title: Cepharanthine improves renal ischemia-reperfusion injury in rats.
abstract: BACKGROUND
  Acute renal damage has numerous causes, including renal ischemia-reperfusion injury. Due to its diverse actions, cepharanthine is used to treat many acute and chronic diseases, including pit viper bites, alopecia areata, and leucopenia in radiation therapy. In this study, we examined whether cepharanthine provides a renal-protective effect in a renal ischemia-reperfusion model.
  
  
  METHODS
  Male Wistar rats were divided into four groups that received the following treatments: induction of renal ischemia-reperfusion (I/R group); subcutaneous injection of cepharanthine (10 mg/kg) followed 1 h later by induction of renal ischemia-reperfusion (Cepha + I/R group); subcutaneous injection of cepharanthine (10 mg/kg) (Cepha group); and subcutaneous injection of saline followed 1 h later by sham treatment (control group). Rats were sacrificed 24 h after renal ischemia-reperfusion or sham treatment. Serum blood urea nitrogen (BUN) and creatinine (Cre) concentrations were determined, histologic examination was performed, and oxidative stress was evaluated in kidney tissue. In addition, antimycin A (AMA)-stimulated RAW264.7 cells were treated with cepharanthine to determine its antioxidant effects.
  
  
  RESULTS
  Serum BUN and Cre levels were increased in the I/R group; however, these increases were significantly inhibited in the Cepha + I/R group. Similarly, kidney tissue damage observed in the I/R group was attenuated in the Cepha + I/R group. In vitro, cells treated with both cepharanthine and AMA showed reduced reactive oxygen species activity compared with cells treated with AMA alone.
  
  
  CONCLUSIONS
  Our findings suggest that cepharanthine may be effective in the treatment of various types of ischemia-reperfusion injuries.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, Oita University Faculty of Medicine, Yufu City, Oita, Japan. j2508@med.oita-u.ac.jp
authors.forename: Junya
authors.initials: J
authors.lastname: Kusaka
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hagiwara
authors.forename: Akira
authors.initials: A
authors.lastname: Hasegawa
authors.forename: Kyosuke
authors.initials: K
authors.lastname: Kudo
authors.forename: Hironori
authors.initials: H
authors.lastname: Koga
authors.forename: Takayuki
authors.initials: T
authors.lastname: Noguchi
mesh_terms: D000208:Acute Disease; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D044182:Benzylisoquinolines / Q000494:pharmacology*; D004195:Disease Models, Animal; D007668:Kidney / Q000187:drug effects / Q000648:ultrastructure; D007674:Kidney Diseases / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D046529:Microscopy, Electron, Transmission; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism; D052117:Benzodioxoles
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D044182:Benzylisoquinolines; D008315:Malondialdehyde; D017382:Reactive Oxygen Species; C006947:cepharanthine; D052117:Benzodioxoles