Polydatin attenuates reactive oxygen species-induced airway remodeling by promoting Nrf2-mediated antioxidant signaling in asthma mouse model

Zeng, Haizhu; Wang, Yumeng; Gu, Yuxia; Wang, Jinrui; Zhang, Huali; Gao, Hongchang; Jin, Qinqin; Zhao, Lei

doi:10.1016/j.lfs.2018.08.013

Cited by 46 publications

(34 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, polydatin has mediated Parkin-dependent mitophagy and protects against mitochondria-dependent apoptosis in ARDS [ 209 , 210 ] niae (MP) infection, MP can infect both the upper and lower respiratory tracts, was found to be suppressed by polydatin treatment through inhibition of the NACHT domain-, leucine-rich repeat-, and pyd-containing protein 3 inflammasome (NLRP3) and the nuclear factor-κB pathway after MP infection [ 211 ]. Actually, several in vivo studies have reported an important protective role of polydatin treatment via different mechanisms in ovalbumin-induced bronchial asthma as well as in LPS-induced acute lung injury [ 212 , 213 ]. Moreover, polydatin protects the respiratory system from the damage caused by fine particulate matters (aerodynamic diameter < 2.5 μm; PM2.5) during air pollution that may cause deleterious effects such as premature death among individuals due to lung disease, lung dysfunction and asthma exacerbation, mainly by the capacity of polydatin to reduce the injury from oxidative stress and inflammation in lung tissues [ 214 ].…”

Section: Polydatinmentioning

confidence: 99%

The upshot of Polyphenolic compounds on immunity amid COVID-19 pandemic and other emerging communicable diseases: An appraisal

Khalil

Tazeddinova

2020

Nat. Prod. Bioprospect.

View full text Add to dashboard Cite

Polyphenols are a large family of more than 10,000 naturally occurring compounds, which exert countless pharmacological, biological and physiological benefits for human health including several chronic diseases such as cancer, diabetes, cardiovascular, and neurological diseases. Their role in traditional medicine, such as the use of a wide range of remedial herbs (thyme, oregano, rosemary, sage, mint, basil), has been well and long known for treating common respiratory problems and cold infections. This review reports on the most highlighted polyphenolic compounds present in up to date literature and their specific antiviral perceptive properties that might enhance the body immunity facing COVID-19, and other viral infectious diseases. In fact, several studies and clinical trials increasingly proved the role of polyphenols in controlling numerous human pathogens including SARS and MERS, which are quite similar to COVID-19 through the enhancement of host immune response against viral infections by different biological mechanisms. Thus, polyphenols ought to be considered as a potential and valuable source for designing new drugs that could be used effectively in the combat against COVID‐19 and other rigorous diseases.

show abstract

Section: Polydatinmentioning

confidence: 99%

The upshot of Polyphenolic compounds on immunity amid COVID-19 pandemic and other emerging communicable diseases: An appraisal

Khalil

Tazeddinova

2020

Nat. Prod. Bioprospect.

View full text Add to dashboard Cite

show abstract

“…Moreover, the renoprotection relys on the activation of Nrf2. Thus we speculate that other Nrf2 activating agents, such as paeonin (Xiao et al, 2018), polydatin (Zeng et al, 2018), salviae (Li et al, 2018b) and umbelliferone (Yin et al, 2018), may be available for renal oxidative damage. There is no doubt that natural product PRO provides a new approach for treatment of nephrotocicity and it is a novel and significant discovery in the process of probing new therapeutic agents to improve survival rate of patients with cisplatin chemotherapy.…”

Section: Discussionmentioning

confidence: 97%

Procyanidin protects HK-2 cells against cisplatin-induced injury through antioxidant action involving Nrf2/HO-1 signaling pathway

Chen

Feng

Jing

et al. 2019

Fundam. Toxicol. Sci.

View full text Add to dashboard Cite

-Cisplatin (CP) is used as a chemotherapeutic drug for the treatment of various kinds of cancer. However, it is becoming increasingly difficult to ignore its side effects, especially nephrotoxicity which has to do with oxidative stress and inflammation. Procyanidin (PRO) has been proved to be a powerful antioxidant. Therefore, we investigated whether PRO could prevent Cisplatin-induced nephrotoxicity and explored the underlying mechanism. In cellular experiment, reactive oxygen species (ROS), the malondialdehyde (MDA) levels, the activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-PX) were measured for the assessment of cisplatin-induced oxidative cell damage. CCK-8 reagent and flow cytometry were used to detect the cell viability and apoptosis. Furthermore, the level of oxidative-related protein Nrf2 and HO-1 were carried out by western blot analysis. We found that cisplatin gave rise to the elevated levels of ROS and MDA and the decrease of the activities of T-SOD and GSH-PX with a related lower viability and higher apoptosis in HK-2 cells. Inversely, the pretreatment of PRO mitigated the oxidative damage, promoted the cell viability and lowered the apoptosis, activated nuclear related factor 2 (Nrf2) and elevated the expression of heme oxygenase-1 (HO-1), the above cytoprotection of PRO was blocked by siNrf2 or siHO-1. These results demonstrated that PRO has the potential to prevent cisplatin-induced nephrotoxicity through activation of Nrf2/HO-1 signaling pathway.

show abstract

“…Glutathione peroxidase functions in cellular oxidation–reduction reactions to protect the cell membrane from oxidative damage caused by ROS (Dauletbaev et al., ). Given that the lung epithelial surface is sensitive to oxidative stress, disorders often occur owing to an imbalance between pro‐oxidants and the antioxidant system (Zeng et al., ). Hydrogen inhalation exerts a potent protective effect on various diseases associated with oxidative and inflammatory stress, such as radiation‐induced heart disease, ischaemia–reperfusion injury, myocardial and brain infarction, storage of the heart and heart transplantation (LeBaron, Kura, Kalocayova, Tribulova, & Slezak, ).…”

Section: Discussionmentioning

confidence: 99%

Hydrogen inhalation attenuated bleomycin‐induced pulmonary fibrosis by inhibiting transforming growth factor‐β1 and relevant oxidative stress and epithelial‐to‐mesenchymal transition

Gao

Jiang

Geng

et al. 2019

Experimental Physiology

View full text Add to dashboard Cite

New Findings What is the central question of this study?The aim was to explore the effects and underlying mechanisms of H2 on bleomycin‐induced pulmonary fibrosis. What are the main findings and its importance?Our results indicate that, in bleomycin‐induced pulmonary fibrosis, H2 inhalation attenuated oxidative stress and reversed the pulmonary epithelial‐to‐mesenchymal transition process by reducing reactive oxygen species production and inhibiting the expression of transforming growth factor‐β1, α‐smooth muscle actin and collagen I to improve fibrotic injury and exert anti‐fibrogenic effects. Thus, H2 inhalation has promising therapeutic potential as a useful adjuvant treatment for patients with idiopathic pulmonary fibrosis, which deserves further study and evaluation. Abstract Hydrogen (H2) can protect against tissue damage. The effect of H2 inhalation therapy on the pathogenesis of pulmonary fibrosis remains unknown. This study was designed to explore the effects and underlying mechanisms of H2 inhalation on bleomycin (BLM)‐induced pulmonary fibrosis. A rat model of pulmonary fibrosis was established with BLM. Rats were randomly divided into control and H2 inhalation groups. Haematoxylin and Eosin staining and Mason's Trichrome staining were performed to evaluate pulmonary fibrosis injury, inflammatory cell infiltration, structural disorder and collagen deposition. qRT‐PCR and western blot assays were used to determine the expression of TNF‐α, TGF‐β1, α‐SMA, E‐cadherin, N‐cadherin, vimentin, VEGF and collagen type I at both mRNA and protein levels. The contents of reactive oxygen species, TGF‐β1, TNF‐α, malondialdehyde and hydroxyproline were determined with biochemical test kits or ELISA kits. Bleomycin‐stimulated rats exhibited typical symptoms of pulmonary fibrosis, which featured an increase in collagen deposition, alveolitis, fibrosis and parenchymal structural disorder in the lung. However, BLM‐induced oxidative stress was attenuated by H2 inhalation therapy, which reduced the contents of reactive oxygen species, malondialdehyde and hydroxyproline, enhanced the activity of glutathione peroxidase and decreased the expression of TGF‐β1 and TNF‐α. In addition, H2 inhalation also inhibited BLM‐induced epithelial‐to‐mesenchymal transition by inhibiting TGF‐β1, increasing the expression level of the epithelial cell marker E‐cadherin, and decreasing the expression level of the mesenchymal cell marker vimentin in a time‐dependent manner. In addition, H2 inhalation downregulated α‐SMA expression and suppressed collagen I generation, exerting anti‐fibrogenic effects. Hydrogen inhalation therapy attenuates BLM‐induced pulmonary fibrosis by inhibiting TGF‐β1, relevant oxidative stress and epithelial‐to‐mesenchymal transition.

show abstract

Polydatin attenuates reactive oxygen species-induced airway remodeling by promoting Nrf2-mediated antioxidant signaling in asthma mouse model

Cited by 46 publications

References 26 publications

The upshot of Polyphenolic compounds on immunity amid COVID-19 pandemic and other emerging communicable diseases: An appraisal

The upshot of Polyphenolic compounds on immunity amid COVID-19 pandemic and other emerging communicable diseases: An appraisal

Procyanidin protects HK-2 cells against cisplatin-induced injury through antioxidant action involving Nrf2/HO-1 signaling pathway

Hydrogen inhalation attenuated bleomycin‐induced pulmonary fibrosis by inhibiting transforming growth factor‐β1 and relevant oxidative stress and epithelial‐to‐mesenchymal transition

Contact Info

Product

Resources

About