Naringin Attenuates the Fibrosis of Transforming Growth Factor-Beta 1 Induced Human Embryonic Lung Fibroblasts through Nuclear Factor Kappa B Pathway DOI Open Access

Y. Kong,

Fei Long Sun,

Xiaojing Wang

et al.

Indian Journal of Pharmaceutical Sciences, Journal Year: 2022, Volume and Issue: 85(2)

Published: Jan. 1, 2022

To investigate the effect of naringin on fibrosis transforming growth factor-beta 1 induced human embryonic lung fibroblasts MRC-5 and its potential mechanism. cells were treated with different concentrations naringin, 5 ng/ml 2 μmol/l nuclear factor kappa B activator phorbol myristate acetate. The experiment was divided into blank group, 1+naringin group 1+naringin+phorbol acetate group. 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide, flow cytometry scratch experiments used to analyze cell viability, cycle distribution migration ability. Western blot examine protein levels. With increase concentration, viability gradually decreased. Compared cycle, rate, alpha-smooth muscle actin, collagen I alpha 1, fibronectin, phosphorylatednuclear p65 phosphorylated-nuclear factor-kappa inhibitor expression in increased. Naringin inhibited factorbeta proliferation, through inactivating pathway. Besides, could reverse naringinmediated inhibition compared reduced 1-induced by inhibiting

Language: Английский

The Dual Roles of Activating Transcription Factor 3 (ATF3) in Inflammation, Apoptosis, Ferroptosis, and Pathogen Infection Responses DOI Open Access
Shuang Liu,

Zhangcheng Li,

Shimei Lan

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(2), P. 824 - 824

Published: Jan. 9, 2024

Transcription factors are pivotal regulators in the cellular life process. Activating transcription factor 3 (ATF3), a member of ATF/CREB (cAMP response element-binding protein) family, plays crucial role as cells respond to various stresses and damage. As factor, ATF3 significantly influences signal transduction regulation, orchestrating variety signaling pathways, including apoptosis, ferroptosis, differentiation. In addition, serves an essential link between inflammation, oxidative stress, immune responses. This review summarizes recent advances research on activation its regulating inflammatory responses, cell ferroptosis while exploring dual functions these processes. Additionally, this article discusses diseases related pathogenic microbial infections. Our may be helpful better understand responses disease progression, thus promoting advancements clinical treatments for inflammation stress-related diseases.

Language: Английский

Citations

38

Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions DOI Creative Commons
Megh Pravin Vithalkar, Shaili Pradhan, K. Sandra

et al.

Cell Biochemistry and Biophysics, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 19, 2025

Abstract Idiopathic Pulmonary Fibrosis (IPF) is a severe, rapidly advancing disease that drastically diminishes life expectancy. Without treatment, it can progress to lung cancer. The precise etiology of IPF remains unknown, but inflammation and damage the alveolar epithelium are widely thought be pivotal in its development. Research has indicated activating NLRP3 inflammasome crucial mechanism pathogenesis, as triggers release pro-inflammatory cytokines such IL-1β, IL-18, TGF-β. These contribute myofibroblast differentiation extracellular matrix (ECM) accumulation. Currently, treatment options for limited. Only two FDA-approved medications, pirfenidone nintedanib, available. While these drugs decelerate progression, they come with range side effects do not cure disease. Additional strategies primarily involve supportive care therapy. Emerging research highlighted numerous flavonoids derived from traditional medicines inhibit critical regulators responsible inflammasome. show promise potential therapeutic agents managing IPF, offering new avenue targets core inflammatory processes this debilitating condition. Graphical

Language: Английский

Citations

1

Flavonoids for treating pulmonary fibrosis: Present status and future prospects DOI
Anju Sharma, Sarika Wairkar

Phytotherapy Research, Journal Year: 2024, Volume and Issue: 38(9), P. 4406 - 4423

Published: July 10, 2024

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with an unknown underlying cause. There no complete cure for IPF; however, two anti-fibrotic agents (Nintedanib and pirfenidone) are approved by the USFDA to extend patient's life span. Therefore, alternative therapies supporting survival of fibrotic patients have been studied in recent literature. The abundance phenolic compounds, particularly flavonoids, has gathered attention due their potential health benefits. Various like naringin, quercetin, baicalin, baicalein, puerarin, silymarin, kaempferol, exhibit anti-inflammatory anti-oxidant properties, which help decrease fibrosis. databases, including PubMed, EBSCO, ProQuest, Scopus, as well particular websites, such World Health Organisation National Institutes Health, were used conduct literature search. Several mechanisms action flavonoids reported vivo cell line studies emphasizing ability modulate oxidative stress, inflammation, processes lungs. They restoration biomarkers hydroxyproline, cytokines, superoxide dismutase, malondialdehyde others associated IPF modulating various pathways responsible progression Yet, some drawbacks, poor solubility, challenging drug loading, stability issues, scarce bioavailability. novel formulations explored, liposomes, solid lipid microparticles, polymeric nanoparticles, nanogels, nanocrystals, enhance therapeutic efficacy This review focuses on role mitigating idiopathic fibrosis, mode formulations.

Language: Английский

Citations

7

Natural plant resource flavonoids as potential therapeutic drugs for pulmonary fibrosis DOI Creative Commons

Meng-chuan Wang

Heliyon, Journal Year: 2023, Volume and Issue: 9(8), P. e19308 - e19308

Published: Aug. 1, 2023

Pulmonary fibrosis is an enduring and advancing pulmonary interstitial disease caused by multiple factors that ultimately lead to structural changes in normal lung tissue. Currently, a global with high degree of heterogeneity mortality rate. Nitidine pirfenidone have been approved for treating fibrosis, the quest effective therapeutic drugs remains unabated. In recent years, anti-pulmonary properties natural flavonoids garnered heightened attention, although further research needed. this paper, resources, characteristics, mechanisms were reviewed. We hope provide potential opportunities application fight against fibrosis.

Language: Английский

Citations

15

Potential Beneficial Effects of Naringin and Naringenin on Long COVID—A Review of the Literature DOI Creative Commons
Siqi Liu,

Mengli Zhong,

Hao Wu

et al.

Microorganisms, Journal Year: 2024, Volume and Issue: 12(2), P. 332 - 332

Published: Feb. 4, 2024

Coronavirus disease 2019 (COVID-19) caused a severe epidemic due to acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Recent studies have found that patients do not completely recover from infections, but instead, suffer variety of post-acute sequelae SARS-CoV-2 infection, known as long COVID. The effects COVID can be far-reaching, with duration up six months and range symptoms such cognitive dysfunction, immune dysregulation, microbiota dysbiosis, myalgic encephalomyelitis/chronic fatigue syndrome, myocarditis, pulmonary fibrosis, cough, diabetes, pain, reproductive thrombus formation. However, recent shown naringenin naringin palliative on various COVID-19 sequelae. Flavonoids naringenin, commonly in fruits vegetables, positive effects, including reducing inflammation, preventing viral providing antioxidants. This article discusses the molecular mechanisms clinical treating above diseases. It proposes them potential drugs for treatment COVID, it inferred exhibit extended medications, future likely serving nutraceuticals or supplements comprehensive alleviation manifestations complications.

Language: Английский

Citations

4

Therapeutic effects of flavonoids on pulmonary fibrosis: A preclinical meta-analysis DOI Creative Commons

Qi Geng,

Lan Yan,

Changqi Shi

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: 132, P. 155807 - 155807

Published: June 7, 2024

The efficacy of flavonoid supplementation in animal models pulmonary fibrosis has been demonstrated.

Language: Английский

Citations

4

Novel therapeutic strategies and drugs for idiopathic pulmonary fibrosis DOI

Zezhou Shi,

Min Zhou, Jingfang Zhai

et al.

Archiv der Pharmazie, Journal Year: 2024, Volume and Issue: 357(10)

Published: July 3, 2024

Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease of unknown etiology. Currently, drugs used to treat IPF in clinical practice exhibit severe side effects and limitations. To address these issues, this paper discusses the therapeutic preclinical targeted (such as STAT3 TGF-β/Smad pathway inhibitors, chitinase PI3K phosphodiesterase etc.) natural products on IPF. Through summary current research progress, it found that possess multitarget effects, stable efficacy, low nondrug dependence. Furthermore, we discuss significant prospects product molecules combating by influencing immune system, expecting analytical data will aid development new or investigation active ingredients for potential treatments future.

Language: Английский

Citations

4

ATF3 Knockdown Exacerbates Astrocyte Activation by Inhibiting Phosphorylation of Drp1 in Ischemic Stroke DOI Creative Commons
Rong Huang, Xiaoyan Huang,

Hongmei Yang

et al.

Biologics, Journal Year: 2025, Volume and Issue: Volume 19, P. 15 - 29

Published: Feb. 1, 2025

Introduction: ATF3, a stress-induced transcription factor, has been implicated in the injury processes of various cell types, including neurons. It is recognized as common marker for neuronal damage following neurotrauma. However, its role other types glial cells, particularly astrocytes, response to ischemic remains unclear. Mitochondrial dysfunction key factor pathogenesis stroke, and impaired mitochondrial function astrocytes associated with astrocyte activation. This study aimed explore relationship between stroke investigate how ATF3 regulates activation context injury. Methods: In transient middle cerebral artery occlusion (tMCAO) mouse model, we knocked down assessed infarct size, motor deficits, activation, damage. vitro, used oxygen-glucose deprivation reoxygenation (OGD-R) simulate ischemia evaluated impact knockdown on function. Results: exacerbated vivo, increased depletion worsened interacted Drp1 via Akt2, inhibiting fission protecting astrocytes. Conclusion: protects highlighting potential therapeutic target recovery. Keywords: activating 3, acute AIS, dysfunction, dynamics-related protein 1, Drp1, threonine/serine kinase 2, Akt2

Language: Английский

Citations

0

Mitochondrial dysfunction and alveolar type II epithelial cell senescence: The destroyer and rescuer of idiopathic pulmonary fibrosis DOI Creative Commons
Suqi Liu, Qian Xi,

Xuannian Li

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2025, Volume and Issue: 13

Published: March 31, 2025

Idiopathic pulmonary fibrosis (IPF) is a chronic respiratory disease with an unknown origin and complex pathogenic mechanisms. A deeper understanding of these mechanisms essential for effective treatment. Pulmonary associated the senescence alveolar type II epithelial (ATⅡ) cells. Additionally, ATⅡ can lead to senescence-associated secretory phenotype, which affects cellular communication disrupts lung tissue repair, contributing development IPF. The role mitochondrial dysfunction in senescence-related diseases increasingly recognized. It induce through apoptosis, impaired autophagy, disrupted energy metabolism, potentially playing key IPF progression. This article explores therapeutic potential targeting dysfunction, emphasizing their significant roles pathogenesis.

Language: Английский

Citations

0

Monomeric compounds from natural products for the treatment of pulmonary fibrosis: a review DOI
Zhuqing Li, Yanyong Yang, Fu Gao

et al.

Inflammopharmacology, Journal Year: 2024, Volume and Issue: 32(4), P. 2203 - 2217

Published: May 9, 2024

Language: Английский

Citations

3