Resveratrol inhibits Lin28A expression and induces its degradation via the proteasomal pathway in NCCIT cells DOI Open Access

Sandra Cotino‐Nájera,

Enrique García‐Villa,

Samantha Cruz‐Rosales

et al.

Oncology Letters, Journal Year: 2024, Volume and Issue: 28(6)

Published: Sept. 30, 2024

Lin28A is an oncoprotein overexpressed in several cancer types such as testicular, ovarian, colon, breast and lung cancers. As a pluripotency factor that promotes tumorigenesis, associated with more undifferentiated aggressive tumors phenotypes. Moreover, highly stable protein difficult to downregulate. The compound resveratrol (RSV) has anticancer effects. present study aimed elucidate the mechanisms underlying downregulation of expression by RSV NCCIT cell line. cells were treated different concentrations investigate its effects on expression. mRNA levels ubiquitin-specific protease 28 (USP28) assessed using reverse transcription-quantitative PCR. Western blot analysis was employed evaluate Lin28A, USP28 phosphorylated Lin28A. In addition, some experiments, MAPK/ERK pathway inhibitor, other experiments involved transfecting small interfering RNAs targeting USP28. results demonstrated significantly reduced destabilizing protein; this effect mediated ability suppress USP28, deubiquitinase normally protects from ubiquitination degradation. Additionally, inhibited phosphorylation via pathway; event previously been shown enhance stability increasing half-life. This resulted degradation through proteasomal cells. provide further evidence activity RSV, identified promising therapeutic targets. oncoprotein, downregulating challenging. However, can overcome hurdle inhibiting signaling promote Furthermore, elucidating these provides avenues for developing targeted therapies.

Language: Английский

Verbascoside attenuates myocardial ischemia/reperfusion-induced ferroptosis following heterotopic heart transplantation via modulating GDF15/GPX4/SLC7A11 pathway DOI Creative Commons
Yuxi Zhang, Jing Zhan, Zhen Qiu

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: May 5, 2025

Myocardial cold ischemia/reperfusion (I/R) injury is an inevitable consequence of heart transplantation, significantly affecting survival rates and therapeutic outcomes. Growth Differentiation Factor 15 (GDF15) has been shown to regulate GPX4-mediated ferroptosis, playing a critical role in mitigating I/R injury. Meanwhile, verbascoside (VB), active compound extracted from the herbaceous plant, demonstrated myocardial protective effects. In this study, transplantation was performed using modified non-suture cuff technique, with VB administered at dose 20 mg/kg/day via intraperitoneal injection for 3 days vivo. vitro, cardiomyocytes were pretreated 50 µg/ml 24 h. treatment reduced histopathological injury, decreased markers, inhibited ferroptosis oxidative stress during vitro experiments further that GDF15 alleviates induced by hypoxic reoxygenation upregulating GPX4. Therefore, it concluded preconditioning can effectively reduce after heterotopic possibly through up-regulation GDF15/GPX4/SLC7A11 pathway.

Language: Английский

Citations

0

Crosstalk among Reactive Oxygen Species, Autophagy and Metabolism in Myocardial Ischemia and Reperfusion Stages DOI Creative Commons

Yajie Peng,

Yachuan Tao,

Lingxu Liu

et al.

Aging and Disease, Journal Year: 2023, Volume and Issue: unknown, P. 0 - 0

Published: Jan. 1, 2023

Myocardial ischemia is the most common cardiovascular disease. Reperfusion, an important myocardial tool, causes unexpected and irreversible damage to cardiomyocytes, resulting in ischemia/reperfusion (MI/R) injury. Upon stress, especially oxidative stress induced by reactive oxygen species (ROS), autophagy, which degrades intracellular energy storage produce metabolites that are recycled into metabolic pathways buffer initiated during MI/R Excellent cardioprotective effects of autophagy regulators against MI have been reported. Reversing disordered cardiac metabolism ROS also exhibits action patients with ischemia. Herein, we review current knowledge on crosstalk between ROS, MI/R. Finally, discuss possible can be exploited harness therapeutic potential diagnosis treatment

Language: Английский

Citations

9

Hederagenin protects against myocardial ischemia–reperfusion injury via attenuating ALOX5-mediated ferroptosis DOI
Li Zhao, Hongtao Shi,

Fan Zhang

et al.

Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2023, Volume and Issue: 397(5), P. 3411 - 3424

Published: Nov. 13, 2023

Language: Английский

Citations

9

Oxidized DJ-1 activates the p-IKK/NF-κB/Beclin1 pathway by binding PTEN to induce autophagy and exacerbate myocardial ischemia-reperfusion injury DOI
Huiru Liu, Yuqin Wang, Kang He

et al.

European Journal of Pharmacology, Journal Year: 2024, Volume and Issue: 971, P. 176496 - 176496

Published: March 18, 2024

Language: Английский

Citations

2

Protective and Detoxifying Effects of Resveratrol on Zearalenone-Mediated Toxicity: A Review DOI Open Access

Qiongxia Lv,

Wenjing Xu, Fan Yang

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(20), P. 11003 - 11003

Published: Oct. 13, 2024

Zearalenone (ZEA) is a mycotoxin produced by Fusarium spp. fungi and widely found in moldy corn, wheat, barley, other grains. ZEA distributed to the whole body via blood circulation after metabolic transformation animals. Through oxidative stress, immunosuppression, apoptosis, autophagy, mitochondrial dysfunction, leads hepatitis, neurodegenerative diseases, cancer, abortion, stillbirth female animals, decreased sperm motility male In recent years, due influence of climate, storage facilities, factors, problem pollution global food crops has become particularly prominent, resulting serious problems for animal husbandry feed industries, threatening human health. Resveratrol (RSV) natural product with therapeutic activities such as anti-inflammatory, antioxidant, anticancer properties. RSV can alleviate ZEA-induced toxic effects targeting signaling pathways NF-κB, Nrf2/Keap1, PI3K/AKT/mTOR attenuating damage, inflammatory response, regulating cellular autophagy. Therefore, this paper provides review protective effect against toxicity its molecular mechanism, discusses safety potential clinical applications search detoxification agents.

Language: Английский

Citations

2

A focus on c-Jun-N-terminal kinase signaling in sepsis-associated multiple organ dysfunction: Mechanisms and therapeutic strategies DOI

Riya Gagnani,

Mugdha Srivastava, Manisha Suri

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 143, P. 113552 - 113552

Published: Nov. 15, 2024

Language: Английский

Citations

2

Resveratrol production from Polygonum cuspidatum by one-pot green extraction and bioprocessing of polydatin DOI
Shaohua Li, Chi Zhang, Renqiang Yang

et al.

Industrial Crops and Products, Journal Year: 2024, Volume and Issue: 212, P. 118386 - 118386

Published: March 15, 2024

Language: Английский

Citations

1

Inhibition of circ_0073932 attenuates myocardial ischemia‒reperfusion injury via miR-493-3p/FAF1/JNK DOI
Yang Su, Lili Zhao,

Dongli Lei

et al.

In Vitro Cellular & Developmental Biology - Animal, Journal Year: 2024, Volume and Issue: 60(6), P. 628 - 643

Published: April 5, 2024

Language: Английский

Citations

1

Mitochondria-Associated Organelle Crosstalk in Myocardial Ischemia/Reperfusion Injury DOI
Hui Yao,

Yuxin Xie,

Chaoquan Li

et al.

Journal of Cardiovascular Translational Research, Journal Year: 2024, Volume and Issue: 17(5), P. 1106 - 1118

Published: May 28, 2024

Language: Английский

Citations

1

Inhibiting H2AX Can Ameliorate Myocardial Ischemia/Reperfusion Injury by Regulating P53/JNK Signaling Pathway DOI Creative Commons

Ziyang Yu,

Yirong Teng, Hongbo Yang

et al.

Cardiology Research and Practice, Journal Year: 2024, Volume and Issue: 2024(1)

Published: Jan. 1, 2024

Myocardial ischemia‐reperfusion (I/R) injury is a significant area of focus in cardiovascular disease research. I/R can increase intracellular oxidative stress, leading to DNA damage. H2AX plays crucial role repair. This study utilized mouse and cell models myocardial investigate the impact on cardiomyocytes during I/R. initially assessed expression MI/R mice compared sham surgery group. Subsequently, cardiac function, infarct area, mitochondrial damage were evaluated after inhibiting negative control Furthermore, delved into molecular mechanisms by analyzing H2AX, P53, p‐JNK, SHP2, p‐SHP2, p‐RAS, parkin, Drp1, Cyt‐C, Caspase‐3, Caspase‐8 following addition JNK or P53 agonists. The results from western blotting vivo indicated significantly higher group Inhibiting improved reduced mitigated In vitro experiments demonstrated that could attenuate apoptosis cells modulating signaling pathways. These findings suggested may alleviate through regulation P53/JNK pathway, highlighting as potential target for treatment ischemia/reperfusion injury.

Language: Английский

Citations

0