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Biomedical subjects

Zhi Yao

Publications and source records attributed to Zhi Yao.

At least 19 recordsLinked to original sources

CCR2 expression correlates with prostate cancer progression.

Although the primary role of chemokines and their receptors is controlling the trafficking of leukocytes during inflammatory responses, they also play pleoitropic roles in cancer development. There is emerging evidence that cancer cells produce chemokines that induce tumor cell proliferation or chemotaxis in various cancer types. We have previously reported that MCP-1 acts as a paracrine and autocrine factor for prostate cancer (PCa) growth and invasion. As the cellular effects of MCP-1 are mediated by CC chemokine receptor 2 (CCR2), we hypothesized that CCR2 may contribute PCa progression. Accordingly, we first determined CCR2 mRNA and protein expression in various cancer cell lines, including PCa and other cancer types. All cells expressed CCR2 mRNA and protein, but in PCa, more aggressive cancer cells such as C4-2B, DU145, and PC3 expressed a higher amount of CCR2 compared with the less aggressive cancer cells such as LNCaP or non-neoplastic PrEC and RWPE-1 cells. Further, we found a positive correlation between CCR2 expression and PCa progression by analyzing an ONCOMINE gene array database. We confirmed that CCR2 mRNA was highly expressed in PCa metastatic tissues compared with the localized PCa or benign prostate tissues by real-time RT-PCR. Finally, CCR2 protein expression was examined by immunohistochemical staining on tissue microarray specimens from 96 PCa patients and 31 benign tissue controls. We found that CCR2 expression correlated with Gleason score and clinical pathologic stages, whereas lower levels of CCR2 were expressed in normal prostate tissues. These results suggest that CCR2 may contribute to PCa development.

Cell Line↗

The role of the CD95, CD38 and TGFbeta1 during active human cytomegalovirus infection in liver transplantation.

AIM: Human cytomegalovirus (HCMV) has highly evolved mechanisms for avoiding detection by the host immune system. The aim of this study was to analyze the expression levels of TGFbeta1, soluble form of CD95, CD95 ligand (sCD95 and sCD95L, respectively) in plasma and CD95 expression on CD3(+) cells, CD38 expression on CD8(+) cells in liver transplanted recipients with active HCMV infection. METHODS: Blood samples were collected from 15 liver transplanted recipients with active HCMV infection and 15 recipients without HCMV infection. CD95 expression on CD3(+) cells and CD38 expression on CD8(+) cells were quantitatively detected with two-color fluorescence activated cell sorter (FACS) analysis. Lymphocyte surface phenotypes of CD4 and CD8 were detected with FACS analysis. Plasma sCD95, sCD95L and TGFbeta1 levels were determined with enzyme linked-immuno-sorbent assay (ELISA). The results were compared with that from 15 healthy individuals. RESULTS: CD95 expression on CD3(+) T-cells and CD38 expression on CD8(+) cells were significantly increased in active HCMV infection group compared with that in stable group or healthy group (P<0.01). No significant difference was seen between stable group and healthy group (P>0.05). The percentages of CD4(+) T-cell and CD4/CD8 ratio in active HCMV infection group were significantly lower than the values in stable group and healthy group (P<0.05). Plasma levels of TGFbeta1 and sCD95 were significantly increased in active HCMV infection group compared to stable group and healthy group (P<0.05). In contrast, plasma levels of sCD95L in healthy group were not significantly different from that expressed in active HCMV infection group and stable group (P>0.05). CONCLUSION: HCMV suppress proliferation of activated T cells by apoptosis and by releasing immunosuppressive cytokine TGFbeta1. This may provide an important clue to a better understanding of the pathogenesis in liver transplanted recipients with active HCMV infection.

ADP-ribosyl Cyclase 1↗

Monocyte chemotactic protein-1 (MCP-1) acts as a paracrine and autocrine factor for prostate cancer growth and invasion.

BACKGROUND: Monocyte chemotactic protein-1 (MCP-1) plays a key role in the recruitment and activation of monocytes during inflammation. Increased MCP-1 serum levels in patients with various cancers were correlated with advanced stage. Here, we evaluated the role of MCP-1 on prostate cancer (CaP) cell proliferation and invasion. METHODS: Expression of MCP-1 in tissue specimens was analyzed by immunohistochemical staining. MCP-1 production was determined by ELISA in conditioned media collected from primary prostate epithelia (PrEC), LNCaP, C4-2B, PC3 cells, and hFOB. Cell proliferation and invasion were assayed by MTS assay and invasion chambers. RESULTS: All CaP cells, as well as hFOB, produced high amount of MCP-1 compared to PrEC cells. MCP-1 expression levels were associated with advanced pathologic stage. MCP-1 induced proliferation and invasion of CaP cells and this was abolished partially either by CCR2 antagonist or PI3 Kinase inhibitor. CONCLUSION: MCP-1 acts as a paracrine and autocrine factor for CaP growth and invasion.

Cell Line↗

Expression of PTEN, p27, p21 and AKT mRNA and protein in human BEL-7402 hepatocarcinoma cells in transplanted tumors of nude mice treated with the tripeptide tyroservatide (YSV).

The tripeptide, tyroservatide (YSV), has been previously shown to have antitumor effects through unknown mechanism. In the current study, we examined whether YSV modulates the protumorigenic PI3K pathway in human BEL-7402 hepatocarcinoma cells. BEL-7402 hepatocarcinoma was transplanted into the subcutaneous tissues of nude mice, and YSV, at varying doses, was administered. RT-PCR and Western blot were used to analyze the expression of PTEN, AKT, p21 and p27. YSV at doses of 80 microg/kg/day, 160 microg/kg/day and 320 microg/kg/day markedly inhibited the growth of human BEL-7402 hepatocarcinoma (p < 0.05). YSV increased mRNA and protein expression of the tumor-suppressor genes, PTEN, p21 and p27, and inhibited the mRNA and protein expression of the oncogene AKT. Furthermore, YSV administration was associated with dephosphorylation of both PTEN (which activates PTEN) and AKT (which inhibits AKT). These results are consistent with the possibility that YSV mediates inhibition of tumor growth through inhibition of the PI3K pathway and suggests that YSV should be explored for use as an antitumor agent for hepatocarcinoma.

Animals↗

Inhibition of interleukin-6 with CNTO328, an anti-interleukin-6 monoclonal antibody, inhibits conversion of androgen-dependent prostate cancer to an androgen-independent phenotype in orchiectomized mice.

Initially, prostate cancer is androgen dependent. However, most cases progress to an androgen-independent state through unknown mechanisms. Interleukin-6 (IL-6) has been associated with prostate cancer progression including activation of the androgen receptor (AR). To determine if IL-6 plays a role in the conversion of prostate cancer from androgen dependent to androgen independent, we established androgen-dependent LuCaP 35 human prostate cancer xenografts in nude mice, castrated the mice, and blocked IL-6 activity using a neutralizing antibody (CNT0328) for a period of 18 weeks. IL-6 inhibition increased survival of mice and inhibited tumor growth, as reflected by decreased tumor volume and prostate-specific antigen levels, compared with that in mice receiving isotype control antibody. To test the effect of IL-6 inhibition on the conversion from androgen dependent to androgen independent, tumor cells from the treated mice were assessed for their androgen dependence both in vitro and by implanting them into sham-operated or orchiectomized mice. Tumor cells derived from the isotype-treated animals converted to androgen-independent state, whereas tumor cells from the anti-IL-6 antibody-treated mice were still androgen dependent in vitro and in vivo. Although there was no difference in AR levels between the androgen-independent and androgen-dependent tumors, IL-6 inhibition promoted both apoptosis and inhibited cell proliferation in tumors and blocked the orchiectomy-induced expression of histone acetylases, p300 and CBP, which are AR cofactors. These data show that IL-6 contributes to the development of androgen independence in prostate cancer and suggest that it mediates this effect, in part, through modulation of p300 and CBP.

Animals↗

Metastasis suppressor gene Raf kinase inhibitor protein (RKIP) is a novel prognostic marker in prostate cancer.

BACKGROUND: Diminished expression of Raf kinase inhibitor protein (RKIP), an inhibitor of the Raf signaling cascade, promotes prostate cancer (PCa) metastasis in a murine model, suggesting that it is a metastasis suppressor gene. However, the prognostic significance of RKIP expression and its association with metastasis in PCa patients is unknown. METHODS: To investigate RKIP protein expression is a prognostic marker in PCa we performed immunohistochemical staining for RKIP expression in tissue microarrays consisting of 758 non-neoplastic prostate tissues, primary tumors and metastases from 134 PCa patients. The Cox proportional-hazards model was used to adjust for covariates including Gleason score, tumor volume, tumor weight, clinical stage, digital rectal exam findings, serum PSA level and surgical margins. RESULTS: RKIP expression was low in approximately 5%, 48%, and 89% of non-neoplastic prostate, primary tumors and metastases, respectively. Low RKIP expression in primary tumors was a strong positive predictive factor for PCa recurrence based on PSA levels. In patients whose primary tumors expressed high RKIP levels, the 7-year PSA recurrence rate was <10%; whereas in patients with tumors with low RKIP expression the recurrence rate was 50% (P<0.001). Multivariate analysis revealed RKIP was an independent prognostic factor (P<0.001). CONCLUSION: In contrast to increased expression of pro-tumorigenic genes, these results demonstrate decreased protein expression of a gene, for example, RKIP, can serve as a prognostic marker in PCa patients.

Biomarkers, Tumor↗

Gene-chip analysis of the effect of tripeptide tyroservatide (YSV) on gene-expression in human hepatocarcinoma BEL-7402 tumors transplanted to nude mice.

Tyroservatide (YSV) is a bioactive tripeptide of tyrosyl-seryl-valine. In this study, we studied the effects of YSV on human hepatocarcinoma BEL-7402 tumors transplanted in BALB/c (nu/nu) nude mice, and gene expression in the tumor cells with gene-chip analysis. Results show that YSV significantly inhibits the growth of transplanted human hepatocarcinoma BEL-7402 in nude mice (n = 12) compared with the control group (P < 0.05); with an inhibition rate of 55% at 320 microg/kg/d. Seven hundred eighty-one genes were different between the YSV group and the control group. Fifty-two genes changed in expression level by onefold or more including 37 downregulated genes and 15 upregulated genes. Probably, YSV exhibits a significant antitumor activity by inhibiting the expression of tumor cells histone genes, then damaging tumor cell chromosome and killing tumor cells.

Animals↗

[Inhibitory effect of tripeptide compound tyroservaltide on invasion and metastasis of mouse melanoma cell line B16-F10].

BACKGROUND & OBJECTIVE: Tripeptide compound tyroservaltide (YSV) has obvious inhibitory effect on experimental liver cancer. This study was to evaluate the inhibitory effect of YSV on the invasion and metastasis of mouse melanoma cell line B16-F10. METHODS: The cytotoxic effect of YSV on B16-F10 cells was assessed by MTT assay, and the effects of YSV on the adhesiveness and invasiveness of B16-F10 cells were determined using Matrigel and a transwell system. B16-F10 cells were injected into the tail veins of C57BL/6 mice to establish an experimental lung metastasis model, and the effect of YSV on lung metastasis was observed. The effect of YSV on the expression of intercellular adhesion molecule-1 (ICAM-1) in lung tissue was detected by immunohistochemistry. RESULTS: YSV (100 microg/ml, 48 h) inhibited the proliferation of B16-F10 cells, with an inhibitory rate of 24.36%; YSV (100 microg/ml, 24 h) inhibited the adhesiveness of B16-F10 cells to Matrigel, with an inhibitory rate of 36.51%; YSV (10 microg/ml, 48 h) inhibited the invasiveness of B16-F10 cells, with an inhibitory rate of 36.53%; YSV [640 microg.(kg.d)-1] inhibited lung metastasis by B16-F10 cells, with an inhibitory rate of 62.21%. The expression of ICAM-1 in lung tissue was lower in YSV group than in normal saline group. CONCLUSION: YSV can inhibit the growth, invasion, and metastasis of B16-F10 cells.

Animals↗

[Tyroservatide inhibits the growth of human hepatocarcinoma in nude mice].

OBJECTIVE: To investigate the inhibitory effects of tyroservatide and its amino acid mixture on growth of hepatocarcinoma. METHODS: Hepatocarcinoma in nude mice was induced by implantation of cells of human hepatocarcinoma cell line BEL-7402. The inhibition of hepatocarcinoma growth was determined by calculating the tumor volume and measuring the tumor weight. The effects of tyroservatide on tumor cells in nude mice were assessed by immunohistochemical staining of proliferating cell nuclear antigen (PCNA), electron microscopic observation of ultrastructure, and apoptosis of tumor cells using terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL). RESULTS: Tyroservatide significantly inhibited the growth of human hepatocarcinoma in nude mice, with an inhibiting rate more than 60%. But the mixture of amino acid did not show a significant inhibitory effect on the tumor growth. Tyroservatide also induced apoptosis of tumor cells and decreased the expression of PCNA in tumor cells. CONCLUSION: Tyroservatide may significantly inhibit the growth of human hepatocarcinoma in nude mice by inducing apoptosis and inhibiting proliferation of tumor cells.

Animals↗

Vascular endothelial growth factor contributes to prostate cancer-mediated osteoblastic activity.

Prostate cancer frequently metastasizes to bone resulting in the formation of osteoblastic metastases through unknown mechanisms. Vascular endothelial growth factor (VEGF) has been shown recently to promote osteoblast activity. Accordingly, we tested if VEGF contributes to the ability of prostate cancer to induce osteoblast activity. PC-3, LNCaP, and C4-2B prostate cancer cell lines expressed both VEGF-165 and VEGF-189 mRNA isoforms and VEGF protein. Prostate cancer cells expressed the mRNA for VEGF receptor (VEGFR) neuropilin-1 but not the VEGFRs Flt-1 or KDR. In contrast, mouse pre-osteoblastic cells (MC3T3-E1) expressed Flt-1 and neuropilin-1 mRNA but not KDR. PTK787, a VEGFR tyrosine kinase inhibitor, inhibited the proliferation of human microvascular endothelial cells but not prostate cancer proliferation in vitro. C4-2B conditioned medium induced osteoblast differentiation as measured by production of alkaline phosphatase and osteocalcin and mineralization of MC3T3-E1. PTK787 blocked the C4-2B conditioned medium-induced osteoblastic activity. VEGF directly induced alkaline phosphatase and osteocalcin but not mineralization of MC3T3-E1. These results suggest that VEGF induces initial differentiation of osteoblasts but requires other factors, present in C4-2B, to induce mineralization. To determine if VEGF influences the ability of prostate cancer to develop osteoblastic lesions, we injected C4-2B cells into the tibia of mice and, after the tumors grew for 6 weeks, administered PTK787 for 4 weeks. PTK787 decreased both intratibial tumor burden and C4-2B-induced osteoblastic activity as measured by bone mineral density and serum osteocalcin. These results show that VEGF contributes to prostate cancer-induced osteoblastic activity in vivo.

Alkaline Phosphatase↗

Tripeptide tyroserleutide enhances the antitumor effects of macrophages and stimulates macrophage secretion of IL-1beta, TNF-alpha, and NO in vitro.

Tyroserleutide (YSL) is a type of active, low molecular weight polypeptide, comprised of three amino acids, which has antitumor effects. YSL has various advantages over the other bioactive peptides such as its low molecular weight, simple construction, nonimmunogenicity, specificity, few side effects, and ease of synthesis. However, the biological activities contributing to it's antitumor effects are not yet known. We studied the effects of YSL on the in vitro cytotoxic activity of BALB/c mice peritoneal macrophages (PEMphi) against the target tumor cell lines BEL-7402 and B16-F10. We also measured the concentrations of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and nitric oxide (NO) produced by YSL-activated Mphi, and we determined the concentrations of IL-1beta and NO secreted by YSL-activated murine macrophage RAW264.7 cells. YSL activated Mphi in vitro, inhibited BEL-7402 proliferation, enhanced PEMphi antitumor effects, and stimulated IL-1beta, TNF-alpha, and NO production by RAW264.7 cells. These data suggest that YSL activates the monocyte-macrophage system, which enhances Mphi antitumor effects against BEL-7402 and B16-F10 cells and stimulates the secretion by Mphi of cytotoxic effectors such as IL-1beta, TNF-alpha, and NO.

Animals↗

Preliminary investigation of the inhibitory effects of the tyroservaltide (YSV) tripeptide on human hepatocarcinoma BEL-7402.

This study aimed to investigate the inhibitory effect of tyroservaltide (YSV) on the human hepatocarcinoma BEL-7402 transplanted into nude mice and to explore its possible anti-tumor mechanism. Nude mice bearing xenografts of the human BEL-7402 hepatoma were given daily i.p. injections of YSV or saline (as a control) after the tumor were transplanted. Calculating tumor volume and measuring tumor weight determined the extent of inhibition of xenografts. The ultrastructure of tumor cells was observed by electron microscopy. Proliferating cell nuclear antigen (PCNA) expression in tissues of the YSV-treated group was observed by immunohistochemistry. Apoptosis of tumor tissue cells was assayed by the terminal transferase uridyl nick end labeling (TUNEL) method. At doses of 80 microg/kg/d and 160 microg/kg/d, YSV could significantly inhibit growth of tumors transplanted into nude mice, with inhibition rates of 60% and 64%, respectively, compared with that of the controls (P < 0.05). Moreover, YSV changed the ultrastructure of tumor cells, resulting in necrosis and apoptosis of the tumor cells. Compared with the saline group, the expression of PCNA in tumor tissue decreased and the count of apoptotic cell increased. Therefore, YSV can significantly inhibit the growth of human hepatocarcinoma BEL-7402 in nude mice, decrease the expression of PCNA in tumor tissue, and induce tumor cell apoptosis.

Animals↗

Bone morphogenetic protein-6 promotes osteoblastic prostate cancer bone metastases through a dual mechanism.

Prostate cancer frequently metastasizes to bone where it forms osteoblastic lesions through unknown mechanisms. Bone morphogenetic proteins (BMP) are mediators of skeletal formation. Prostate cancer produces a variety of BMPs, including BMP-6. We tested the hypothesis that BMP-6 contributes to prostate cancer-induced osteosclerosis at bone metastatic sites. Prostate cancer cells and clinical tissues produced BMP-6 that increased with aggressiveness of the tumor. Prostate cancer-conditioned medium induced SMAD phosphorylation in the preosteoblast MC3T3 cells, and phosphorylation was diminished by anti-BMP-6 antibody. Prostate cancer-conditioned medium induced mineralization of MC3T3 cells, which was blocked by both the BMP inhibitor noggin and anti-BMP-6. Human fetal bones were implanted in severe combined immunodeficient mice and after 4 weeks, LuCaP 23.1 prostate cancer cells were injected both s.c. and into the bone implants. Anti-BMP-6 or isotype antibody administration was then initiated. Anti-BMP-6 reduced LuCaP 23.1-induced osteoblastic activity, but had no effect on its osteolytic activity. This was associated with increased osteoblast numbers and osteoblast activity based on bone histomorphometric evaluation. As endothelin-1 has been implicated in bone metastases, we measured serum endothelin-1 levels but found they were not different among the treatment groups. In addition to decreased bone production, anti-BMP-6 reduced intraosseous, but not s.c., tumor size. We found that BMP-2, BMP-4, BMP-6, and BMP-7 had no direct effect on prostate cancer cell growth, but BMP-2 and BMP-6 increased the in vitro invasive ability of prostate cancer cell. These data show that prostate cancer promotes osteoblastic activity through BMP-6 and that, in addition to its bone effects, suggest that BMPs promote the ability of the prostate cancer cells to invade the bone microenvironment.

Animals↗

The effect of tripeptide tyroserleutide (YSL) on animal models of hepatocarcinoma.

This study aimed to observe the effects of tyroserleutide (tyrosyl-seryl-leucine, YSL) on the survival time of mice transplanted with the ascitic fluid-type hepatocarcinoma H22, as well as the inhibitory effect of tyroserleutide on the human hepatocarcinoma Bel-7402 that was transplanted into nude mice. At doses of 80, 20 and 5 microg/kg/d, tyroserleutide significantly prolonged the survival of mice transplanted with H22 tumor cells, producing survival rates of 89%, 39% and 49%, respectively, which were statistically significantly different from the saline group (P < 0.05). YSL, at doses of 80, 160 and 320 microg/kg/d significantly inhibited the growth of the human hepatocarcinoma Bel-7402 tumor in nude mice, producing inhibition of 40%, 64% and 59%, respectively; this inhibition was significantly greater than that by saline (P < 0.05). HE staining and electron microscopy of the pathological changes of the tumor in nude mice showed that YSL changed the structure Bel-7402 tumor cells that were transplanted into nude mice, and also induced tumor cell apoptosis and necrosis, which could be a mechanism by which YSL inhibits the tumor growth in animal models.

Animals↗

Experimental study of the inhibition of human hepatocarcinoma Bel7402 cells by the tripeptide tyroserleutide(YSL).

PURPOSE: To investigate the antitumor effects of tyroserleutide (tyrosyl-seryl-leucine, YSL) on human Bel7402 hepatocarcinoma in vitro and in vivo, with preliminary exploration of its antitumor mechanism. METHODS: MTT was used to observe the anticarcinogenic effects of YSL on human hepatocarcinoma Bel7402 cells in vitro. The ultrastructure of tumor cells was observed by electron microscopy. Nude mice bearing xenografts of human hepatocarcinoma Bel7402 were given daily i.p. injections of YSL or saline and an admixture of amino acids as controls, after tumor implantation. The inhibition of xenografts was determined by calculating the tumor volume and measuring tumor weight. The effects of YSL on the cell cycle and apoptosis of Bel7402 cells were determined by flow cytometry, and the effects on the ultrastructure of the cells by electron microscopy. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and proliferating-cell nuclear antigen (PCNA) immunohistochemical staining were used to investigate apoptosis in tumor tissue in nude mice. RESULTS: In vitro YSL inhibited the proliferation of human Bel7402 tumor cells and changed their ultrastructure, resulting in the necrosis and apoptosis of the tumor cells. YSL at 80, 160, or 320 microg/kg/d inhibited tumor growth in nude mice by 40.26, 64.17, and 59.19%, respectively, which are significantly lower than the inhibition exerted by saline and an admixture of YSL amino acids (P<0.05). The ultrastructure and cell cycle of human hepatocarcinoma Bel7402 cells were changed by treatment with YSL, with a rate of apoptosis higher than that of the control group. TUNEL and PCNA analysis showed that YSL inhibited the proliferation of tumor cells and induced apoptosis at the level of the cell. CONCLUSIONS: YSL significantly inhibited human hepatocarcinoma Bel7402 growth in vitro and in vivo. The growth inhibition of the tumor may involve necrosis and apoptosis of the tumor induced by YSL.

Animals↗

Correlation of CD95 and soluble CD95 expression with acute rejection status of liver transplantation.

AIM: To analyze the expression levels of soluble form of CD95, CD95 ligand (sCD95 and sCD95L, respectively) in plasma and CD95 expression on CD3+ cells in liver-transplanted recipients with acute rejection (AR). METHODS: Peripheral blood mononuclear cells (PBMCs) were isolated from 30 clinically liver transplanted recipients. CD95 expression on CD3+ cells was quantitatively measured by two-color fluorescence activated cell sorter (FACS) analysis. Lymphocyte surface phenotypes of CD4, CD8, CD16 and CD56 were determined by flow cytometry. Plasma levels of sCD95 and sCD95L were detected by Enzyme Linked-Immuno-Sorbent Assay (ELISA). The results were compared with that from normal healthy volunteers (n = 15 individuals). RESULTS: FACS analysis showed that CD95 expression on CD3+ T cells was significantly increased in liver transplanted recipients with AR compared to that in stable recipients without rejection and infection or healthy individuals who did not undergo transplantation (18,676.93+/-11,588.34/molecule, 6,848.20+/-1 712.96/molecule, 6,418.01+/-2,001.95/molecule, respectively, P<0.01). Whereas no significant difference was seen between liver-transplanted stable recipients and healthy individuals. Furthermore, no significant differences were detected between each group with CD4/CD8 ratio or the percentage of CD16+56+ cells. Plasma levels of sCD95 were significantly higher in transplanted recipients with AR compared to that in stable recipients or healthy individuals (391.88+/-196.00, 201.37+/-30.30, 148.83+/-58.25 pg/mL, respectively, P<0.01). In contrast, the plasma levels of sCD95L in liver- transplanted recipients were not significantly different from that in healthy individuals. CONCLUSION: The present results indicate that the increased CD95 expression on CD3+ cells and the increased levels of sCD95 in plasma may modify the immunological situation of the recipients after transplantation or represent the ongoing graft rejection.

Acute Disease↗

Immunosuppressive sesquiterpenes from Tripterygium wilfordii.

Five new sesquiterpenes, 1beta-furanoyl-2beta,3alpha,7alpha,8beta,11-pentaacetoxy-4alpha,5alpha-dihydroxy-dihydroagarofuran (1), 1beta,2beta,3alpha,5alpha,7beta,8beta,11-heptaacetoxy-dihydroagarofuran (2), 1beta-furanoyl-2beta,3alpha,7alpha,8beta,11-pentaacetoxy-5alpha-hydroxy-dihydroagarofuran (3), 1beta,7beta,8alpha-triacetoxy-2beta-furanoyl-4alpha-hydroxy-11-isobutyryloxy-dihydroagarofuran (4), and 1beta-nicotinoyl-2beta,5alpha,7beta-triacetoxy-4alpha-hydroxy-11-isobutyryloxy-8alpha-furanoyl-dihydroagarofuran (5), were isolated from the xylem of Tripterygium wilfordii, together with a known compound (6). Their structures were elucidated on the basis of spectroscopic studies. Compounds 2-5 showed significant immunosuppressive activities.

Drugs, Chinese Herbal↗

Tyroserleutide tripeptide affects calcium homeostasis of human hepatocarcinoma BEL-7402 cells.

This study aimed to observe the effects of tyroserleutide (tyrosyl-seryl-leucine, YSL) on the growth of human hepatocarcinoma BEL-7402 that was transplanted into nude mice, and explore its anti-tumor mechanism preliminarily. YSL, at doses of 80 microg x kg(-1) x d(-1), 160 microg x kg(-1) x d(-1) and 320 microg x kg(-1) x d(-1) significantly inhibited the growth of the human hepatocarcinoma BEL-7402 tumor in nude mice, producing inhibition of 21.66%, 41.34%, and 34.78%, respectively. Ultra structure of BEL-7402 tumor in nude mice showed that YSL could induce tumor cells apoptosis and necrosis, cell organelle mitochondria and endoplasmic reticulum damage, and calcium overload. By confocal laser scanning microscopy and flow cytometry, we found that 10 microg/mL YSL rapidly induced an increase of the concentration of cytoplasmic free calcium in BEL-7402 cells in vitro, and maintained high concentrations of cytoplasmic free calcium for 1 h. Then the calcium concentration began to decrease after 2 h, and was lower than that of the control group at 4 h and 24 h (p < 0.05). YSL also decreased the mitochondrial transmembrane potential of BEL-7402 cells in vitro, but had no effect on the calcium homeostasis or mitochondrial transmembrane potential of Chang liver hepatocytes. So affecting calcium homeostasis, then inducing apoptosis and necrosis may be a mechanism by which YSL inhibits the tumor growth in animal model.

Animals↗