Effects of Yugong Qili Duoming Capsule on Expression of Bc1-2 in Brain Tissue of Cerebral Bleeding Model Rats / 中国中医药信息杂志

Objective To explore the curative mechanism of Yugong Qili Duoming Capsule for cerebral hemorrhage. Methods The model rats were established by being injected its blood to its own basal segmental, which induced cerebral bleeding. Bc1-2 was determined with immunohistochemical method and was used to evaluate the effect of Yugong Qili Duoming Capsule on the treatment group and other comparative group. Results The Bc1-2 cells in brain issue of model groups began to increase at the 1st day, reached its highest level at the 2nd day and decreased greatly at the 7th day. However, the Bcl-2 cells of the treatment group were much more than those of the model groups in the 2nd, 4th and 7th day. Conclusion Yugong Qili Duoming Capsule can increase expression of Bc1-2 in brain tissue of cerebral bleeding model rats.

Bcl-2 FAMILY:THE IMPORTANT REGULATING PROTEINS DURING GINSENOSIDE RG1 PROTECTION AGAINST APOPTOSIS OF NIGRA NEURONS / 解剖学报

Objective To explore the role of Bc1\|2,Bc1\|x1 and Bax during the process of Ginsenoside Rg1 protecting against apoptosis of substantia nigra neurons in Parkinson disease(PD) mouse model. Methods C57BL mice were administrated i.p. with MPTP to produce PD mouse model.And different doses of Rg1(2 5,5 0,10 0?mg/kg) were given i.p. prior 3 days to MPTP in preventive groups.Nissl staining,tyrosine hydroxythase(TH) immunostaining and TUNEL staining were used to observe the changes of nigra neurons.Bc1\|2,Bc1\|x1 and Bax immunostaining were used to detect the expression of these proteins. Results Pretreatment with Rg1(5 0,10 0?mg/kg) could prevent the loss of Nissl staining neurons and TH\|positive neurons,and decrease TUNEL\|staining ratio.Rg1 could enhance the expression level of Bc1\|2 and Bc1\|x1,and reduce the expression level of Bax. Conclusion\ Rg1 has protective effect on apoptosis of substantia nigra neurons in PD mouse model.The increased expression level of Bc1\|2 and Bc1\|x1,and the decreased expression level of Bax may be the important mechanism during Rg1 protection against apoptosis.

Relationship between activity of protein kinase C and apoptosis of cultured neurons after hypoxia / 第三军医大学学报

Objective To explore the effect and possible mechanism of protein kinase C (PKC) on the apoptosis of cultured neurons after hypoxia Methods Model of cultured rat neurons under hypoxia condition was established. Calphostin C, an inhibitor for the catalytic subunit of PKC, at 4 different concentrations were separately cocultured for 2 h with the neurons having been cultivated under hypoxic condition for different times The activity of membrane PKC (mPKC), the expression of Bcl 2 and the situation of neuron apoptosis were studied Results With the prolonging of hypoxic time the activity of mPKC was increased significantly And the expression of Bcl 2 was decreased obviously and positive rate of TUNEL were significantly increased in a calphostin C concentration dependent manner Conclusion ① The activation of mPKC and Bcl 2 are involved in the apoptosis of neurons after hypoxia ② Hypoxia and calphostin C can aggravate the hypoxic neuronal apoptosis through the signal transduction of Bcl 2 ③ The activation of PKC can protect neuron against hypoxia

Expression of bcl-2 and p53 Protein in Invasive Cervical Cancer / 대한부인종양콜포스코피학회잡지

Recently, the bcl-2 and p53 protein have been recognized as important factors that is contributed to programmed cell death. The objective of this study was to evaluate the prognostic significance of bcl-2 and p53 protein expression in uterine cervical carcinoma. The expression of bcl-2 and p53 in 59 cases of uterine cervical carcinoma (stage IB to IIB) were surgically treated from January 1993 to June 1994. The expression of bcl-2 and p53 was examined by immunohistochemical method using formalin fixed paraffin embedded tissue specimens. The 48 cases were squamous cell carcinoma and 11 cases were adenocarcinoma. The results were as follows: 1. The expression rate of bcl-2 protein was 28.8%(17/59) and there was no significant correlaltion between the expression of bcl-2 protein and the clinicopathologic parameters (histologic type, grade, FIGO stage, cervical invasion depth, lymph node metastasis, parametrial invasion, tumor size, neoadjuvant chemotherapy response, recurrence, survival). 2. The expression rate of p53 protein was 32.2%(19/59) and there was no significant correlation between expression of p53 protein and the clinicopathologic parameters. 3. There was significant correlation between and expression of bcl-2 and p53 protein (P 0.05). In conclusion, bcl-2 and p53 protein are thought to be possible factors in the carcinogenesis of uterine cervical carcinoma and correlate with progression of it. But further study will be required to clarify the role of bcl-2 and p53 in carcinogenesis of the uterine cervix.

Immunohistochemical Study on the Expression of p53 and bcl-2 Protein in Gallbladder Adenocarcinoma / 대한암학회지

PURPOSE: This study was carried out to evaluate the expression of p53 and bcl-2 protein in the adenocarcinoma of gallbladder. MATERIALS AND METHODS: Thirty three cases of adenocarcinoma of gallbladder were immunohistochemically stained for p53 and bcl-2 protein. RESULTS: p53 protein was expressed in 51.5%(17/33) of adenocarcinoma. p53 protein expression was not significantly correlated with histologic grade of adenocarcinoma, depth of invasion, lymph node metastasis, distant metastasis and TNM stage, respectively(p>0.05). bcl-2 protein was expressed in 12.1%(4/33) of adenocarcinoma. bcl-2 protein expression was not significantly correlated with tumor size, histologic grade, depth of invasion, lymph node metastasis, distant metastasis and TNM stage, respectively(p>0.05). There is no correlation between expression of p53 and bcl-2 in gallbladder adenocarcioma(p > 0.05). CONCLUSION: This study suggest that p53 gene mutation plays an important role in carcinogenesis of gallbladder adenocarcinoma. The role of bcl-2 protein in gallbladder adenocarcinoma may be not significant.

Immunohistochemical Studies of bc1-2 Protein in a Skin Tumor of Neuroectodermal Origin / 대한피부과학회지

BACKGROUND: Protooncogene, bcl-2 is known to inhibit, apoptosis induced by various stimuli. Its expression has been reported in various fetal and adult tissues, and also in tumors of neural origin. OBJECTIVE: The purpose of this study was to evaluate the expression of bcl-2 in a skin tumor of neuroectodermal origin and to estimate whether this expression was useful in the different,ial diagnosis of tumors of neural origin or not. METHOD: Immunohistochemical stains by the LSAB(labelled streptavidin biotin) method for bcl-2 protein were performed in normal special nerve end-organs and a skin tumor of neural origin. RESULTS: The immunohistochemical findings revealed strong positive results in Meissners corpuscles, but weak week positive results in Vater-Pacini corpuscles. There were also strong positive results in neurilernmomas which were mostly composed of Schwann cells, but results were mostly negative in neurofibromas and neurofibrosarcomas which were composed primarily of endoneurial fibroblasts of mesodermal origin except a few cells of Schwann cell origin. Benign granular cell tumors arising from Schwann cells, and Merkel cell carcinoma known to arise from the Merkel cells of neural crest origin showed strong positive reactions. CONCLUSION: The strong expression of bcl-2 protein exclusively in the tumor of neuroectodermal origin suggests a useful indicator for the differential diagnosis of skin tumors of neural origin.

bc1 - 2 Expresseion in Malignant Melanoma and Melanocytic Nevus / 대한피부과학회지

BACKGROUND: The bcl-2 is a newly known oncogene involved in tumorigenisis by blocking apoptosis or programmed cell death. Overexpression of bcl-2 protein has been detected in a variety of human malignancies. However, recent studies of the expression of bcl-2 protein in human melanoma and melanocytic nevus have been controversial. OBJECTIVE: The purpose of this study was to examine whether there are any differences in the expression of bcl-2 protein between melanocytic nevus and rnalignant melanoma. METHODS: Immunohistochemical analysis of bcl-2 protein expression was performed on the formalin-fixed, paraffin-embedded tissue sections of 22 melanocytic nevus and 29 malignant melanomas (20 primary and 9 metastatic) using anti bcl-2 monoclonal antibody with an avidin-biotin peroxidase complex procedure. RESULTS: The results were as follows. 1. The positive rate for bcl-2 protein was observed in 95.4% (21/22) of melanocytic nevus and 95.0% (19/20) of primary malignant melanomas. Therefore, there was no significant difference between the two groups in the positive rate for bcl-2 prtoein. 2. The percentage of stained cells and the staining intensity of bcl-2 protein were significantly increased in melanocytic nevus compared to malignant melanoma (p<0.05). 3. The positive rate for bcl-2 expression of metastatic malignant melanoma [44.4% (4/9)] was significantly decreased compared to that of primary malignant melanoma [95.0%(19/20) ] (p<0. 05). But, there was no significant difference betweeen tumor thickness and histological type of malignant, melanoma in the expression of bcl-2 protein. 4. In melanocytic nevus, immunoreactivity of bcl-2 protein gradually diminished or even disappeared towards the deep dermis. CONCLUSION: the bcl-2 expression was decreased in malignant melanoma compared to melanocytic nevus. It. suggests that the loss of bcl-2 expression may play a significant role in the progression and metastasis of malignant melanoma.

Induction of apoptosis in PC12 cells by homocysteine / 中国病理生理杂志

AIM: To explore the effects of homocysteine on the apoptosis in PC12 cells and the relationship between the apoptosis and the expression of the bcl-2 as well as bax gene. METHODS: Cell viability was determined by MTT assay. Cell apoptosis was assessed by phase-contrast microscope, fluorescence microscopy and flow cytometry (FCM). The expression of bcl-2 and bax mRNA was measured by semiquantitative reverse transcription polymerse chain reaction (RT-PCR). RESULTS: Treatment of PC12 cells with Hcy plus 10 ?mol/L copper for 12 h, in the range of 0.125, 0.25, 0.5, 1.0 mmol/L, caused a great decrease in cell viability: 81%, 79%, 69%, 57%, and induced typical morphological changes of apoptosis in a dose-dependent manner. The apoptosis ratios were respectively 8.00%, 10.37%, 17.26% and 20.19%, respectively. The expression of bcl-2 was significantly decreased (from 0.517 to 0.198) whereas bax was significantly increased (from 0.302 to 0.619). CONCLUSION: Homocysteine plus copper may induce apoptosis in PC12 cells through the down-regulation of bcl-2 and the up-regulation of bax gene expression.