Protective effects of polydatin on lipopolysaccharide-induced acute lung injury through TLR4-MyD88-NF-κB pathway

Jiang, Qi; Yi, Min; Guo, Qianqian; Wang, Ciman; Wang, Huimin; Meng, Shanshan; Liu, Chao; Fu, Yeliu; Ji, Hui; Chen, Tong

doi:10.1016/j.intimp.2015.10.027

Cited by 163 publications

(84 citation statements)

References 35 publications

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“…LTA, a specific endotoxin embedded in the cell wall of S. aureus , has been reported to activate the inflammatory response . Although PD has been showed a potent anti‐inflammatory effects , previous studies have focused on the inhibition of pro‐inflammatory factors to exert anti‐inflammatory effects, Recently, it has been found that the level of intracellular ROS also causes the tissue injury in many inflammatory disease, such as atherosclerosis . However, our study has confirmed PD may play a protective role by reducing intracellular ROS levels, which might provide a new therapeutic target for the development of anti‐inflammatory drugs.…”

Section: Discussionsupporting

confidence: 55%

“…A), as a natural precursor of resveratrol, which is a naturally occurring stilbene endowed with multiple health‐promoting effects, is the main active phenolic compound extracted from the root of Polygonum cuspidatum , which has been widely used as a traditional Chinese medicine for centuries. Given the potent antioxidant effects , anti‐inflammatory effects and antitumour effects , it has received worldwide attention for its beneficial effects on cardiovascular, inflammatory, neurodegenerative, metabolic and age‐related diseases . Studies have shown that LTA can induce a high level of intracellular ROS in various cell types, leading to injury, such as inflammation .…”

Section: Introductionmentioning

confidence: 99%

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Polydatin reduces Staphylococcus aureus lipoteichoic acid‐induced injury by attenuating reactive oxygen species generation and TLR2‐NFκB signalling

Zhao

Jiang

et al. 2017

J Cellular Molecular Medi

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Staphylococcus aureus (S. aureus) causes severe inflammation in various infectious diseases, leading to high mortality. The clinical application of antibiotics has gained a significant curative effect. However, it has led to the emergence of various resistant bacteria. Therefore, in this study, we investigated the protective effect of polydatin (PD), a traditional Chinese medicine extract, on S. aureus lipoteichoic acid (LTA)‐induced injury in vitro and in vivo. First, a significant improvement in the pathological conditions of PD in vivo was observed, suggesting that PD had a certain protective effect on LTA‐induced injury in a mouse model. To further explore the underlying mechanisms of this protective effect of PD, LTA‐induced murine macrophages were used in this study. The results have shown that PD could reduce the NF‐κB p65, and IκBα phosphorylation levels increased by LTA, resulting in a decrease in the transcription of pro‐inflammatory factors, such as TNF‐α, IL‐1β and IL‐6. However, LTA can not only activate NF‐κB through the recognition of TLR2 but also increase the level of intracellular reactive oxygen species (ROS), thereby activating NF‐κB signalling. We also detected high levels of ROS that activate caspases 9 and 3 to induce apoptosis. In addition, using a specific NF‐κB inhibitor that could attenuate apoptosis, namely NF‐κB p65, acted as a pro‐apoptotic transcription factor in LTA‐induced murine macrophages. However, PD could inhibit the generation of ROS and NF‐κB p65 activation, suggesting that PD suppressed LTA‐induced injury by attenuating ROS generation and TLR2‐NFκB signalling.

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Section: Discussionsupporting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Polydatin reduces Staphylococcus aureus lipoteichoic acid‐induced injury by attenuating reactive oxygen species generation and TLR2‐NFκB signalling

Zhao

Jiang

et al. 2017

J Cellular Molecular Medi

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“…Inflammatory process is highly related to various coronary diseases including acute MI, microvascular reperfusion injury and ischaemic heart disease myocardial necrosis 26. Some studies suggested that a substantial amount of TNF‐α is produced in cardiac myocytes exposed to LPS 27, 28. The pro‐inflammatory cytokines including TNF‐α and IL‐6 are involved in the initiation and regulation of inflammatory response 29.…”

Section: Discussionmentioning

confidence: 99%

Salidroside suppressing LPS‐induced myocardial injury by inhibiting ROS‐mediated PI3K/Akt/mTOR pathway in vitro and in vivo

Chen

Liu

Feng

et al. 2017

J Cellular Molecular Medi

198

104

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The purpose of the present study was to investigate the effect of salidroside (Sal) on myocardial injury in lipopolysaccharide (LPS)‐induced endotoxemic in vitro and in vivo. SD rats were randomly divided into five groups: control group, LPS group (15 mg/kg), LPS plus dexamethasone (2 mg/kg), LPS plus Sal groups with different Sal doses (20, 40 mg/kg). Hemodynamic measurement and haematoxylin and eosin staining were performed. Serum levels of creatine kinase (CK), lactate dehydrogenase, the activities of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH‐px), glutathione, tumour necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6), and interleukin‐1β (IL‐1β) were measured after the rats were killed. iNOS, COX‐2, NF‐κB and PI3K/Akt/mTOR pathway proteins were detected by Western blot. In vitro, we evaluated the protective effect of Sal on rat embryonic heart‐derived myogenic cell line H9c2 induced by LPS. Reactive oxygen species (ROS) in H9c2 cells was measured by flow cytometry, and the activities of the antioxidant enzymes CAT, SOD, GSH‐px, glutathione‐S‐transferase, TNF‐α, IL‐6 and IL‐1β in cellular supernatant were measured. PI3K/Akt/mTOR signalling was examined by Western blot. As a result, Sal significantly attenuated the above indices. In addition, Sal exerts pronounced cardioprotective effect in rats subjected to LPS possibly through inhibiting the iNOS, COX‐2, NF‐κB and PI3K/Akt/mTOR pathway in vivo. Furthermore, the pharmacological effect of Sal associated with the ROS‐mediated PI3K/Akt/mTOR pathway was proved by the use of ROS scavenger, N‐acetyl‐l‐cysteine, in LPS‐stimulated H9C2 cells. Our results indicated that Sal could be a potential therapeutic agent for the treatment of cardiovascular disease.

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“…Upon ISO stimulated inflammation and oxidative stress, IκB is phosphorylated at serine residues and the phosphorylation of p65 subunit is also promoted. Then p65 phosphorylation enhances NF-κB-driven transcriptional activity and the degradation of IκBα [40,41]. Researchers clarified that NF-κB p65 phosphorylation and nuclear translocation were down-regulated by Rho kinase inhibition [42,43].…”

Section: Discussionmentioning

confidence: 99%

Crocetin ester improves myocardial ischemia via Rho/ROCK/NF-κB pathway

Huang

Chen

Wang

et al. 2016

International Immunopharmacology

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Protective effects of polydatin on lipopolysaccharide-induced acute lung injury through TLR4-MyD88-NF-κB pathway

Cited by 163 publications

References 35 publications

Polydatin reduces Staphylococcus aureus lipoteichoic acid‐induced injury by attenuating reactive oxygen species generation and TLR2‐NFκB signalling

Polydatin reduces Staphylococcus aureus lipoteichoic acid‐induced injury by attenuating reactive oxygen species generation and TLR2‐NFκB signalling

Salidroside suppressing LPS‐induced myocardial injury by inhibiting ROS‐mediated PI3K/Akt/mTOR pathway in vitro and in vivo

Crocetin ester improves myocardial ischemia via Rho/ROCK/NF-κB pathway

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