Attenuation of PM2.5-Induced Lung Injury by 4-Phenylbutyric Acid: Maintenance of [Ca2+]i Stability between Endoplasmic Reticulum and Mitochondria DOI Creative Commons
Zhenhua Ma, Xiaohui Du,

Yize Sun

и другие.

Biomolecules, Год журнала: 2024, Номер 14(9), С. 1135 - 1135

Опубликована: Сен. 8, 2024

Fine particulate matter (PM2.5) is a significant cause of respiratory diseases and associated cellular damage. The mechanisms behind this damage have not been fully explained. This study investigated two types (inflammation pyroptosis) induced by PM2.5, focusing on their relationship with organelles (the endoplasmic reticulum mitochondria). Animal models demonstrated that PM2.5 induces excessive stress (ER stress), which lung in rats. was confirmed pretreatment an ER inhibitor (4-Phenylbutyric acid, 4-PBA). We found that, vitro, the intracellular Ca2+ ([Ca2+]i) dysregulation rat alveolar macrophages stress. Changes mitochondria-associated membranes (MAMs) result abnormal mitochondrial function. further massive expression NLRP3 GSDMD-N, detrimental to cell survival. In conclusion, our findings provide valuable insights into between [Ca2+]i dysregulation, damage, inflammation pyroptosis under PM2.5-induced conditions. Their interactions ultimately impact health.

Язык: Английский

Cardamom extract alleviates tamoxifen-induced liver damage by suppressing inflammation and pyroptosis pathway DOI Creative Commons
Wedad S. Sarawi, Hala Attia,

Afraa Alzoubi

и другие.

Scientific Reports, Год журнала: 2025, Номер 15(1)

Опубликована: Фев. 8, 2025

Tamoxifen (TAM) is extensively used to manage estrogen receptor-positive breast cancer. Despite its effectiveness, administration can negatively impact various organs, including the liver. This research focused on effects of TAM pyroptotic pathway in liver and evaluated potential cardamom extract (CRDE) lessen hepatic damage female rats. Rats received 45 mg/kg injections for 10 days, while groups treated with CRDE 12 ml/kg 20 commencing days before administration. exposure resulted apparent degenerations tissue inflammatory cell infiltration loss architectures. Serum levels enzymes alanine aminotransferase, aspartate aminotransferase alkaline phosphatase were elevated, along oxidative stress, as shown by increased lipid peroxidation lower reduced glutathione. caused inflammation indicated higher tumor necrosis factor-α interleukin-6 well expression CD68; a phagocytic Kupffer's cells marker. Additionally, protein analysis revealed high markers NLRP3-inflammasome, caspase-1, gasdermin D. Conversely, treatment effectively neutralized biochemical, histological, alterations induced TAM. In conclusion, demonstrated protect from TAM-induced regulating mechanisms involving damage, inflammation, pyroptosis.

Язык: Английский

Процитировано

0

N-acetylserotonin derivative ameliorates hypoxic-ischemic brain damage by promoting PINK1/Parkin-dependent mitophagy to inhibit NLRP3 inflammasome-induced pyroptosis DOI

Fang Fang,

Jiaxin Tang,

Jiaqing Geng

и другие.

International Immunopharmacology, Год журнала: 2025, Номер 153, С. 114469 - 114469

Опубликована: Март 18, 2025

Язык: Английский

Процитировано

0

Attenuation of PM2.5-Induced Lung Injury by 4-Phenylbutyric Acid: Maintenance of [Ca2+]i Stability between Endoplasmic Reticulum and Mitochondria DOI Creative Commons
Zhenhua Ma, Xiaohui Du,

Yize Sun

и другие.

Biomolecules, Год журнала: 2024, Номер 14(9), С. 1135 - 1135

Опубликована: Сен. 8, 2024

Fine particulate matter (PM2.5) is a significant cause of respiratory diseases and associated cellular damage. The mechanisms behind this damage have not been fully explained. This study investigated two types (inflammation pyroptosis) induced by PM2.5, focusing on their relationship with organelles (the endoplasmic reticulum mitochondria). Animal models demonstrated that PM2.5 induces excessive stress (ER stress), which lung in rats. was confirmed pretreatment an ER inhibitor (4-Phenylbutyric acid, 4-PBA). We found that, vitro, the intracellular Ca2+ ([Ca2+]i) dysregulation rat alveolar macrophages stress. Changes mitochondria-associated membranes (MAMs) result abnormal mitochondrial function. further massive expression NLRP3 GSDMD-N, detrimental to cell survival. In conclusion, our findings provide valuable insights into between [Ca2+]i dysregulation, damage, inflammation pyroptosis under PM2.5-induced conditions. Their interactions ultimately impact health.

Язык: Английский

Процитировано

3