Potential Anti-inflammatory Effect of Telmisartan In Experimentally Induced Acute Pancreatitis in Rats.
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Background: Acute pancreatitis (AP) is an acute inflammatory disorder of the pancreas. The destruction of pancreatic parenchyma induces a systemic activation of coagulation, kinin, complement and fibrinolytic cascades with liberation of cytokines and reactive oxygen metabolites. Peroxisome proliferator—activated receptors (PPARs) play key roles in the processes of fat metabolism, adipocyte differentiation, tumorigenesis, inflammation and variety of immune processes. Telmisartan is the only angiotensin receptor blocker (ARB) that may modulate PPARy activation at physiologic plasma concentrations. Telmisartan may reduce markers of inflammation, such as interleukin-6 and C-reactive protein, oxidative stress and improves markers of vascular function. The aim of the current article was to investigate the possible antiinflammatory, antioxidant effects, and peroxisome proliferator-activated receptor-y (PPARy) properties of the angiotensin type I receptor blocker telmisartan in experimentally induced acute pancreatitis. Materials and Methods:Fifty male albino rats were divided randomly into 5 groups; control normal group and 4 acute pancreatic groups group (n=40). Acute pancreatitis were induced by i.p. injection of 20% L-arginine hydrochloride in saline (2x250 mg/100 g at I h interval) and subdivided equally into acute pancreatic group (no treatment); AP treatedt with Tel or Ros alone or their combination groups. Serum amylase and lipase activity were determined. Also TNF-a, IL-6, MDA and CAT were estimated in addition to histopathological examination. Results: Ros alone or in combination with Tel induced significant attenuation of serum amylase and lipase activity. Also TNF-a, IL-6, MDA and CAT were improved. While Tel induced insignificant improvement of previous parameters Conclusion: Use of rosiglitazone associated with a reduced risk of AP by improving inflammatory status and oxidative stress reflecting the important role of PPAR-y in AP. Furthermore, telmisartan does not ameliorate acute pancreatic inflammation. Both agents have affinity for PPAR-y, telmisartan binds to the receptor in a different manner, resulting in distinct pharmacological actions.