Effect of hemin on severe acute pancreatitis-associated lung injury in rats and its mechanism.
- Author:
Zhiyong LIU
1
;
Yuhang AI
;
Lina ZHANG
Author Information
1. Department of Anesthesiology, Xiangya Hospital, Central South University, Changsha 410008, China.
- Publication Type:Journal Article
- MeSH:
Acute Lung Injury;
drug therapy;
etiology;
Animals;
Cytokines;
genetics;
metabolism;
Female;
Heme Oxygenase (Decyclizing);
genetics;
metabolism;
Hemin;
therapeutic use;
Male;
NF-kappa B;
genetics;
metabolism;
Pancreatitis, Acute Necrotizing;
complications;
drug therapy;
RNA, Messenger;
genetics;
metabolism;
Rats;
Rats, Sprague-Dawley;
Reverse Transcriptase Polymerase Chain Reaction
- From:
Journal of Central South University(Medical Sciences)
2009;34(3):242-246
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of hemin on lung injury following severe acute pancreatitis (SAP) in rats and to explore its rudimentary mechanism.
METHODS:Thirty-six rats were randomly divided into 3 groups: a control group, a SAP model group, and a hemin-pretreated group. Rats were sacrificed 12 hours after inducing SAP model. The pathological changes of the pancreas and lungs were observed under light microscope. Expression of heme oxygenase (HO-1) mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR), NF-kappaB activity in the lung tissues was detected by enzyme linked immunosorbent assay (ELISA), and the serum levels of TNF-alpha and IL-6 were measured by ELISA.
RESULTS:HO-1 was induced during experimental SAP, NF-kappaB activity in the lung tissues was elevated after the induction of SAP and the serum levels of TNF-alpha and IL-6 were significantly elevated. Hemin further upregulated the expression of HO-1 mRNA, decreased NF-kappaB activity drastically, and inhibited the serum levels of TNF-alpha and IL-6 significantly (P < 0.05). Hemin could treat SAP by alleviating the pancreatic and lung injury.
CONCLUSION:Hemin moderates the inflammatory reaction and decreases the lung injury following SAP, the mechanism of which may be closely related to the upregulation of expression of HO-1 mRNA, the inhibitory effect on NF-kappaB, and adjustment of cytokines.
