title: N-acetyl cysteine promotes angiogenesis and clearance of free oxygen radicals, thus improving wound healing in an alloxan-induced diabetic mouse model of incisional wound.
abstract: BACKGROUND
  This study investigated whether N-acetyl cysteine induces any favourable effects on cutaneous incisional wound healing in diabetic and nondiabetic mice. The wounds were assessed using detection of vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) expression, and wound-breaking strength (WBS) measurements.
  
  
  METHODS
  In total, 48 BALB/c mice were used. These were divided into four groups, each consisting of 12 mice. Incisional wounds were made on the back of each mouse. Two of the groups consisted of healthy animals and the other two groups consisted of mice with alloxan-induced diabetes. One group of healthy mice and one group of diabetic mice received intraperitoneal N-acetyl cysteine (NAC) 150 mg/kg for 5 consecutive days, while the other two groups were untreated. On the fifth day all animals were killed, and the WBS, oxidative stress parameters, histopathological and immunohisotchemical results were assessed.
  
  
  RESULTS
  Both diabetic and nondiabetic mice receiving NAC had lower levels of oxidative stress markers and higher WBS measurements than untreated counterparts.
  
  
  CONCLUSIONS
  A mouse model of incisional wound treated with NAC resulted in lower levels of tissue oxidative stress, higher levels of tissue glutathione, and downregulation of iNOS expression coupled with upregulation of VEGF expression, producing an overall favourable clinical outcome of higher WBS and a shorter wound-healing period both in diabetic and nondiabetic mice. Both antioxidant and anti-inflammatory properties of NAC may be involved in this improved healing process for incisional wounds.
authors.affiliation: Department of Family Medicine, School of Medicine, Zonguldak Karaelmas University, Kozlu-Zonguldak, Turkey. aktunc.erol@gmail.com
authors.forename: E
authors.initials: E
authors.lastname: Aktunc
authors.forename: V H
authors.initials: VH
authors.lastname: Ozacmak
authors.forename: H S
authors.initials: HS
authors.lastname: Ozacmak
authors.forename: F
authors.initials: F
authors.lastname: Barut
authors.forename: M
authors.initials: M
authors.lastname: Buyukates
authors.forename: O
authors.initials: O
authors.lastname: Kandemir
authors.forename: N
authors.initials: N
authors.lastname: Demircan
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology*; D000496:Alloxan / Q000633:toxicity; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced; D004195:Disease Models, Animal; D016166:Free Radical Scavengers / Q000494:pharmacology*; D005978:Glutathione / Q000096:biosynthesis; D006909:Hydroxyproline / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D018919:Neovascularization, Physiologic / Q000187:drug effects* / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D012867:Skin / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D042442:Vascular Endothelial Growth Factors / Q000096:biosynthesis; D014945:Wound Healing / Q000187:drug effects*; D014950:Wounds, Penetrating / Q000378:metabolism / Q000473:pathology*
chemical_list: D016166:Free Radical Scavengers; D017382:Reactive Oxygen Species; D042442:Vascular Endothelial Growth Factors; D008315:Malondialdehyde; D000496:Alloxan; D019001:Nitric Oxide Synthase; D005978:Glutathione; D006909:Hydroxyproline; D000111:Acetylcysteine