Exp Biol Med (Maywood)
July 2023
The objective of the present investigation was to assess the protective impact of gentiopicroside (GPS) on acute myocardial infarction (AMI) through the modulation of NF-E2-related factor 2 (Nrf2)/nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing 3 (NLRP3) signaling. H9c2 cells were subjected to varying concentrations of GPS, and subsequently, the cells and Sprague-Dawley (SD) rats were segregated into control, model, GPS, t-BHQ (an Nrf2 activator), and GPS + ML385 (an Nrf2 inhibitor) groups. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were analyzed.
View Article and Find Full Text PDFWe aimed to investigate the effects and mechanism of Atorvastatin on Myocardial Ischaemia-Reperfusion Injury and . The effects of Atorvastatin on Silent information regulator l (SIRT1) and endoplasmic reticulum (ER) stress were investigated in Myocardial ischaemia-reperfusion (MI/R) injury rat model and hypoxia/reoxygenation (H/R)-treated H9c2 cells. Pathological changes, inflammatory and heart injury markers, cell apoptosis and cell death, SIRT1 and cleaved Caspase-12 expressions, and ER stress relative proteins were measured through HE, enzyme-linked immunosorbent assay, quantitative TUNEL and flow cytometry, immunofluorescence and Western blotting with the assistance of the SIRT1 specific inhibitor EX527 and ER stress pathway blocker treatment.
View Article and Find Full Text PDFParaquat (PQ) intoxication causes thousands of mortalities every year, worldwide. Its pulmonary-targeted accumulation and the acute lung injury it subsequently causes, remain a challenge for detoxification treatment. A previous study has demonstrated that the upregulation of nuclear factor erythroid-2 related factor 2 (Nrf2) prevents PQ toxicity in cell line and murine models.
View Article and Find Full Text PDFZhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
January 2014
Objective: To investigate the protective effect of curcumin (CU) on type II alveolar epithelial cells (A549 cells) during paraquat (PQ)-induced oxidative damage and its underlying mechanism.
Methods: Routinely cultured A549 cells were divided into blank control group, CU control group, PQ group, and PQ+Cu group to receive respective treatments for 24 h. Cell viability was determined by MTT assay.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
March 2013
Objective: To investigate the intervention effect of thalidomide on paraquat-induced acute lung injury in mice and its mechanism.
Methods: Male ICR mice were randomly allocated to negative control group (n = 30), thalidomide control group (n = 30), paraquat poisoning group (n = 30), 50 mg/kg thalidomide treatment group (n = 30), 100 mg/kg thalidomide treatment group (n = 30), and 150 mg/kg thalidomide treatment group (n = 30). The negative control group was intraperitoneally injected with the same volume of saline; the thalidomide control group was intraperitoneally injected with thalidomide (150 mg/kg); the paraquat poisoning group was intraperitoneally injected with diluted paraquat solution (22 mg/kg); each thalidomide treatment group was intraperitoneally injected with the same volume of paraquat solution (22 mg/kg) and was injected with thalidomide (50, 100, or 150 mg/kg) 1 h later.