Objective: To investigate the effect of propofol on the expression of thrombospondin-1 (THBS-1) mRNA and protein in purified newborn rat cortical astrocytes in vitro.
Methods: Astrocytes were isolated from newborn rat cortex and grown in culture before exposure to propofol at 3, 10, 30, 100 or 300 µmol/L for 6 h, 12, or 24 h. The mRNA level of THBS-1 was detected by RT-PCR, and the protein level of THBS-1 was detected by immunofluorescence cytochemistry and Western blotting.
Results: Propofol exposure caused significantly upregulated THBS-1 level in cultured astrocytes (P<0.05) to a level about 1.3 times higher than that in control cells. The mRNA and protein levels of THBS-1 in cultured rat cortical astrocytes were upregulated by exposures to 10, 30 and 100 µmol/L propofol (P<0.01). High expression of THBS-1 mRNA and protein was detected in the cells with exposures for different durations (P<0.05), especially in the 12 h group (P<0.01).
Conclusion: Propofol at clinically relevant concentrations can modulate the level of THBS-1 secreted by astrocytes of rat cerebral cortex in vitro.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Early maternal undernutrition induces sex-related metabolic changes in adult offspring.
J Dev Orig Health Dis
January 2025
Postgraduate Program in Physiological Sciences, State University of Londrina, Londrina, Parana, Brazil.
Nutritional status during the developmental periods leads to predisposition to several diseases and comorbidities, highlighting metabolic and reproductive changes throughout adult life, and in the next generations. One of the experimental models used to induce undernutrition is litter size expansion, which decreases the availability of breast milk to pups and delays development. This work evaluated the effects of maternal undernutrition induced by litter size expansion, a maternal undernutrition preconception model, on the metabolic and reproductive alterations of the offspring.
View Article and Find Full Text PDFPPARγ activation attenuates neonatal CRD-induced visceral pain sensitization and anxiety in male rats by alleviating oxidative stress.
BMC Gastroenterol
January 2025
Department of Anesthesiology, First Affiliated Hospital, Fujian Medical University, No. 20, Cha Zhong Road, Fuzhou, Fujian Province, People's Republic of China.
Background: Visceral pain sensitization and emotional reactions due to irritable bowel syndrome (IBS) occur frequently in the general population. Oxidative stress plays a crucial role in the pathogenesis of IBS. Previous studies have demonstrated that activation of peroxisome proliferator-activated receptor gamma (PPARγ) has analgesic effects.
View Article and Find Full Text PDFNovel peptidomimetic compounds attenuate hypoxic-ischemic brain injury in neonatal rats.
Exp Neurol
January 2025
Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA. Electronic address:
Hypoxic-ischemic (HI) brain injury is a common neurological problem in neonates. The postsynaptic density protein-95 (PSD-95) is an excitatory synaptic scaffolding protein that regulates synaptic function, and represents a potential therapeutic target to attenuate HI brain injury. Syn3 and d-Syn3 are novel high affinity cyclic peptides that bind the PDZ3 domain of PSD-95.
View Article and Find Full Text PDFDifferentiation of primary retinal progenitor cells into retinal ganglion-like cells using low dose cytarabine.
Biochem Biophys Res Commun
January 2025
Department of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China. Electronic address:
The death of retinal ganglion cells (RGCs) is a key factor in the pathophysiology of all forms of glaucoma. RGC culture serves as a simple system for establishing and testing candidate therapies. This study aimed to explore the differentiation of primary retinal progenitor cells (RPCs) into RGC-like cells induced by low-dose cytarabine (Ara-C).
View Article and Find Full Text PDFEdaravone Mitigates Hippocampal Neuronal Death and Cognitive Dysfunction by Upregulating BDNF Expression in Neonatal Hypoxic-Ischemic Rats.
Int J Dev Neurosci
February 2025
Department of Digestive and Nutrition, College of Clinical Medicine for Obstetrics & Gynecology and Pediatrics, Fujian Medical University, Fuzhou, Fujian, China.
Neonatal hypoxic-ischemic encephalopathy (HIE) is a severe neurological injury during infancy, often resulting in long-term cognitive deficits. This study aimed to investigate the neuroprotective effects of Edaravone (EDA), a free radical scavenger, and elucidate the potential role of brain-derived neurotrophic factor (BDNF) in mediating these effects in neonatal HIE rats. Using the Rice-Vannucci model, HIE was induced in neonatal rats, followed by immediate administration of EDA after the hypoxic-ischemic insult.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!