Effect of triptolide on airway smooth muscle proliferation and the expression of nuclear factor-kappa B, Bcl-2 in asthmatic rats.
- Author:
Bi-Wen MO
1
;
Jiang-Hong WEI
;
Jian-Wei HUANG
;
Chang-Ming WANG
;
Jin-Rong ZENG
;
Mei-Xi CHEN
;
Yan ZHOU
;
Qing XU
;
Yun LIN
Author Information
- Publication Type:Journal Article
- MeSH: Airway Remodeling; Animals; Apoptosis; Asthma; metabolism; pathology; Bronchi; cytology; drug effects; Diterpenes; pharmacology; Epoxy Compounds; pharmacology; Male; Myocytes, Smooth Muscle; drug effects; metabolism; NF-kappa B; metabolism; Phenanthrenes; pharmacology; Proto-Oncogene Proteins c-bcl-2; metabolism; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2010;26(4):385-390
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effect of triptolide on airway remodeling and the expression of nuclear factor-kappaB, Bcl-2 in asthmatic rats.
METHODS40 rats were randomly divided into 5 groups (n = 8): (1) Control group; (2) Asthmatic 4 week group; (3) Asthmatic 6 week group; (4) Therapeutic 4 week group; (5) Therapeutic 6 week group. The airway resistance and eosinophilic inflammation of airway wall were observed. The airway wall thickness (WA/Pi), the bronchial smooth muscle thickness (smooth muscle area/Pi) and the number of bronchial smooth muscle nucleus (N/Pi) were measured by image analysis system. The expression of PCNA, nuclear factor-kappaB and Bcl-2 protein were determined by immunohistochemical staining and Western blot. The expression of Bcl-2 mRNA was determined by reverse transcription-polymerase chain reaction(RT-PCR).
RESULTS(1) The expression of NF-kappaB protein in asthmatic 4 week group and asthmatic 6 week group was significantly higher than that in control group, respectively (P < 0.01). The above-mentioned parameters of therapeutic 6 week group were significantly lower than those of asthmatic 4 week group, asthmatic 6 week group and therapeutic 4 week group, respectively (P < 0.01, P < 0.01 P < 0.05). (2) The expression of Bcl-2 protein and mRNA of asthmatic 4 week group and asthmatic 6 week group were significantly higher than those in control group respectively (P < 0.01). The expression of Bcl-2 protein of therapeutic 6 week group was significantly lower than those of asthmatic 4 week group, asthmatic 6 week group and therapeutic 4 week group respectively (P < 0.05, P < 0.01, P < 0.01), but the expression of Bcl-2 mRNA was significantly higher than the above-mentioned groups respectively (P < 0.01), the expression of Bcl-2 protein and mRNA of therapeutic 6 week group were higher than control group respectively (P < 0.05, P < 0.01). (3) The expression of PCNA protein of asthmatic 4 week group and asthmatic 6 week group were significantly higher than those of control group respectively (P < 0.01). (4) The WA/ Pi, the smooth muscle area/Pi and the N/Pi of asthmatic 4 week group and asthmatic 6 week group were significantly higher than those of control group, respectively (P < 0.01). The above-mentioned parameters of therapeutic 6 week group were significantly lower than those of asthmatic 4 week group, asthmatic 6 week group and therapeutic 4 week group, respectively (P < 0.01). (5) The airway resistance of asthmatic 4 week group and asthmatic 6 week group were significantly higher than those of the control group, respectively (P < 0.01). The above-mentioned parameters of therapeutic 6 week group were significantly lower than those of asthmatic 4 week group, asthmatic 6 week group and therapeutic 4 week group, respectively (P < 0.01, P < 0.01, P < 0.05).
CONCLUSIONThe proliferation of airway smooth muscle(ASM) is related with apoptosis of airway smooth muscle cells in asthma. NF-kappaB may be involved in the process. Triptolide may prevent apoptosis of ASMCs and decrease the proliferation of ASM by inhibiting the expression of NF-kappaB, Bcl-2.
