Pravastatin is an inhibitor of 3-hydroxy-3-methyl- glutaryl-coenzyme A reductase that has been reported to have therapeutic applications in a range of inflammatory conditions. The aim of the present study was to assess the radioprotective effects of pravastatin in an experimental animal model. Mice were divided into two groups: The control group received ionizing radiation with no prior medication, while the pravastatin group received pravastatin prior to ionizing radiation. Pravastatin was administered orally at 30 mg/kg body weight in drinking water at 24 and 4 h before irradiation. Intestinal crypt epithelial cell survival and the incidence of apoptosis in the intestine and lung were measured post-irradiation. The effect of pravastatin on intestinal DNA damage was determined by immunohistochemistry. Finally, the effect of pravastatin on tumor response to radiotherapy was examined in a mouse mesothelioma xenograft model. Pravastatin increased the number of viable intestinal crypts and this effect was statistically significant in the ileum (P<0.0001). The pravastatin group showed significantly lower apoptotic indices in all examined parts of the intestine (P<0.0001) and tended to show reduced apoptosis in the lung. Pravastatin reduced the intestinal expression of ataxia-telangiectasia mutated and gamma-H2AX after irradiation. No apparent pravastatin-related differences were observed in the response of xenograft tumors to irradiation. In conclusion, pravastatin had radioprotective effects on the intestine and lung and reduced radiation-induced DNA double-strand breaks. Pravastatin may increase the therapeutic index of radiotherapy.
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http://dx.doi.org/10.3892/etm.2017.4192 | DOI Listing |
Clin Pharmacol Drug Dev
December 2024
Gossamer Bio, Inc., San Diego, CA, USA.
Seralutinib, an inhaled, small-molecule tyrosine kinase inhibitor in clinical development for the treatment of pulmonary arterial hypertension (PAH), was evaluated for its potential as a perpetrator or victim of a metabolic and transporter-based drug-drug interactions in 2 phase 1 studies. In study 1, 24 participants received a cocktail of probe substrates: caffeine (CYP1A2), montelukast (CYP2C8), flurbiprofen (CYP2C9), midazolam (CYP3A), and pravastatin (OATP1B1/1B3), plus digoxin (P-gp) with or without seralutinib. In study 2, 19 participants received seralutinib with/without itraconazole, a strong CYP3A inhibitor, or fosaprepitant, a weak CYP3A inhibitor.
View Article and Find Full Text PDFEur J Hum Genet
December 2024
Department of Family Medicine, Public Health and Primary Care (PHEG), Mayo Clinic, Rochester, MN, USA.
Aligned with the mission of the Dutch Pharmacogenetics Working Group (DPWG) to promote the implementation of pharmacogenetics (PGx), this guideline is specifically designed to optimize pharmacotherapy of cholesterol lowering medication (statins) and glucose lowering medication (sulfonylureas). The SLCO1B1 c.521 T > C variant reduces the activity of the SLCO1B1 transporter involved in statin transport out of the blood into the liver.
View Article and Find Full Text PDFJ Neurol Sci
December 2024
Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan; Department of Neurology, Iseikai Hospital, Osaka, Japan.
Background And Aims: We aimed to investigate long-term changes in carotid intima-media thickness (IMT) based on baseline blood pressure (BP) levels in non-cardioembolic stroke patients.
Methods: Patients aged 45-80 years with dyslipidemia who were not on statins before enrollment and had experienced a non-cardioembolic stroke were assigned to either the pravastatin group or the control group in a randomized trial. Patients were classified into three groups according to BP levels: normal BP (N-group: systolic BP [sBP] <140 mmHg and diastolic BP [dBP] <90 mmHg), highly elevated BP (G2 group: sBP ≥160 mmHg or dBP ≥100 mmHg), and mildly elevated BP (G1 group: the remaining patients).
Clin Auton Res
December 2024
ECRI-Penn Evidence-Based Practice Center, 5200 Butler Pike, Plymouth Meeting, PA, 19462, USA.
Purpose: For Long COVID autonomic dysfunction, we have summarized published evidence on treatment effectiveness, clinical practice guidelines, and unpublished/ongoing studies.
Methods: We first interviewed 11 stakeholders (clinicians, clinician/researchers, payors, patient advocates) to gain clinical insights and identify key areas of focus. We searched Embase, CINAHL, Medline, PsycINFO, and PubMed databases for relevant English-language articles published between 1 January 2020 and 30 April 2024.
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