Hemin attenuated oxidative stress and inflammation to improve wound healing in diabetic rats.
Administration, Cutaneous
Animals
Antioxidants
/ administration & dosage
Blood Glucose
/ analysis
Diabetes Mellitus, Experimental
/ drug therapy
Heme Oxygenase (Decyclizing)
/ antagonists & inhibitors
Hemin
/ administration & dosage
Inflammation Mediators
/ metabolism
Male
Metalloporphyrins
/ administration & dosage
Ointments
Oxidative Stress
/ drug effects
Protoporphyrins
/ administration & dosage
Rats
Skin
/ drug effects
Streptozocin
Wound Healing
/ drug effects
Diabetes
Hemin
Inflammation
Oxidative stress
Tin protoporphyrin
Wound
Journal
Naunyn-Schmiedeberg's archives of pharmacology
ISSN: 1432-1912
Titre abrégé: Naunyn Schmiedebergs Arch Pharmacol
Pays: Germany
ID NLM: 0326264
Informations de publication
Date de publication:
11 2019
11 2019
Historique:
received:
03
02
2019
accepted:
21
06
2019
pubmed:
6
7
2019
medline:
21
8
2020
entrez:
6
7
2019
Statut:
ppublish
Résumé
Oxidative stress and persistent inflammation play crucial role in the progression of diabetic wound complications. Hemeoxgenase-1 (HO-1) by degrading hemin has been shown to display anti-oxidant and anti-inflammatory effects. Further, hemin is a potent HO-1 inducer. Thus, the current study was aimed to evaluate the effect of topical application of hemin on diabetic wound in rats. Four hundred square millimeter open excision wound were created 2 weeks after induction of diabetes with single intraperitoneal injection of streptozotocin (60 mg/kg), and the diabetic rats were divided into three groups namely diabetic control, hemin, and tin protoporphyrin (SnPPIX). Ointment base, hemin (0.5% in ointment base), and SnPPIX (0.5% in ointment base) were applied topically to wounded area in diabetic control, hemin, and SnPPIX group rats, respectively, twice daily for 19 days. Hemin significantly increased the wound contraction in comparison to control and SnPPIX-treated rats. Time-dependent analysis revealed significant increase in anti-oxidants with concomitant decrease in oxidants in hemin-treated rats as compared to diabetic control rats. Further, mRNA expression decreased for inflammatory cytokine and increased for anti-inflammatory cytokine in hemin group as compared to diabetic control rats. Expression of HO-1 also increased in hemin group as compared to diabetic control rats. However, SnPPIX group results were in disagreement with results of hemin which is clearly reflected in histopathology. Results indicate the ability of hemin to accelerate wound healing in diabetic rats by combating inflammation and oxidative stress probably via HO-1.
Identifiants
pubmed: 31273394
doi: 10.1007/s00210-019-01682-7
pii: 10.1007/s00210-019-01682-7
doi:
Substances chimiques
Antioxidants
0
Blood Glucose
0
Inflammation Mediators
0
Metalloporphyrins
0
Ointments
0
Protoporphyrins
0
Streptozocin
5W494URQ81
Hemin
743LRP9S7N
tin protoporphyrin IX
DIO3JT9G2P
Heme Oxygenase (Decyclizing)
EC 1.14.14.18
Hmox1 protein, rat
EC 1.14.14.18
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1435-1445Références
Am J Pathol. 1995 Sep;147(3):782-9
pubmed: 7677189
Pharmacol Res. 2008 Aug;58(2):165-71
pubmed: 18617006
J Vasc Surg. 2010 Feb;51(2):417-28
pubmed: 20022212
Int J Low Extrem Wounds. 2002 Mar;1(1):27-32
pubmed: 15871949
Naunyn Schmiedebergs Arch Pharmacol. 2014 Oct;387(10):955-61
pubmed: 24969350
Indian J Biochem Biophys. 1998 Jun;35(3):184-8
pubmed: 9803669
Diabetes. 2010 Sep;59(9):2306-14
pubmed: 20566667
Eur J Pharmacol. 2010 Oct 25;645(1-3):165-70
pubmed: 20638379
Free Radic Res. 1997 Feb;26(2):93-101
pubmed: 9257121
Proc Natl Acad Sci U S A. 2009 Mar 31;106(13):5171-6
pubmed: 19286972
PLoS One. 2009 Jun 04;4(6):e5803
pubmed: 19495412
J Pharm Pharmacol. 2013 Jul;65(7):995-1004
pubmed: 23738727
Toxicol Lett. 1984 Jun;21(3):333-7
pubmed: 6740722
Clin Sci (Lond). 1998 Jun;94(6):623-32
pubmed: 9854460
Eur J Pharmacol. 2011 Jul 1;661(1-3):102-8
pubmed: 21549697
Clin Plast Surg. 1998 Jul;25(3):341-56
pubmed: 9696897
Am J Respir Cell Mol Biol. 1996 Jul;15(1):9-19
pubmed: 8679227
Biomaterials. 2005 Nov;26(33):6664-73
pubmed: 15978664
Nature. 2001 Dec 13;414(6865):813-20
pubmed: 11742414
Biochem Biophys Res Commun. 1999 Nov;265(1):194-9
pubmed: 10548513
Pharmacol Rev. 2008 Mar;60(1):79-127
pubmed: 18323402
Circ Res. 1998 Apr 20;82(7):810-8
pubmed: 9562441
J Invest Dermatol. 2000 Aug;115(2):245-53
pubmed: 10951242
PLoS One. 2010 Mar 04;5(3):e9539
pubmed: 20209061
Science. 1973 Feb 9;179(4073):588-90
pubmed: 4686466
Naunyn Schmiedebergs Arch Pharmacol. 2013 Mar;386(3):217-26
pubmed: 23254361
Anal Biochem. 1968 Oct 24;25(1):192-205
pubmed: 4973948
Circ Res. 2010 Oct 29;107(9):1058-70
pubmed: 21030723
Diabetes Res Clin Pract. 2001 May;52(2):119-23
pubmed: 11311966
Biochemistry. 1977 Feb 8;16(3):419-23
pubmed: 836794
Curr Pharm Des. 2003;9(30):2541-51
pubmed: 14529552
Am J Respir Crit Care Med. 2005 Sep 15;172(6):660-70
pubmed: 15901614
J Invest Dermatol. 2004 Jul;123(1):87-92
pubmed: 15191547
JAMA. 2009 May 27;301(20):2129-40
pubmed: 19470990
Endocrinology. 2009 May;150(5):2098-108
pubmed: 19106228
Methods. 2001 Dec;25(4):402-8
pubmed: 11846609
Antioxidants (Basel). 2018 Jul 24;7(8):null
pubmed: 30042332
Dis Model Mech. 2013 Jul;6(4):1012-20
pubmed: 23592614
Methods Enzymol. 1984;105:121-6
pubmed: 6727660
J Diabetes Res. 2016;2016:9726503
pubmed: 26798657
Exp Diabetes Res. 2007;2007:43603
pubmed: 17641741
Am J Pathol. 1990 Jun;136(6):1235-46
pubmed: 2356856