dysfunction syndrome with high mortality. There is no effective clinical therapy for SAP, yet daphnetin, a coumarin extracted from Dracaena marginata, has analgesic and anti-inflammatory effects, and has been used clinically in several diseases. The objective of this study was to investigate the role and underlying mechanisms of daphnetin in a rat SAP model. Male Wistar rats were pretreated with daphnetin via intraperitoneal injection, 30[Formula: see text]min before retrograde infusion of 5% sodium taurocholate into the biliopancreatic duct. Twelve hours after sodium taurocholate administration, rats were sacrificed and tissues and blood were harvested. Then, histological, chemical, and molecular analyses were performed. Daphnetin treatment reduced the levels of serum alanine transaminase and creatinine (CR), increased superoxide dismutase(SOD) activity, and decreased neutrophil infiltration and cell apoptosis of the pancreatic tissues in rat SAP. Daphnetin treatment significantly decreased expression of pro-inflammatory cytokines and increased expression of anti-inflammatory cytokines in rat SAP. Molecular analyses revealed that daphnetin reduced TLR4 expression and inhibited NF-[Formula: see text]B signaling pathway activation. These findings demonstrate that daphnetin attenuates acute pancreatic injury by regulating the TLR4/NF-[Formula: see text]B signaling pathway and inflammation in rat SAP model. Daphnetin may be a potential therapeutic agent for SAP.

scholarly journals Antiulcerogenic Activity of Li-Zhong Decoction on Duodenal Ulcers Induced by Indomethacin in Rats: Involvement of TLR-2/MyD88 Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Houpan Song ◽  
Meiyan Zeng ◽  
Xiaojuan Chen ◽  
Xinyi Chen ◽  
Jun Peng ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Duodenal Mucosa ◽  
Interleukin 4 ◽  
Prostaglandin E ◽  
Sprague Dawley ◽  
Serious Adverse Events ◽  
Inflammatory Infiltration ◽  
Expression Levels ◽  
Anti Inflammatory ◽  
Myd88 Signaling

Background. Administration of nonsteroidal anti-inflammatory drugs (NSAIDs) often causes small intestinal ulcers in patients, but few effective drugs are currently available to manage such serious adverse events of NSAIDs. Li-Zhong decoction (LZD), a well-known traditional Chinese medicine (TCM) formula, is commonly prescribed for treatment of gastrointestinal diseases. The present study aimed to investigate the anti-ulcerogenic activity of LZD on indomethacin- (IND-) induced duodenal ulcer in rats. Mechanistic studies of action of LZD were focused on involvement of TLR-2/MyD88 signaling pathway. Methods. Fifty male Sprague-Dawley (SD) rats were randomly and evenly divided into five groups: normal control, ulcer control (IND, 25 mg/kg), IND + esomeprazole (ESO, 4.17 mg/kg), and IND + low and high doses of LZD (3.75 and 7.50 g/kg). Macroscopic and histopathological examinations were performed for evaluation of ulcer index (UI), curative index (CI), and microscopic score (MS). Levels of duodenal inflammatory biomarkers and cytoprotective mediators including interleukin-4 (IL-4), IL-10, tumor necrosis factor-α (TNF-α), and prostaglandin E2 (PGE2) were measured by ELISA. Expression levels of TLR-2 and MyD88 mRNA were assessed by qRT-PCR. The expression and distribution of TLR-2 and MyD88 proteins were analyzed by western blot and immunohistochemistry, respectively. Results. Gross and microscopic examinations of the IND-treated rats revealed severe duodenal hemorrhagic necrosis, inflammatory infiltration, villus destruction, and crypt abscess, while LZD-treated rats manifested these pathological events to a markedly lesser degree. LZD significantly decreased UI and MS, increased CI, preserved the integrity of the villus and crypt, and normalized the tissue architecture of the duodenum of rats. The elevated TNF-α levels in the IND-treated rats were markedly diminished in the LZD-treated rats, while lower levels of IL-4, IL-10, and PGE2 observed in IND-treated rats were significantly increased in LZD-treated rats. Interestingly, improvement of immune function in duodenal mucosa by reduction of mRNA and protein expression levels of TLR-2 and MyD88 was also observed in rats treated with LZD. Consistently, immunohistochemical analyses revealed a lower co-localization of TLR-2 and MyD88 proteins in the duodenal mucosa of LZD-treated rats as compared to the IND-induced rats. Conclusions. Our data demonstrate that LZD protects the duodenal mucosa from IND-caused lesions, which is at least partially attributable to the interaction of its potential cytoprotective and anti-inflammatory mechanisms together with enhancement of the mucosal immunity through TLR-2/MyD88 signaling pathway.

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