ABSTRACT
Cortex Periplocae Radicis(CPR)is the dried root barks of Periploca spium Bge. It has been used in China for treat?ing rheumatoid arthritis and strengthening the bone and the musculature for thousands of years. Recently,an increasing number of bio?activities of CPR have been recognized,including tumor suppression and anti-chronic heart failure function. However,long-term use or large doses of CPR may produce adverse reactions,which constrains its applications in clinical therapy. Therefore,it is critical to know the chemical components of CPR in order to understand the toxicity mechanism. Nearly a hundred chemical compositions have been found,however,various classes,obfuscated names of different compounds,and disaccord between chemical structure and name were major obstacles to studying pharmacodynamics and toxicity of CPR. In this paper,94 chemical components of CPR are classified and reviewed,which is valuable for the comprehensive understanding of its biological functions and safe clinical use.
ABSTRACT
Cortex Periplocae Radicis (CPR) is the dried root barks of Periploca spium Bge. It has been used in China for treating rheumatoid arthritis and strengthening the bone and the musculature for thousands of years. Recently, an increasing number of bioactivities of CPR have been recognized, including tumor suppression and anti-chronic heart failure function. However, long-term use or large doses of CPR may produce adverse reactions, which constrains its applications in clinical therapy. Therefore, it is critical to know the chemical components of CPR in order to understand the toxicity mechanism. Nearly a hundred chemical compositions have been found, however, various classes, obfuscated names of different compounds, and disaccord between chemical structure and name were major obstacles to studying pharmacodynamics and toxicity of CPR. In this paper, 94 chemical components of CPR are classified and reviewed, which is valuable for the comprehensive understanding of its biological functions and safe clinical use.
ABSTRACT
Objective To investigate the effects of periplocin from Cortex Periplocae (CPP) on apoptosis of human lung cancer A549 cells and expression of survivin, and demonstrate its anti-tumor effect and the possible mechanism. Methods Inhibitory effect of CPP at different concentrations (1. 25, 2. 50, 5. 00, 10. 00, 20. 00 ng·mL-1 ) and for different time length (24, 48, 72 h) on A549 cell proliferation was tested by MTT method. Apoptosis rate of A549 cells treated with CPP at different concentrations (2. 50, 5. 00, 10. 00 ng·mL-1 ) were measured using flow cytometry (FCM) for 6, 12, 24, 48, 72 h, respectively. The morphological and ultrastructural changes of the apoptosis cells were observed by acridine orange/ ethidium bromide (AO/ EB) staining and transmission electron microscopy (TEM). The effects of CPP on mRNA and protein expression of apoptosis associated gene survivin were assessed by RT-PCR and Western blotting. Results CPP could significantly inhibit the growth of A549, and the inhibition rate reached (93. 46±2. 35)% . The results of FCM showed that the apoptosis rate of A549 cells treated with CPP was increased significantly as compared to the control group ( P<0. 05). Meanwhile, typical apoptotic peaks were detected. The characteristic morphological changes of apoptosis were observed in A549 exposed to CPP, including cell shrinkage, the nuclei became yellow-red by AO/ EB staining, and typical ultrastructural changes, including nuclear chromatin condensation along the nuclear membrane, vacuolar degeneration of cytoplasm observed by TEM. The result of RT-PCR indicated that survivin mRNA expression decreased obviously in A549 cells exposed to CPP. The protein expression of survivin in A549 cells treated with 10. 0 ng·mL-1 CPP(0. 251±0. 012)was weaker than that in control group(0. 928±0. 016). Conclusion CPP can induce apoptosis in human lung cancer cell lines A549, and the probable mechanism is related to the down-regulation of survivin mRNA and protein.
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Objective To investigate the inhibitory effects of periplocin from cortex periplocae (CPP) on human lung cancer cell line QG56 and to discuss its mechanism. Methods QG56 cells were cultured in vitro. The final concentrations of CPP in control group were 1.25, 2.50, 5.00, 10.00 and 20.00μg/L. QG56 cells were treated with ascending concentration of CPP for 24 h, 48 h and 72 h. The cell proliferation was measured using MTT method. The morphological changes of QG56 cells were observed under inverted microscope. Flow cytometry (FCM) was used to detect the effects of CPP on cell cycle and cell apoptosis. The expression of apoptosis associated gene bax mRNA in QG56 cells was detected by RT-PCR. The expres-sion of bax protein before and after treatment of CPP was examined by SP immunocytochemistry. Results The inhibitory ef-fect of CPP on the proliferation of QG56 cells was increased with the increasing concentrations of CPP and the prolonged du-ration of treatment. The morphological changes were displayed in QG56 exposed to CPP. The results of FCM showed that CPP caused cell cycle arrest at G0/G1 phase. The apoptotic rate of QG56 cells was significantly increased after CPP treatment for 48 h (P<0.05). The expression of bax mRNA was increased in QG56 exposed to CPP. The result of immunocytochemis-try indicated that CPP up-regulated the expression of bax protein. Conclusion CPP showed significant inhibitory effect on human lung cancer cell lines QG56 through inducing cell cycle arrest and apoptosis.
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Objective:To investigate the effect of ethyl acetate extract from Cortex periplocae (CPEAE) on apoptosis of human esophageal carcinoma cell line TE-13 and to elucidate its mechanism. Methods:Inhibitory effect of CPEAE on TE-13 proliferation was tested by MTT assay. The morphological changes of cell apoptosis were observed by Giemsa staining and transmission electron microscopy. Cell cycle and apoptotic ratio were tested by flow cytometry (FCM). The protein expression of CDK4 was observed by Western blotting.Results:CPEAE inhibited proliferation of TE-13 cells in a concentration-dependent and time-dependent manner, and its IC_(50) value was (2.443±0.005) μg/mL at 48 h (P<0.05). The characteristic morphological changes of apoptosis were observed in TE-13 cells after treatment with CPEAE under transmission microscope. A typical subdiploid peak was detected by flow cytometry. CPEAE decreased the expression of gene CDK4 in TE-13 cells. Conclusion:CPEAE can induce apoptosis of TE-13 cells. The effect is related with down-regulation of CDK4 expression.
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AIM: To investigate the immune mechanisms for Periplocin from Cortex Periplocae (CPP) in tumor-bearing mice. METHODS: H_(22) tumor-bearing model BALB/c mice were applied to evaluated in vivo immunoregulatory effect of CPP. The influence of different dose CPP (0.25, 0.50 and 1.00 mg/kg) on immune organs in tumorbearing mice were observed. T cell subsets of mice spleen were detected by flow cytometry. MTT assay was used to determine the influence of CPP on lymphocyte proliferation of mice spleen stimulated by ConA. The levels of TNF-α, IL-2 and IL-12 in serum from mice were detected by means of ELISA. RESULTS: Thymus index and spleen index of H_(22) tumor-bearing model control mice became less than that of normal mice (P < 0.05). Compared to both model and normal control groups, thymus index and spleen index of H_(22) tumor-bearing mice treated with CPP increased obviously (P < 0.05). CPP had no influence on the number of CD8~+ T cells, but up-regulated markedly the number of CD3~+, CD4~+ T cells and the ratio of CD4~+/CD8~+ in tumorbearing mice. In CPP-treated mice, the percentage of CD3~+, CD4~+ T cells were not different from normal mice (P<0.05), the ratio of CD4~+/CD8~+ was higher than that of normal mice (P < 0.05). CPP enhanced obviously lymphocyte proliferation of mice spleen induced by ConA, the SI scores were even higher than that of nornal mice. The levels of TNF-α, IL-2 and IL-12 in serum from CPP-treated mice, increased significantly compared to model control group (P<0.05) in a dose-dependent manner, were similar to or higher than that of normal mice. CONCLUSION: CPP protected immune organs of tumor-bearing mice, increased obviously the percentage of CD4~+ and CD4~+/ CD8~+ among the T cell line, and enhanced lymphocyte proliferation of mice spleen significantly, stimulated the production of TNF-α, IL-2 and IL-12. The results suggested that CPP possessed potent immunoregulatory effect.
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Objective To investigate the effect of periplocin of cortex periplocae (CPP) on Stat3 signaling and its probable molecular mechanism of inducing apoptosis and anti-tumor activity. Methods Cell proliferation was detected by MTT. Cell apoptosis and cell cycle were investigated by flow cytometry. Expression of Stat3 protein in SMMC-7721 cells was analyzed by Western blot. Mcl-1, Survivin and XIAP mRNA expressions were measured by RT-PCR. Results CPP inhibited the proliferation of SMMC-7721 cells significantly, induced their apoptosis and arrested their cell cycle at G2/M phase. Decreased expression of Stat3 protein in the cell nucleus was observed after CPP treatment, but no significant changes were found in cytoplasma. Mcl-1, Survivin and XIAP mRNA expression levels were decreased in a time-dependent manner. Conclusion CPP inhibits cell proliferation and induces apoptosis by inhibiting Stat3 signal transduction in human hepatocellular carcinoma cell line SMMC-7721.
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Objective To study the inductive effect of Cortex Periplocae extract(CPE) on apoptosis of human gastric cancer cells BGC-823 and its mechanism.Methods The cell morphology and super-microstructural changes of apoptosis were analysed by Giemsa staining and electric microscope,respectively.The BGC-823 apoptosis ratio,cell cycles,and changes of apoptosis in DNA level were studied by Flow Cytometry and agarose gel electrophoresis.The genes mRNA and protein expression of apoptosis-related genes bcl-2,bax,and survivin were studied by RT-PCR and immunology cell chemistry method.Results After treatment with CPE,BGC-823 cells showed some typical morphologic features and super-microstructural changes of apoptosis.DNA agarose gel electrophoresis showed characteristic "DNA ladder" pattern.Most BGC-823 cells were arrested at G_2/M phase.Some typical subdiploid peaks before G_0/G_1 phase were observed.The apoptotic rate of BGC-823 was 18.9% after 250 ?g/mL CPE treated for 48 h.The gene mRNA and protein expression of bcl-2 and survivin were inhibited by CPE,whereas that of bax was up-regulated.CPE could enhance the life span of S_(180) bearing mice in a dose-dependent manner.Conclusion(CPE can) inhibit the tumor growth by arresting the BGC-823 cell cycle at G_2/M phase and inducing BGC-823 apoptosis.Its mechanism is related to the inhibition on gene mRNA and protein expression of bcl-2 and survivin,and enhancement of those of bax.