[The influence of Qi-lan granulates on the variation of proliferating cell nuclear antigen during the course of SD rat tongue carcinogenesis].

PURPOSE: To study the cancer blocking effect of the Qi-lan granulates in SD rats. METHODS: A total of 150 SD rats were divided into five groups A,B,C,D,E. Rats in group A, B, C, D were fed with 0.002% 4NQO dissolved in drinking water to induce tongue carcinogenesis in rats. Different concentration of the herb Qi-lan granulates was given to the rats of group B, C, D during oral carcinogenesis. Group A was model group, group E was normal group. The rats were sacrificed at 9, 18, 27 and 36 weeks respectively from the beginning of the experiment. The samples were collected for histophology and PCNA immunohistochemistry. The date was analyzed by Chi-square test and Kruskal-Wallis test using SPSS13.0 software package. RESULTS: The overall canceration rate of group B (14.29%), C (3.57%), D (14.29%) was significantly lower than group A (39.29%) (P<0.05), the effect of Qi-lan granulates in group C was the best. Immunohistochemistry result showed that 6 cases of normal oral mucosa in group A had positive expression of PCNA. In 11 cases of dysplasia, 8 had positive express of PCNA, 11 rats with oral cancerous tissues had positive expression of PCNA.In group A, the expression of PCNA was normal tissue0.05). In general, the expression of PCNA in group A was significantly higher than the Qi-lan granulates group, the difference was statistically significant (P<0.05). The expression of PCNA in group E was negative. CONCLUSIONS: Qi-lan granulates have significant inhibitory effect on tongue cancer, through blocking cell proliferation.

[Significance of cell immunoreactions and cell apoptosis in oral lichen planus].

OBJECTIVE: To evaluate the expression of CD4+, CD8+ T cells and cell apoptosis in oral lichen planus (OLP) and investigate the role and the relationship of immunological reaction and cell apoptosis in the pathogenesis of OLP2. METHODS: Immunohistochemical technique was used to study the expression of CD4+, CD8+ T cells in 27 OLP cases. TUNEL was used for detecting the cell apoptotic index (AI) in 17 OLP2 cases. RESULTS: The expression of CD4+, CD8+ T cells were obviously elevated in lamina propria of OLP group compared with control group (P<0.05). There was a strong significance when compared the ration of CD4/CD8 in both group. AI was remarkably increased in epithelia cells and significantly decreased in lymphocytes in lamina propria in OLP cases compared with its expression in the control group respectively. CONCLUSION: The increased amount of CD4+, CD8+ T cells in lamina propria of OLP and the change ration of CD4/CD8 suggest that immune response is involved in the pathogenesis of OLP. The abnormal cell apoptosis plays an important role in the pathogenesis of OLP.

[Expression of TGF-beta1, Smad7 and cell apoptosis in epithelium of oral lichen planus].

OBJECTIVE: To examine the expression of TGF-beta1, Smad7 and cell apoptosis in oral lichen planus (OLP) and to evaluate the possible pathogenesis of oral lichen planus. METHODS: Immunohistochemical technique was used to study the expression of TGF-beta1 and Smad7 in the epithelia cells of 17 OLP cases and 7 normal oral mucosa (NOM). TUNEL was used for detecting the cell apoptosis in 17 OLP cases and 7 NOM. RESULTS: TGF-beta1 was moderately positive in the epithelia cells of OLP. All the epithelia cells in OLP showed strong cytoplasmic staining. The expression of TGF-beta1 and Smad7 were significantly increased in OLP compared with that in NOM (P < 0.05). Cell apoptotic index (AI) was remarkably increased in epithelia cells in OLP cases, and the cell apoptosis was localized in basal and suprabasal epithelial layers. There was a positive correlation between TGF-beta1 expression and cell apoptosis in the epithelia of OLP (r = 0.69, P <0.05). CONCLUSIONS: High expression of TGF-beta1 and Smad7 in the epithelia of OLP suggests that TGF-beta1-Smad7 signal pathway was disturbed in oral lichen planus. The imbalance of TGF-beta1-Smad7 pathway may contribute to the mechanisms of cell apoptosis of epithelial cells in OLP.