[Antitumour effect of total saponins of Rubus parvifolius on malignant melanoma].

OBJECTIVE: To evaluate the antitumor effect of total saponins of R. parvifolius on malignant melanoma. METHOD: The human malignant melanoma A375 cells were regularlly subcultured in vitro, and were divided into five groups contained positive control group (CTX), high concentration (0.01 mg x mL(-1)) and middle concentration (0.001 mg x mL(-1)) and low concentration (0.000 1 mg x mL(-1)) total saponins of R. parvifolius groups and negative control group. By using MTT colorimetric method, the cell viability was measured. B16 melanoma cells were transplanted to mice, which were divided into positive control group, high dose (100 mg x kg(-1)) and middle dose (50 mg x kg(-1)) and low dose (25 mg x kg(-1)) total saponins of R. parvifolius groups and negative control group. The inhibition effect of the tumor in vivo, mean survival time and rate of life-elongation of the mice were observed. TUNEL method was used to detect the apoptosis of B16 malignant melanoma. RESULT: Antitumor assay in vitro showed that the absorbency increased in the concentration of 0.01, 0.001 mg x mL(-1) with statistical significance (P < 0.05 vs negative control). Antitumor assay in vivo showed that the tumor inhibitory rate of high dose (100 mg x kg(-1)) and middle dose (50 mg x kg(-1)) of total saponins of R. parvifolius were 37.02% and 30.61%, respectively. Loaded tumor mouse survival duration could be prolonged. The apoptosis indexes of B16 tumor cells in three treatment groups were 32.5%, 20.5% and 5.5%, respective and there was statistical significance (P < 0.05 vs negative control). CONCLUSION: The total saponins of R. parvifolius has remarkable inhibition of proliferation of malignant melanoma cells in vivo and in vitro and exerts antitumor activities through promoting tumor cell apoptosis.

[Experimental study on the mechanism of nonablative skin photorejuvenation].

OBJECTIVE: To explore the Mechanism of nonablative skin rejuvenation. METHOD: The Kunming mice be used as subjects and divided into three groups (A, B, C). A, B, C groups were irradiated with 1 320 nm cooltouch laser (20 J/cm2) in the skin of left back; B and C groups were irradiated two and three times respectively; the skin of right back of A, B, C groups was adopted as control. The expression of bFGF and TGF-beta1 in the mouse skin was examined by the immunohistochemistry . The fibroblasts were isolated from the foreskin and cultured. One group is a control and other three ones are low, intermediate and high energetic groups respectively. The fibroblasts were irradiated by laser with 15 J/cm2 ,20 J/cm2 and 24 J/cm2 energy for three times. We examined the levels of bFGF and TGF-beta1 by ELISA in 0, 24, 48 and 72 hours. RESULTS: According to this research on immunohistochemistry result, there are significant differences in the expression of bFGF and TGF-beta1 between the group irradiated by three times and others (P < 0.01). The number of fibroblasts get increased after being irradiated by laser. The ELISA result indicates that the secretion of bFGF increased in the group of intermediate and high energetic level after laser irradiating and may reach the peak at 24 hours (P < 0.01). The amount of TGF-beta1 secretion, however, seems to get decreased in each group at all energetic levels, and at 24 hours it can reach the top level as well. CONCLUSION: The direct influence of laser on the fibroblasts is to promote secretion of bFGF and to inhibit secretion of TGF-beta1, while its influence on the tissue is to promote the secretions of the both. Nonablative skin rejuvenation not only can induce fibroblasts to secrete more bFGF but also induce the blood vessels to release cytokines which stimulate endothelial cell to express more of bFGF and TGF-beta1. Furthermore, fibroblastic proliferation can accelerate by laser's irradiating.

[Microsatellite instability and allele-specific chromosome 3p deletion in breast cancer and precancerous lesions].

OBJECTIVE: To investigate the incidence and clinicopathologic significance of MSI and LOH on 3P in breast carcinoma and its precancerous lesions, intraductal papillary adenoma and ductal carcinoma in situ. METHODS: 41 paired sporadic invasive breast carcinomas, 13 archival precancerous lesion specimens of the breast and 14 couples of benign hyperplasia were collected. Twelve microsatellites on chromosomes 2p, 3p, 5q, 6q, 16q, 17q, eleven markers on chromosome 3p were amplified for MSI and LOH, respectively, by polymerase chain reaction ( PCR ) with designed primers and detecting after polyacrylamide gel electrophoresis. In addition, the expression of protein of hMSH2, hMLHI, FHIT, ER, and PR were detected by immunohistochemistry. RESULTS: MSI was observed, at least two microsatellite markers, in 15 out of 41 (36. 6%) of the carcinomas, almost all belonging to poorly or intermediately differentiated carcinoma. Instability was shown in 9 of the 13 cases of precancerous lesions, but only 2 among them had more than 2 MSI sites. There was no MSI in benign hyperplasia. MSI was targeted predominately at D3S1766, D2S2739 in both carcinomas and precancerous lesions. Of the 11 loci examined, D3S1295, D3S1029 and D3S1038 were identified as the locus with most frequent LOH which were all correlated significantly with some clinicopathological parameters such as histological type, lymph node metastasis in breast cancer, while D3S1295 and D3S1029 were the most frequent markers in precancerous lesions. LOH of D3S1295 had significant correlation with negative expression of FHIT. Positive expression of hMLH1 and hMSH2 protein was detected in breast carcinomas in scattered distribution and their positive rate was 45% and 40% , respectively. In precancerous lesions, hMLH1 and hMSH2 protein showed diffuse expression and their positive rate was 61. 54% and 76. 92% , respectively, significantly lower than that in the control tissues. CONCLUSION: Defective expression of MMR genes is closely associated with the development of breast cancer. Genomic instability might play a role in the early stage during multi-step mammary carcinogenesis. MSI indicates poor histological differentiation in breast carcinoma. D3S1766 and D2S2739 might be the sensitive sites to detect MSI in breast carcinoma and precancerous lesions. The smallest common LOH deletion regions seem likely to be situated between 3p14 and 3p25, indicating the existence of breast tumor related genes in those regions and some of them might affect tumor development.