The regulative effects of polydatin on toll-like receptor 4 signal transduction pathway in lung ischemia/reperfusion injury in rabbits.
- Author:
Xiao-Feng JIN
1
;
Zheng-Jie XU
;
Wan-Tie WANG
;
Yi-Xiao XU
;
Xiao-Long ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Female; Glucosides; pharmacology; Intercellular Adhesion Molecule-1; genetics; metabolism; Ischemia; metabolism; physiopathology; Lung; blood supply; Male; Protective Agents; pharmacology; RNA, Messenger; genetics; metabolism; Rabbits; Reperfusion Injury; metabolism; prevention & control; Signal Transduction; drug effects; Stilbenes; pharmacology; Toll-Like Receptor 4; genetics; metabolism; Transcription Factor RelA; genetics; metabolism
- From: Chinese Journal of Applied Physiology 2009;25(1):41-44
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate protective effects of polydatin(PD) during lung ischemia/reperfusion in rabbits and its potential mechanisms.
METHODSRabbit lung model of ischemia/reperfusion (I/R) injury was constituted in vivo. Thirty rabbits were divided into groups randomly: Control (C), I/R, PD group, respectively. Endotoxin (ET) in plasma was analyzed by End-point Chromogenic Assay, the expression of Toll-like receptor 4 (TLR4) mRNA, nuclear factor (NF)-kappaBp65 mRNA, intracellular adhesion molecule-1 (ICAM-1) mRNA were measured by RT-PCR, the morphological changes of lung tissue were observed with hematoxylin-eosin (HE) staining.
RESULTSThere was no significant difference in ET concentration of plasma between groups (all of P > 0.05). The expression of TLR-4 mRNA, NF-kappaBp65 mRNA and ICAM-1mRNA in I/R group were significantly increased as compared to C group and PD group, while those expressions in PD group were evidently higher than those in C group (all of P < 0.01). Light microscope showed that the lung pathological injuries in PD group were obviously alleviated as compared to I/R group.
CONCLUSIONPD might have a protective effect on lung ischemia/reperfusion injury by down-regulating TLR4 and NF-kappaB expression, then inhibiting the release of mediators of inflammation as ICAM-1.
