Protective effect of astragaloside against cadmium toxicity on expression of connexin 43 and ultrastructure of TM3 cells
10.7644/j.issn.1674-9960.2014.11.010
- VernacularTitle:黄芪甲苷对镉致TM3细胞损伤的保护作用
- Author:
Yi WANG
;
Wei NING
;
Yaping LIU
;
Xiaogang LIAO
- Publication Type:Journal Article
- Keywords:
astragaloside;
cadmium;
TM3 cell;
apoptosis;
connexin43;
immunohistochemistry;
electron microscope
- From:
Military Medical Sciences
2014;(11):879-884
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the destructive effect of cadmium (Cd)and the protective effect of astragaloside ( Asd) on TM3 cells.Methods The best protective concentration of Asd on TM 3 cells after Cd treatment was selected by MTT cell viability experiment .The apoptosis rate of TM3 cells was measured by flow cytometry .The expression of connexin 43(Cx43) was detected by immunohistochemistry .The morphological changes of TM3 cells were observed by electron mi-croscopy .Results The viability of TM3 cells in both control and Asd-treated group was not significantly different after 24 h or 48 h,but it was significantly decreased in Cd group .However , the viability of TM3 cells in Cd +As group was higher than that in Cd group .Flow cytometry showed that there was no significant difference in the apoptosis rate of TM 3 cells be-tween the control and Asd-treated group after 24 h,but it was obviously increased with the Cd concentration .The apoptosis rate of Cd+Asd group was lower than that in Cd group (P<0.01).Immunohistochemistry demonstrated that the average optical density (AOD) of the positive product of Cx43 in Cd-treated TM3 cells was obviously decreased (P<0.01), but the average gray value (AGV) was significantly increased when compared with the control group (P<0.01).The ultra-structural changes in TM3 cells were obvious after Cd treatment ,but those in Cd+Asd group were improved when compared with Cd group.Conclusion Cd reduces the expression of Cx 43 and damages the morphology of TM 3 cells.Asd has protec-tive effect on Cd-induced TM3 cell injury.