MicroRNAs: Important Regulatory Molecules in Acute Lung Injury/Acute Respiratory Distress Syndrome DOI Open Access
Qianying Lu, Sifan Yu, Xiangyan Meng

et al.

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(10), P. 5545 - 5545

Published: May 16, 2022

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is an overactivated inflammatory response caused by direct or indirect injuries that destroy parenchymal cells and dramatically reduce function. Although some research progress has been made in recent years, the pathogenesis of ALI/ARDS remains unclear due to its heterogeneity etiology. MicroRNAs (miRNAs), a type small noncoding RNA, play vital role various diseases. In ALI/ARDS, miRNAs can regulate immune responses targeting specific molecules. Regulation miRNA expression damage promote recovery ALI/ARDS. Consequently, are considered as potential diagnostic indicators therapeutic targets Given inflammation plays important we review involved process provide new ideas for pathogenesis, clinical diagnosis, treatment

Language: Английский

Network pharmacology and molecular docking analyses on Lianhua Qingwen capsule indicate Akt1 is a potential target to treat and prevent COVID‐19 DOI Creative Commons
Qi‐Dong Xia, Yang Xun, Junlin Lu

et al.

Cell Proliferation, Journal Year: 2020, Volume and Issue: 53(12)

Published: Nov. 3, 2020

Abstract Objectives Coronavirus disease 2019 (COVID‐19) is rapidly spreading worldwide. Lianhua Qingwen capsule (LQC) has shown therapeutic effects in patients with COVID‐19. This study aimed to discover its molecular mechanism and provide potential drug targets. Materials Methods An LQC target COVID‐19–related gene set was established using the Traditional Chinese Medicine Systems Pharmacology database seven disease‐gene databases. Gene ontology (GO), Kyoto Encyclopedia of Genes Genomes (KEGG) enrichment analysis protein‐protein interaction (PPI) network were performed mechanism. Molecular docking visualize patterns interactions between effective molecule targeted protein. Results A 65 genes generated. We then constructed a compound‐target that contained 234 nodes active compounds 916 edges pairs. The GO KEGG indicated can act by regulating immune response, apoptosis virus infection. PPI subnetworks identified nine hub genes. conducted on most significant Akt1, which involved lung injury, fibrogenesis Six enter pocket namely beta‐carotene, kaempferol, luteolin, naringenin, quercetin wogonin, thereby exerting Conclusions pharmacological strategy integrates unravel LQC. Akt1 promising reduce tissue damage help eliminate

Language: Английский

Citations

211
Sitagliptin activates the p62–Keap1–Nrf2 signalling pathway to alleviate oxidative stress and excessive autophagy in severe acute pancreatitis-related acute lung injury DOI Creative Commons
Lingming Kong, Jie Deng, Xiang Zhou

et al.

Cell Death and Disease, Journal Year: 2021, Volume and Issue: 12(10)

Published: Oct. 11, 2021

Abstract Acute lung injury (ALI) is a complication of severe acute pancreatitis (SAP). Sitagliptin (SIT) DPP4 inhibitor that exerts anti-inflammatory and antioxidant effects; however, its mechanism action in SAP-ALI remains unclear. In this study, we investigated the effects SIT on specific pathways involved SAP-induced inflammation, including oxidative stress, autophagy, p62–Kelch-like ECH-associated protein 1 (Keap1)–NF-E2-related factor 2 (Nrf2) signalling pathways. Nrf2 knockout (Nrf2 −/− ) wild-type (WT) mice were pre-treated with (100 mg/kg), followed by caerulein lipopolysaccharide (LPS) administration to induce pancreatic injury. BEAS-2B cells transfected siRNA-Nrf2 treated LPS, changes reactive oxygen species (ROS) levels, autophagy measured. reduced histological damage, oedema, myeloperoxidase activity lung, decreased expression pro-inflammatory cytokines, inhibited excessive ROS production via activation p62–Keap1–Nrf2 pathway promotion nuclear translocation Nrf2. Nrf2-knockout mice, effect was reduced, resulting accumulation autophagy. cells, LPS induced activated further enhanced knockdown. This study demonstrates reduces SAP-ALI-associated stress through Nrf2, suggesting therapeutic potential SAP-ALI.

Language: Английский

Citations

144
Melatonin attenuates LPS-induced pyroptosis in acute lung injury by inhibiting NLRP3-GSDMD pathway via activating Nrf2/HO-1 signaling axis DOI
Jia‐Ying Kang, Mengmeng Xu, Ying Sun

et al.

International Immunopharmacology, Journal Year: 2022, Volume and Issue: 109, P. 108782 - 108782

Published: April 23, 2022

Language: Английский

Citations

88
Cadmium exposure caused cardiotoxicity in common carps (Cyprinus carpio L.): miR-9-5p, oxidative stress, energetic impairment, mitochondrial division/fusion imbalance, inflammation, and autophagy DOI
Yuhao Liu, Lin Xu, Zhiyu Hao

et al.

Fish & Shellfish Immunology, Journal Year: 2023, Volume and Issue: 138, P. 108853 - 108853

Published: May 27, 2023

Language: Английский

Citations

53
New perspectives on the therapeutic potential of quercetin in non-communicable diseases: Targeting Nrf2 to counteract oxidative stress and inflammation DOI Creative Commons
Li Zhang,

Li-Yue Xu,

Fei Tang

et al.

Journal of Pharmaceutical Analysis, Journal Year: 2024, Volume and Issue: 14(6), P. 100930 - 100930

Published: Jan. 3, 2024

Non-communicable diseases (NCDs), including cardiovascular diseases, cancer, metabolic and skeletal pose significant challenges to public health worldwide. The complex pathogenesis of these is closely linked oxidative stress inflammatory damage. Nuclear factor erythroid 2-related 2 (Nrf2), a critical transcription factor, plays an important role in regulating antioxidant anti-inflammatory responses protect the cells from damage inflammation-mediated injury. Therefore, Nrf2-targeting therapies hold promise for preventing treating NCDs. Quercetin (Que) widely available flavonoid that has properties. It modulates Nrf2 signaling pathway ameliorate inflammation. Que mitochondrial function, apoptosis, autophagy, cell biomarkers regulate inflammation, highlighting its efficacy as therapeutic agent against Here, we discussed, first time, close association between NCD pathway, involved neurodegenerative disease, cancers, organ damage, bone Furthermore, reviewed availability, pharmacokinetics, pharmaceutics, applications In addition, focused on prospects clinical use. represents promising candidate treatment NCDs due

Language: Английский

Citations

21
Ginseng-derived nanoparticles alleviate inflammatory bowel disease via the TLR4/MAPK and p62/Nrf2/Keap1 pathways DOI Creative Commons
Song Yang, Wenjing Li, Xueyuan Bai

et al.

Journal of Nanobiotechnology, Journal Year: 2024, Volume and Issue: 22(1)

Published: Feb. 1, 2024

Abstract Inflammatory bowel disease (IBD) is closely linked to the homeostasis of intestinal environment, and exosomes can be used treat IBD due their high biocompatibility ability effectively absorbed by tract. However, Ginseng-derived nanoparticles (GDNPs) have not been studied in this context mechanism action remains unclear. Here, we investigated GDNPs mediate intercellular communication a complex inflammatory microenvironment order IBD. We found that scavenge reactive oxygen species from immune cells epithelial cells, inhibit expression pro-inflammatory factors, promote proliferation differentiation stem as well enhancing diversity flora. significantly stabilise barrier thereby promoting tissue repair. Overall, proved ameliorate inflammation oxidative stress vivo vitro, acting on TLR4/MAPK p62/Keap1/Nrf2 pathways, exerting an anti-inflammatory antioxidant effect. mitigated mice reducing factors improving environment. This study offers new evidence potential therapeutic effects IBD, providing conceptual ground for alternative strategy. Graphical

Language: Английский

Citations

20
Quercetin attenuates sepsis-induced acute lung injury via suppressing oxidative stress-mediated ER stress through activation of SIRT1/AMPK pathways DOI
Aming Sang, Yun Wang, Shun Wang

et al.

Cellular Signalling, Journal Year: 2022, Volume and Issue: 96, P. 110363 - 110363

Published: May 27, 2022

Language: Английский

Citations

62
Diosmetin alleviated cerebral ischemia/reperfusion injuryin vivoandin vitroby inhibiting oxidative stressviathe SIRT1/Nrf2 signaling pathway DOI
Zhigang Mei, Lipeng Du, Xiaolu Liu

et al.

Food & Function, Journal Year: 2021, Volume and Issue: 13(1), P. 198 - 212

Published: Nov. 27, 2021

Cerebral ischemia/reperfusion (I/R) injury is caused by blood flow recovery after an ischemic stroke, and effective treatments targeting I/R are still insufficient. Oxidative stress known to play a pivotal role in the pathogenesis of cerebral injury. Previous studies have revealed that diosmetin could protect against oxidative injury, but underlying mechanisms not been fully revealed. The present study was undertaken investigate effects action on In vivo, rats were orally gavaged with for seven days, middle artery occlusion (MCAO) established simulate neurological deficit score, infarct volume, cortical pathological lesions measured. vitro, PC12 cells exposed oxygen-glucose deprivation/reoxygenation (OGD/R). To clarify mechanism, SIRT1 inhibitor EX527 small interfering RNA (siRNA) used downregulate protein level, respectively. contents superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), malondialdehyde (MDA) determined commercial kits. expressions SIRT1, total Nrf2 (T-Nrf2), nucleus (N-Nrf2), NQO1 HO-1 measured western blotting. results showed pretreatment improved outcomes, decreased volume lesions, inhibited rats. cells, increased cell viability, reduced lactate dehydrogenase (LDH) release reactive oxygen species (ROS) stress. Besides, T-Nrf2, N-Nrf2, both vivo vitro. However, administration or silencing gene its siRNA eliminated beneficial diosmetin. Meanwhile, inhibition levels downstream antioxidants HO-1. conclusion, our data suggested attenuate inhibiting via SIRT1/Nrf2 signaling pathway.

Language: Английский

Citations

59
Vitamin C Attenuates Oxidative Stress, Inflammation, and Apoptosis Induced by Acute Hypoxia through the Nrf2/Keap1 Signaling Pathway in Gibel Carp (Carassius gibelio) DOI Creative Commons

Liyun Wu,

Wenjie Xu, Hongyan Li

et al.

Antioxidants, Journal Year: 2022, Volume and Issue: 11(5), P. 935 - 935

Published: May 9, 2022

Previous studies have found that vitamin C (VC) has protective effects in fish. However, the efficacy of VC on hypoxia-induced liver injury fish remains unknown. Therefore, to investigate mechanism after acute hypoxic stimulation fish, gibel carp were fed a diet containing for eight weeks, then subjected hypoxia stimulation. The specific growth rate was increased by supplementation VC. Plasma stress markers (glucose, lactic acid, and cortisol) decreased supplementation. Moreover, levels inflammatory cytokines (tnf-α, il-2, il-6, il-12) enhancing Nrf2/Keap1 signaling pathway. Upregulation antioxidant enzymes activity (CAT, SOD, GPx); T-AOC; anti-inflammatory factors (il-4 tgf-β) highlighted activities results showed reduced apoptotic index hypothalamus. expression GRP78 protein endoplasmic reticulum apoptosis induced inhibited Taken together, indicate can attenuate oxidative damage, inflammation, via identify new defense strategy response conditions.

Language: Английский

Citations

51
Novel neutrophil extracellular trap-related mechanisms in diabetic wounds inspire a promising treatment strategy with hypoxia-challenged small extracellular vesicles DOI Creative Commons

Ziqiang Chu,

Qilin Huang, Kui Ma

et al.

Bioactive Materials, Journal Year: 2023, Volume and Issue: 27, P. 257 - 270

Published: April 14, 2023

Neutrophil extracellular traps (NETs) have been considered a significant unfavorable factor for wound healing in diabetes, but the mechanisms remain unclear. The therapeutic application of small vesicles (sEVs) derived from mesenchymal stem cells (MSCs) has received considerable attention their properties. Hypoxic preconditioning is reported to enhance potential MSC-derived sEVs regenerative medicine. Therefore, aim this study illustrate detailed mechanism NETs impairment diabetic and develop promising NET-targeting treatment based on hypoxic pretreated (Hypo-sEVs). Excessive were found wounds high glucose (HG)-induced neutrophils. Further research showed that concentration impaired function fibroblasts through activating endoplasmic reticulum (ER) stress. Hypo-sEVs efficiently promoted reduced excessive NET formation by transferring miR-17-5p. Bioinformatic analysis RNA interference experiment revealed miR-17-5p obstructed targeting TLR4/ROS/MAPK pathway. Additionally, overexpression decreased overcame NET-induced fibroblasts, similar effects Hypo-sEVs. Overall, we identify previously unrecognized NET-related provide strategy treatment.

Language: Английский

Citations

41