Candesartan Cilexetil Decreases Genes Expression of p53 and TNF-α in Mice Serum

Abstract

Background: Candesartan is an angiotensin II receptor blocker available as Candesartan Cilexetil tablets used for hypertension treatment. Candesartan Cilexetil is converted to active Candesartan during gastrointestinal absorption. Tumor necrosis factor - alpha (TNF-α) is a cytokine associated with pro-inflammation, which has emerged as a critical modulator of blood pressure. Tumor suppressor protein (p53) is a cytokine responsible for cell apoptosis. Hypertension can induce apoptosis, especially in cardiac muscle. Recently, research referred to increased levels of TNF-α and P53 in serum with increasing angiotensin II releasing. This study is designed to investigate the impact of Candesartan Cilexetil on reducing these cytokines in serum.
Methods: Forty Albino Swiss male mice were incubated under ideal conditions. Mice were divided into two groups; one was given many doses of Candesartan Cilexetil (0.1, 0.3, and 0.5 mg kg-1day-1) and a control group. After treatment for 21 days the concentration of p53 and TNF-α in serum was determined using Elisa sandwich method.
Results: Candesartan Cilexetil reduced P53 and TNF–α concentration significantly at (p≤0.05). But a highly significant decrease for the two cytokines was recorded in mice that were treated with 0.3 mg kg-1 of Candesartan cilexetil.
Conclusion: Candesartan Cilexetil can reduce TNF-α and P53 concentration in mice serum by blocking the angiotensin II receptor because angiotensin II enhances releasing of these cytokines.