Effects of IFNα-2b on cell apoptosis and expression of hTERT and bcl-2 mRNA in keloid fibroblasts
- VernacularTitle:α-2b干扰素对瘢痕疙瘩成纤维细胞凋亡及端粒酶逆转录酶、bcl-2 mRNA表达的影响
- Author:
Yong HUANG
;
Qiang MENG
;
Xin XING
- Publication Type:Journal Article
- Keywords:
Keloid;
hTERT;
Apoptosis;
IFNα-2b
- From:
Chinese Journal of Medical Aesthetics and Cosmetology
2008;14(4):261-264
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effects of IFNα-2b on keloid fibroblasts in cell prolifera-tion, apoptosis, expression of hTERT and bcl-2 mRNA and to explore its anti-keloid mechanism. Methods Primary cultures of dermal fibroblasts derived from 8 keloid and 8 normal skin samples were established, strains of fibroblasts at passages 3 to 4 were used in this study. Keloid and normal skin fibroblasts in culture medium in vitro were given IFNα-2b and were obsevered in different time. The proliferation of the fibroblasts was measured by MTT assay, the apoptosis was analysed by flow cytometry(FCM), and the expression of hTERT and bcl-2 mRNA were obsevered by semi-qnantitativere verse transcriptase-polymerase chain reaction (RT-PCR). The data were analyzed by statistical software (SPSS11. 5). Results IFNα-2b could inhibit the growth of keloid and nomal skin fibroblasts. The suppression of keloid and nomal skin fibroblasts was time-dependent. After the effect of 10 000 U/ml INFα-2b on cultured fibroblast of keloid and normal skin,the fibroblasts apoptosis was induced and the expression of hTERT and bcl-2 mRNA was lower than that of controlled group . The result was significantly different between control group and treatment group and was related with the treatment time of INFα-2b (P<0.01). Conclusions As a negative regulatory factor,interferon α-2b can suppress growth and proliferation of keloid fibroblasts and induce apoptosis. Decreasing the telomerase activity of keloid fibroblasts may be one of the most important mechamisms. That IFNa-2b inhibited telomerase activity in keloid fibroblasts is an important pathway that may play a key role in the anti- keloid therapy.
