Characterization of cellular senescence in radiation ulcers and therapeutic effects of mesenchymal stem cell-derived conditioned medium DOI Creative Commons
Wanchao Chen, Yang Wang, Jiancheng Zheng

et al.

Burns & Trauma, Journal Year: 2023, Volume and Issue: 11

Published: Jan. 1, 2023

Abstract Background Radiation ulcers are a common and severe injury after uncontrolled exposure to ionizing radiation. The most important feature of radiation is progressive ulceration, which results in the expansion nonirradiated area refractory wounds. Current theories cannot explain progression ulcers. Cellular senescence refers as irreversible growth arrest that occurs stress, contributes tissue dysfunction by inducing paracrine senescence, stem cell chronic inflammation. However, it not yet clear how cellular facilitates continuous Here, we aim investigate role promoting indicate potential therapeutic strategy for Methods ulcer animal models were established local 40 Gy X-ray continuously evaluated >260 days. roles assessed using pathological analysis, molecular detection RNA sequencing. Then, effects conditioned medium from human umbilical cord mesenchymal cells (uMSC-CM) investigated models. Results with features clinical patients primary mechanisms responsible We have characterized being closely associated found exogenous transplantation senescent significantly aggravated them. Mechanistic studies sequencing suggested radiation-induced secretions facilitating Finally, uMSC-CM was effective mitigating inhibiting senescence. Conclusions Our findings only characterize but also their treatment.

Language: Английский

Orally administration of cerium oxide nanozyme for computed tomography imaging and anti-inflammatory/anti-fibrotic therapy of inflammatory bowel disease DOI Creative Commons

Yameng Cao,

Kai Cheng, Mei Yang

et al.

Journal of Nanobiotechnology, Journal Year: 2023, Volume and Issue: 21(1)

Published: Jan. 19, 2023

Inflammatory bowel disease (IBD) is a chronic nonspecific with unknown etiology. Currently, the anti-inflammatory therapeutic approaches have achieved certain extent of effects in terms inflammation alleviation. Still, final pathological outcome intestinal fibrosis has not been effectively improved yet.In this study, dextran-coated cerium oxide (D-CeO2) nanozyme superoxide dismutase (SOD) and catalase (CAT) activities was synthesized by chemical precipitation. Our results showed that D-CeO2 could efficiently scavenge reactive species (ROS) as well downregulate pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, iNOS) to protect cells from H2O2-induced oxidative damage. Moreover, suppress expression fibrosis-related gene levels, such α-SMA, Collagen 1/3, demonstrating anti-fibrotic effect. In both TBNS- DSS-induced colitis models, oral administration chitosan/alginate hydrogel alleviated inflammation, reduced colonic damage scavenging ROS, decreased inflammatory factor levels. Notably, our findings also suggested cytokine predicting contribution alleviating fibrosis. Meanwhile, be employed CT contrast agent for noninvasive gastrointestinal tract (GIT) imaging.We introduced novel approach computed tomography (CT)-guided therapy management IBD. Collectively, without appreciable systemic toxicity, held promise integrated applications diagnosis therapy, pioneering exploration nanozymes ROS capacity treatment

Language: Английский

Citations

66
Oxidative Stress in Radiation-Induced Cardiotoxicity DOI Creative Commons
Zhang Ping, Peng Yang,

Lang Hong

et al.

Oxidative Medicine and Cellular Longevity, Journal Year: 2020, Volume and Issue: 2020, P. 1 - 15

Published: March 2, 2020

There is a distinct increase in the risk of heart disease people exposed to ionizing radiation (IR). Radiation-induced (RIHD) one adverse side effects when are radiation. IR may come from various forms, such as diagnostic imaging, radiotherapy for cancer treatment, nuclear disasters, and accidents. However, RIHD was mainly observed after chest malignant tumors, especially left breast cancer. Radiation therapy (RT) has become main ways treat all kinds cancer, which used reduce recurrence improve survival rate patients. The potential cause radiation-induced cardiotoxicity unclear, but it be relevant oxidative stress. Oxidative stress, an accumulation reactive oxygen species (ROS), disrupts intracellular homeostasis through chemical modification damages proteins, lipids, DNA; therefore, results series related pathophysiological changes. purpose this review summarise studies stress radiotherapy-induced provide prevention treatment methods cardiac damage.

Language: Английский

Citations

136
TGF-β in radiotherapy: Mechanisms of tumor resistance and normal tissues injury DOI
Bagher Farhood, Ehsan Khodamoradi, Mojtaba Hoseini‐Ghahfarokhi

et al.

Pharmacological Research, Journal Year: 2020, Volume and Issue: 155, P. 104745 - 104745

Published: March 4, 2020

Language: Английский

Citations

117
Imidacloprid-induced liver fibrosis in quails via activation of the TGF-β1/Smad pathway DOI

Yueying Lv,

Qizheng Bing,

Zhanjun Lv

et al.

The Science of The Total Environment, Journal Year: 2019, Volume and Issue: 705, P. 135915 - 135915

Published: Dec. 6, 2019

Language: Английский

Citations

80
Free radicals, antioxidants, nuclear factor‐E2‐related factor‐2 and liver damage DOI Creative Commons
Erika Ramos‐Tovar, Pablo Muriel

Journal of Applied Toxicology, Journal Year: 2019, Volume and Issue: 40(1), P. 151 - 168

Published: Aug. 6, 2019

Abstract Oxidative/nitrosative stress is proposed to be a critical factor in various diseases, including liver pathologies. Antioxidants derived from medicinal plants have been studied extensively and are relevant many illnesses, diseases. Several hepatic disorders, such as viral hepatitis alcoholic or nonalcoholic steatohepatitis, involve free radicals/oxidative agents that cause at least exacerbate injury, which can result chronic fibrosis, cirrhosis end‐stage hepatocellular carcinoma. In this scenario, nuclear factor‐E2‐related factor‐2 (Nrf2) appears an essential counteract attenuate oxidative nitrosative cells. fact, growing body of evidence indicates Nrf2 plays complex multicellular roles inflammation, hepatocarcinogenesis regeneration via the induction its target genes. Inflammation most common feature triggering Increasing counteracts proinflammatory process by modulating recruitment inflammatory cells inducing endogenous antioxidant response cell. review, interactions between molecular pathways analyzed.

Language: Английский

Citations

78
Blockade of Platelets Using Tumor-Specific NO-Releasing Nanoparticles Prevents Tumor Metastasis and Reverses Tumor Immunosuppression DOI
Yan Xu, Ji‐Wei Liu,

Zhangya Liu

et al.

ACS Nano, Journal Year: 2020, Volume and Issue: 14(8), P. 9780 - 9795

Published: July 31, 2020

The tumor microenvironment maintains a sufficient immunosuppressive state owing to the existence of factors. most prominent such factor is transforming growth β (TGF-β), which mainly provided by platelets. Moreover, platelets have been shown be main accomplice in assisting metastasis. Therefore, blocking tumor-associated endowed with functions enhancing immunity and reducing Herein, we designed microenvironment-responsive nitric oxide (NO) release nanoparticle, Ptx@AlbSNO, was able specifically safely co-deliver antiplatelet agent NO chemotherapeutic paclitaxel (Ptx) into tissues inhibit platelet–tumor cell interactions. We discovered that Ptx@AlbSNO could successfully block tumor-specific platelet functions, thereby suppressing process epithelial–mesenchymal transition (EMT), preventing adhesion around circulating cells (CTCs) distant In vivo studies demonstrate co-delivery Ptx can suppress primary growth. With ability effectively activated TGF-β secretion tumors, enhance intratumoral immune infiltration reverse microenvironment.

Language: Английский

Citations

75
Nonalcoholic steatohepatitis and mechanisms by which it is ameliorated by activation of the CNC-bZIP transcription factor Nrf2 DOI Creative Commons

Boushra Bathish,

Holly Robertson, John Dillon

et al.

Free Radical Biology and Medicine, Journal Year: 2022, Volume and Issue: 188, P. 221 - 261

Published: June 18, 2022

Non-alcoholic steatohepatitis (NASH) represents a global health concern. It is characterised by fatty liver, hepatocyte cell death and inflammation, which are associated with lipotoxicity, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, iron overload oxidative stress. NF-E2 p45-related factor 2 (Nrf2) transcription that combats Remarkably, Nrf2 downregulated during the development of NASH, probably accelerates disease, whereas in pre-clinical studies upregulation inhibits NASH. We now review scientific literature proposes downregulation NASH involves its increased ubiquitylation proteasomal degradation, mediated Kelch-like ECH-associated protein 1 (Keap1) and/or β-transducin repeat-containing (β-TrCP) HMG-CoA reductase degradation (Hrd1, also called synoviolin (SYVN1)). Additionally, Nrf2-mediated may involve diminished recruitment coactivators Nrf2, due to levels activating 3 (ATF3) nuclear factor-kappaB (NF-κB) p65, or competition for promoter binding BTB CNC homology (Bach1). Many processes downregulate triggered transforming growth factor-beta (TGF-β), stress amplifying signalling. Oxidative increase suppression β-TrCP through facilitating formation DSGIS-containing phosphodegron glycogen synthase kinase-3. In animal models, knockout increases susceptibility while pharmacological activation inducing agents target Keap1 These counter affected β-TrCP, Hrd1/SYVN1, ATF3, NF-κB p65 Bach1, suppressing Activation likely inhibit ameliorating ER overload. Crucially, mice has already been established supresses liver steatosis inflammation. There therefore compelling evidence provides comprehensive multipronged strategy treat

Language: Английский

Citations

51
Nuclear and Radiological Emergencies: Biological Effects, Countermeasures and Biodosimetry DOI Creative Commons
Elena Obrador, Rosario Salvador‐Palmer, J.I. Villaescusa

et al.

Antioxidants, Journal Year: 2022, Volume and Issue: 11(6), P. 1098 - 1098

Published: May 31, 2022

Atomic and radiological crises can be caused by accidents, military activities, terrorist assaults involving atomic installations, the explosion of nuclear devices, or utilization concealed radiation exposure devices. Direct damage is when interacts directly with cellular components. Indirect effects are mainly generation reactive oxygen species due to radiolysis water molecules. Acute persistent oxidative stress associates radiation-induced biological damages. Biological impacts deterministic (in a period range posteriori event because destructive tissue/organ harm) stochastic (irregular, for example cell mutation related pathologies heritable infections). Potential countermeasures according specific scenario require considering basic issues, e.g., type radiation, people affected first responders, doses received whether contamination has total body partial. This review focuses on available medical (radioprotectors, radiomitigators, radionuclide scavengers), biodosimetry (biological biophysical techniques that quantitatively correlated magnitude dose received), strategies implement response an accidental exposure. In case large-scale events, most ideal choice triage, assessment victim classification, global networks, in combination automation based modular platforms.

Language: Английский

Citations

46
Reactive oxygen species as signaling molecules in the development of lung fibrosis DOI Creative Commons
Francisco J. González-González, Navdeep S. Chandel, Manu Jain

et al.

Translational research, Journal Year: 2017, Volume and Issue: 190, P. 61 - 68

Published: Oct. 12, 2017

Language: Английский

Citations

86
Radiation-Induced Alterations in the Recurrent Glioblastoma Microenvironment: Therapeutic Implications DOI Creative Commons
Kshama Gupta, Terry C. Burns

Frontiers in Oncology, Journal Year: 2018, Volume and Issue: 8

Published: Nov. 8, 2018

Glioblastoma (GBM) is uniformly fatal with a median survival of just over 1 year, despite best available treatment including radiotherapy (RT). Impacts prior brain RT on recurrent tumors are poorly understood, though increasing evidence suggests RT-induced changes in the microenvironment contribute to GBM aggressiveness. The tumor impacts malignant cells directly and indirectly through stromal that support growth. Changes extracellular matrix (ECM), abnormal vasculature, hypoxia, inflammation have been reported promote aggressiveness could be exacerbated by RT. Prior radiation may long-term microglia brain-infiltrating monocytes, leading lasting alterations cytokine signaling ECM. Tumor-promoting CNS injury responses recapitulated augmented following radiation, impacting cell phenotype, proliferation, infiltration CNS. Since vital management, but substantially alters microenvironment, we here review challenges, knowledge gaps, therapeutic opportunities relevant targeting pro-tumorigenic features microenvironment. We suggest insights from provide target mechanisms, such as cellular senescence, amplified previously radiated

Language: Английский

Citations

83