ABSTRACT
Objective To observe the effect of aspirin on the proliferation inhibition and apoptosis of human adrenal cortical cancer cells, and to explore preliminarily the related mechanisms. Methods The human adrenal cortical cancer cells were cultured in vitro. The experimental group was DEME/F-12 complete medium which contained different concentrations of aspirin (final concentration of 0.125, 0.25, 0.5, 1 mg/ml). The control group was DEME/F-12 complete medium which had no aspirin but 1%anhydrous ethanol instead. After treatment by aspirin at different concentrations for different durations (24, 48, 72 hours), we detected the proliferation inhibition of SW-13 cells and H295R cells by methyl thiazolyl tetrazolium (MTT) method, observed the changes of cell morphology with the inverted microscope; Observed and counted apoptotic cells through Hoechst33258 fluorescent staining, tested the cell apoptosis by flow cytometry, and detected the expression of Bcl-2 and Bax by western blotting. Results The date of MTT showed that after treated by different concentrations of aspirin,the growth inhibition ratio of SW-13 cells and H295R cells were higher than the control group (P＜0.05), and at the same time, the inhibition ratio would increase when the drug concentration increased ( P＜0. 05 ), with a dose-dependent tendency. When the drug concentration was constant, the inhibition ratio increased with the duration of the drug (P＜0.05), which showed a time-dependent tendency. The number of apoptosis cells and the cell apoptosis rate of both SW-13 and H295R which were treated by different concentrations of aspirin for 48 hours were higher than the control group ( P＜0. 01). According to the analysis of grayscale value of western blotting, Aspirin can increase the expression of Bax ( P＜0.05). On the contrary, the expression of bcl-2 in the experimental group was lower than that in the control group (P＜0.05). Conclusion Aspirin may inhibit the growth of human adrenal cortical cancer cell in vitro and induce its apoptosis, and the possible mechanism may be correlated with the up-regulation of the expression of Bax, and down regulation of Bcl-2 expression.
ABSTRACT
Objective To investigate the expression and significance of the endocrine gland-derived vascular endothelial growth factor (EG-VEGF) and vascular endothelial growth factor(VEGF) in adrenocortical lesions of primary aldosteronism. Methods The expressions of EG-VEGF, and VEGF were detected by immunohistochemistry and real-time fluorescence quantitative PCR in samples of 18 cases of adrenocortical adenoma, 6 adrenocortical hyperplasia, and 8 normal adrenal cortex. The correlation between the expressions of EG-VEGF, VEGF, and clinicopathological parameters was analyzed. Results The expression of EG-VEGF or VEGF in adrenocortical adenomas was higher than that in adrenocortical hyperplasia or normal adrenal cortex ( all P＜0. 05 ), and the expression of EG-VEGF or VEGF between adrenocortical hyperplasia samples and normal adrenal cortex samples was indistinctive. There was no statistically significant correlation between EG-VEGF or VEGF expression and sex, age, blood pressure, serum potassium, plasma renin activity, except in case of serum aldosterone( P＜0.05 ). A positive correlation between EG-VEGF and VEGF ( P＜0. 01 ) was found. Conclusions EG-VEGF and VEGF may play a significant role in the formation and development of adrenocortical tumors in primary aldosteronism.
ABSTRACT
The expressions of Ki67 and FHIT were detected by immunohistochemical staining in 15 cases of adrenocortical carcinoma, 42 cases with adrenocortical adenoma,6 cases of adrenocortical hyperplasia, and 10 cases of normal adrenocortical tissue. The results showed that the highest expression of Ki67 and the lowest expression of FHIT were found in adrenocortical carcinoma. There were significant differences in the Ki67 and FHIT between adrenocortical adenoma and adrenocortical carcinoma ( both P < 0. 05 ). There existed negative correlation between the expressions of Ki67 and FHIT( r=-0. 712, P<0.05 ). Ki67 over-expression and loss of FHIT expression may be involved in the occurrence and development of adrenocortical carcinoma. It is suggested that combined detections of Ki67 and FHIT may have reference significance in the differentiation of adrenocortical adenoma from adrenocortical carcinoma.
ABSTRACT
BACKGROUND: Secretion of various neurotrophic factors by Schwann cells plays important roles in neural regeneration. However, the secretion capability is affected by many factors. To seek a feasible method for promoting nerve growth factor secretion by Schwann cells is a key of regeneraion following neurologic defect.OBJECTIVE: To explore the effects of methylprednisolone(solu-medrol) on the secreted function of Schwann cells of cultured rats.METHODS: Schwann cells were isolated and cultured by enzyme digestion method. Cell growth was observed under an inverted phase contrast microscope. Following passage, purity of some Schwann cells was identified using S-100 protein immunity. Other Schwann cells were regulated using cell counting plate into 1×10~9/L, and incubated in a 6-well culture plate (15 wells) for further incubation. Following 4 days of culture, different concentrations of solu-medrol (10~(-3), 10~(-4), 10~(-6), 10~(-8) mol/L) were administrated to the cell, while blank control group (1 well) was given no drug. 24, 48 and 72 hours after administration, reverse trancription-polymerase chain reaction (RT-PCR) was used in the detection of the levels of nerve growth factor mRNA.RESULTS AND CONCLUSION: Number of primarily cultured cells was significantly increased at day 7, and 80% cells were confluent. Subcultured cells were spindle-shaped, with 2 thin long processes, showing positive fluorescence staining. Fibroblasts were round or flat, showing negative reaction of fluorescence staining. Reserve transcription-polymerase chain reaction demonstrated that nerve growth factor number at 72 hours affected by 10~(-8) mol/L radiosone was increased compared with the blank control group and other concentrations and other time points (P < 0.05). Number of nerve growth factor was reduced following treatment of 10~(-3) mol/L radiosone compared with the blank control group and other concentrations (P < 0.05). These results suggested that high concentration of solu-medrol prohibits secreted function of Schwann's cells, but long time and low dosage solu-medrol promotes secreted function of Schwann's cells.
ABSTRACT
Objective To study relationship between Ki67 ,fragile histindine tried (FHIT) and adrenocortical tumors. Methods Ki67 and FHIT was detected by immunohistochemical staining in edrenecortical carcinoma(n=14) ,edrenocortical adenoma(n = 61) and normal adrenocortical tissue adjacent to tumor(n = 10). Results Ki67 was not expressed in normal adrenecortical tissue but highest expressed in adrenocortical carcinoma as well as in adrenocortical adenoma,and however,the expression of FHIT was expressed in a different way to Ki67. Negative correlation was observed between Ki67 and FHIT (r = -0.721 ,P <0.005). Conclusion The correlation of Ki67, FHIT with adrenocortical tumor, suggest that the detection of both Ki67 and FHIT can provide objective and simple diagnosis method to identify adrencortical adenomas from adrencortical carcinomas.
ABSTRACT
In this study we calculate theoretically and use FEM to simulate the effect of plate position relative to bending direction on the overall bending stiffness of the composite system plate-bone. The results show that for different bending directions the effect of the modulus of elasticity of the plate is negligible. Changing the position of a plate will often alter the stress obviously. During the operation, the steel plate should be assigned onto the tension side of the bone.