Depsipeptide (FK228 or FR901228) was evaluated in the mouse bone marrow micronucleus test for its possible protective effect against chromosomal damage induced by benzo(a)pyrene and cyclophosphamide. Three doses of depsipeptide (0.5, 1, and 1.5 mg/kg body weight) were given intravenously to mice for 7 consecutive days prior to administration of genotoxins under investigation. All the three doses of depsipeptide were effective in exerting a protective effect against both benzo(a)pyrene and cyclophosphamide. A significant suppression (34.9% to 67.5%) in the micronuclei formation induced by benzo(a)pyrene and (25.7% to 71.5%) cyclophosphamide was observed following intravenous administration of depsipeptide at doses of 0.5, 1, and 1.5 mg/kg in Swiss albino mice.

Download full-text PDF

Source
http://dx.doi.org/10.1080/10915810601120111DOI Listing

Publication Analysis

Top Keywords

swiss albino
8
albino mice
8
induced benzoapyrene
8
benzoapyrene cyclophosphamide
8
three doses
8
doses depsipeptide
8
depsipeptide
5
inhibitory effects
4
effects histone
4
histone deacetylase
4

Similar Publications

Present study was conducted to evaluate the detrimental impacts of exposure of Multi-walled Carbon Nanotubes (MWCNT-NP) on enzymatic activities and tissue structures in Swiss albino mice. The experimental groups of mice received MWCNT-NP for specific time period (seven or fourteen days). Two distinct doses of the MWCNT-NP solution were given orally: 0.

View Article and Find Full Text PDF

Brivaracitam Ameliorates Increased Inflammation, Oxidative Stress, and Acetylcholinesterase Activity in Ischemic Mice.

Clin Psychopharmacol Neurosci

February 2025

Department of Pharmacology, Amity Institute of Pharmacy, Amity University Uttar Pradesh, Noida, Uttar Pradesh, India.

Objective: Cerebral ischemia is a medical condition that occurs due to poor supply of blood in the brain. Reperfusion being savage further exaggerates the tissue injury causing cerebral ischemia/reperfusion injury (CI/R). CI/R is marked by an impairment in release of neurotransmitter, excitotoxicity, oxidative stress, inflammation, and neuronal apoptosis.

View Article and Find Full Text PDF

Neurotensin receptor agonist PD149163 modulates LPS-induced enterocyte apoptosis by downregulating TNFR pathway and executioner caspase 3 in endotoxemic mice: insights from in vivo and in silico study.

Naunyn Schmiedebergs Arch Pharmacol

January 2025

Department of Zoology, University of Allahabad, Senate House, University Road, Old Katra, Prayagraj, Uttar Pradesh, 211002, India.

This study was designed to evaluate the dose-dependent efficacy of neurotensin receptor-1 (NTSR1) agonist PD149163 in the amelioration of the lipopolysaccharide (LPS)-induced apoptosis in the gastrointestinal tract (GIT) of mice. PD149163 is an analogue of NTS, a GIT tri-decapeptide with anti-inflammatory and anti-oxidative effects. Swiss-albino mice (female/8 weeks/25 ± 2.

View Article and Find Full Text PDF

In the Rutaceae family is the biggest among all fruits, tradtionally used for several purposes due to its diverse ethnomedicinal, phytochemical, and pharmacological activities. Different portions of this plant have been used as sedatives and anti-inflammatory medications, as well as to treat coughs, fevers, asthma, diarrhea, ulcers, and diabetes. There is a scientific potential for the methanolic seed extract to contain bioactive compounds, similar to those found in other parts of the plant.

View Article and Find Full Text PDF

Hepatic steatosis/non-alcoholic fatty liver disease is a major public health delinquent caused by the excess deposition of lipid into lipid droplets (LDs) as well as metabolic dysregulation. Hepatic cells buildup with more fat molecules when a person takes high fat diet that is excessive than the body can handle. At present, millions of people in the world are affected by this problem.

View Article and Find Full Text PDF

Want 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!