title: Telmisartan inhibits hyperalgesia and inflammatory progression in a diabetic neuropathic pain model of Wistar rats.
abstract: OBJECTIVE
  To evaluate the potential therapeutic value of telmisartan (TMT) against diabetic neuropathy (DN) and associated pain in Wistar rats.
  
  
  METHODS
  Peripheral DN was induced by a single intraperitoneal streptozotocin injection (55 mg/kg), and 3 weeks later TMT treatment was started (5 and 10 mg/kg/day), and continued for 4 weeks. Mechanical nociceptive threshold, motor coordination, and thermal nociceptive threshold tests were performed before and after TMT treatment. In serum, glucose, pro-inflammatory cytokines including tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 were assessed. Nerve growth factor (NGF) levels and histopathological changes were estimated in the sciatic nerve. This study was conducted at the Experimental Animal Care Center, Department of Pharmacology, College of Pharmacy, King Saud University, Riyadh, Kingdom of Saudi Arabia between January 2013 and May 2014.
  
  
  RESULTS
  We observed a significant reduction in mechanical nociceptive threshold, motor coordination, and thermal nociceptive threshold in diabetic animals. The TMT treatment significantly enhanced the reduced mechanical nociceptive threshold. The untreated diabetic animals revealed a significant decrease in sciatic NGF, which was markedly attenuated by TMT. The elevated serum levels of cytokines in diabetic animals were inhibited by the TMT treatments. Histopathological evaluation showed obvious nerve degeneration in the diabetic group that was eliminated in the TMT treated diabetic groups.
  
  
  CONCLUSIONS
  Telmisartan has a potential neuro-protective effect on peripheral DN; this is mediated through its anti-inflammatory effects and its dual properties as an angiotensin receptor blocker, and a partial peroxisome proliferator activator receptor-gamma ligand.
authors: Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, PO Box 55760, Riyadh 11544, Kingdom of Saudi Arabia. E-mail: rejaie@ksu.edu.sa.
authors: Salim S
authors: SS
authors: Al-Rejaie
authors: Hatem M
authors: HM
authors: Abuohashish
authors: Mohammed M
authors: MM
authors: Ahmed
authors: Aws S
authors: AS
authors: Arrejaie
authors: Abdulaziz M
authors: AM
authors: Aleisa
authors: Shakir D
authors: SD
authors: AlSharari
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D000818:Animals; D001562:Benzimidazoles / Q000627:therapeutic use*; D001565:Benzoates / Q000627:therapeutic use*; D016207:Cytokines / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000473:pathology; D003929:Diabetic Neuropathies / Q000150:complications* / Q000188:drug therapy* / Q000473:pathology; D006930:Hyperalgesia / Q000188:drug therapy* / Q000473:pathology; D007249:Inflammation / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D010147:Pain Measurement / Q000187:drug effects; D010812:Physical Stimulation; D051381:Rats; D017208:Rats, Wistar; D012584:Sciatic Nerve / Q000473:pathology; D000077333:Telmisartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D001562:Benzimidazoles; D001565:Benzoates; D016207:Cytokines; D000077333:Telmisartan