High-Dose Aspirin Reverses Tartrazine-Induced Cell Growth Dysregulation Independent of p53 Signaling and Antioxidant Mechanisms in Rat Brain.
Nouf AlsalmanAbdulaziz AljafariTanveer A WaniSeema ZargarPublished in: BioMed research international (2019)
Tartrazine, an azo dye used in food, cosmetics, and pharmaceuticals with the effects on cell cycle, is not well understood. Therefore, we investigated the toxicity of tartrazine in rat brain with high-dose aspirin. Male Wistar rats (n = 24) were divided into (C) control, (T) tartrazine (700 mg/kg body weight [BW] at weeks 1 and 2), (A) aspirin (150 mg/kg [BW] at weeks 1, 2, and 3), and (TA) aspirin + tartrazine (150 mg/kg [BW] aspirin at weeks 1, 2, and 3 and 700 mg/kg [BW] tartrazine at weeks 1 and 2) groups. The expression of p53, B cell lymphoma-2 extra-large (Bcl-xL), cyclin-dependent kinase 2 (CDK2), p27, and Ki67 was evaluated by quantitative reverse-transcription PCR. A histopathological analysis of brain tissue and oxidative stress level was assessed based on reduced glutathione (GSH), ascorbic acid (AA), and malondialdehyde levels. We found that Bcl-xL, Ki67, CDK2, and p27 were upregulated and p53 was downregulated in the tartrazine-treated group as compared to the control group. Aspirin administration reversed these changes except P53 expression. Tartrazine had no effect on lipid peroxidation but altered AA and GSH levels with no reversal by aspirin treatment. Histopathological analysis revealed that aspirin prevented tartrazine-induced damage including increased perivascular space and hemorrhage. These results indicate that aspirin protects the brain from tartrazine-induced toxicity independent of p53 signaling and antioxidant mechanisms.
Keyphrases
- low dose
- high dose
- cell cycle
- oxidative stress
- cardiovascular events
- antiplatelet therapy
- diabetic rats
- anti inflammatory drugs
- body weight
- high glucose
- cell proliferation
- acute coronary syndrome
- dna damage
- resting state
- cardiovascular disease
- stem cell transplantation
- drug induced
- gestational age
- white matter
- mass spectrometry
- functional connectivity
- high resolution
- squamous cell carcinoma
- type diabetes
- multiple sclerosis
- brain injury
- percutaneous coronary intervention
- ischemia reperfusion injury
- anti inflammatory
- signaling pathway
- blood brain barrier
- climate change
- endothelial cells
- pi k akt
- highly efficient
- heat stress
- endoplasmic reticulum stress
- smoking cessation
- oxide nanoparticles