Effects of icariin on Bcl-2 and Bax protein expressions and eosinophils apoptosis in bronchial asthmatic mice.
- Author:
Wen-jing DU
1
;
Jing-cheng DONG
;
Cui CAI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Asthma; metabolism; Eosinophils; drug effects; metabolism; Female; Flavonoids; pharmacology; Mice; Mice, Inbred BALB C; bcl-2-Associated X Protein; genetics; metabolism
- From: Chinese Journal of Integrated Traditional and Western Medicine 2011;31(9):1248-1253
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects of icariin on Bcl-2 and Bax protein expressions and eosinophils apoptosis in bronchial asthmatic mice.
METHODS48 female Balb/c mice were randomly divided into 6 groups, i.e., the normal control group, the model group, the Dexamethasone group, the low dose icariin group, the middle dose icariin group, and the high dose icariin group, 8 mice in each group. Bronchial asthma in mice were induced by intraperitoneal sensitization and challenged with nebulized ovalbumin (OVA). The mice of each treatment group were administrated with different doses of icariin by peritoneal injection from the first asthma sensitization (the 3rd week after the modeling) to the day before killing once every other day, while mice in the normal control group were administrated with physiological saline. The mice were killed after 6 weeks of treatment. The apoptosis of eosinophils and the Bcl-2 and Bax protein expressions of the lung tissues were detected by TUNEL and immunohistochemical assay respectively.
RESULTSAs compared with the model group, the apoptosis ratio of eosinophils were higher in the rest four treatment groups (P<0.05). The Bcl-2 protein positive areas in the lung tissues and the airway wall were significantly lowered (P<0.05). The Bax protein positive area significantly increased (P<0.05).
CONCLUSIONIn bronchial asthmatic mice, icariin could enhance the apoptosis of eosinophils and lessen their infiltration by decreasing the expression of Bcl-2 protein and increasing the expression of Bax protein in lung.