1. Biological activities of crude plant extracts from Vitex trifolia L. (Verbenaceae).
Biological assays of Vitex trifolia L. organic extracts have shown relevant activities. Hexanic and dichloromethanic (DCM) extracts, when prepared from stems and foliage, have proved to be very toxic against several cancer cell lines in culture (SQC-1 UISO, OVCAR-5, HCT-15 COLADCAR, and KB). Also, an important antifeeding activity against the insect pest Spodoptera frugiperda (Lepidoptera: Noctuidae) was recorded. The hexanic extract from leaves completely inhibited the growth of the fungal plant pathogen Fusarium sp. within the first 2 days of the experiment, but dropped significantly at day 6 (15% inhibition). The potential of V. trifolia for several uses is discussed.
––Hernandez MM, Heraso C, Villarreal ML, Vargas-Arispuro I, Aranda E. J Ethnopharmacol. 1999 Oct;67(1):37-44.
1. Saw palmetto for prostate disorders
Saw palmetto is an herbal product used in the treatment of symptoms related to benign prostatic hyperplasia. The active component is found in the fruit of the American dwarf palm tree. Studies have demonstrated the effectiveness of saw palmetto in reducing symptoms associated with benign prostatic hyperplasia. Saw palmetto appears to have efficacy similar to that of medications like finasteride, but it is better tolerated and less expensive. There are no known drug interactions with saw palmetto, and reported side effects are minor and rare. No data on its long-term usage are available. The herbal product also has been used to treat chronic prostatitis, but currently there is no evidence of its efficacy.
––Gordon AE, Shaughnessy AF. Am Fam Physician. 2003 Mar 15;67(6):1281-3.
2. Saw palmetto berry extract inhibits cell growth and Cox-2 expression in prostatic cancer cells.
The cytotoxicity of a commonly used material to alleviate the symptoms of benign prostatic hyperplasia (BPH), Saw Palmetto Berry Extract (SPBE), was examined as neat oil using a set of prostatic cell lines; 267B-1, BRFF-41T and LNCaP. Proliferation of these prostatic derived cell lines is inhibited to different degrees when dosed for 3 days with SPBE. The amount of SPBE required to inhibit 50% growth (IC50) of these cell lines was 20-30 nl equivalents of SPBE per ml of medium for cell lines 267B-1 and BRFF-41T and approximately 10-fold more for the LNCaP cell line. The effect of SPBE dosing on these cell lines is not irreversible, since a 30 min treatment with SPBE at an IC50 concentration does not inhibit their growth. Normal prostate cells were inhibited by 20-25% when grown in the presence of 200 nl SPBE equivalent per ml media. Growth of other non-prostatic cancer cell lines, i.e. Jurkat and HT-29, was affected by approx. 50% and 40%, respectively. When LNCaP cells were grown in the presence of dihydrotestosterone and SPBE, the IC50 concentration decreased significantly compared to LNCaP cells grown in the presence of serum and SPBE. Reduced cellular growth after SPBE treatment of these cell lines may relate to decreased expression of Cox-2 and may be due to changes observed in the expression of Bcl-2. Expression of Cox-1 under similar conditions is not affected because of its constitutive expression. Since increased Cox-2 expression is associated with an increased incidence of prostate cancer, and decrease in its expression by SPBE would provide a basis for further investigation of its use against BPH and in prostatic cancer chemoprevention.
––Goldmann WH, Sharma AL, Currier SJ, Johnston PD, Rana A, Sharma CP. Cell Biol Int. 2001;25(11):1117-24.
1. Effect of Rhizoma Curcumate Zedoariae and Rhizoma Sparganii on apoptosis of human lung cancer cell line A549
The object was to study the medhanism of inhibitory and tumor killing effects of two kinds of Chinese traditional herbs, rhizoma Curcumate zeloariae and Rhizoma Sparganii. Lung cancer cell line A549 was adopted as target cell. The research examined tumor cell apoptosis induced by the herbs with flow cytometry when the target cell was cultured with the herb substration for 24h. The substraction both two kinds of herbs can induce tumor cell apoptosis. The great synergic effect to induce target cell apoptosis was also found out. The results suggested that to induce target cells apoptosis is the man mechanism in inhibiting and killing tumor by ther herbs.
––Wang Z, Zhang JF, Fu GF. Journal of Capital University of Medical Sciences. 2001; 22(4): 304~5.
2. Molecular mechanisms of curcumin-induced cytotoxicity: induction of apoptosis through generation of reactive oxygen species, down-regulation of Bcl-XL and IAP, the release of cytochrome c and inhibition of Akt.
Curcumin, a natural, biologically active compound extracted from rhizomes of Curcuma species, has been shown to possess potent anti-inflammatory, anti-tumor and anti-oxidative properties. The mechanism by which curcumin initiates apoptosis remains poorly understood. In the present report we investigated the effect of curcumin on the activation of the apoptotic pathway in human renal Caki cells. Treatment of Caki cells with 50 micro M curcumin resulted in the activation of caspase 3, cleavage of phospholipase C-gamma1 and DNA fragmentation. Curcumin-induced apoptosis is mediated through the activation of caspase, which is specifically inhibited by the caspase inhibitor, benzyloxycarbony-Val-Ala-Asp-fluoromethyl ketone. Curcumin causes dose-dependent apoptosis and DNA fragmentation of Caki cells, which is preceded by the sequential dephosphorylation of Akt, down-regulation of the anti-apoptotic Bcl-2, Bcl-XL and IAP proteins, release of cytochrome c and activation of caspase 3. Cyclosporin A, as well as caspase inhibitor, specifically inhibit curcumin-induced apoptosis in Caki cells. Pre-treatment with N-acetyl-cysteine, markedly prevented dephosphorylation of Akt, and cytochrome c release, and cell death, suggesting a role for reactive oxygen species in this process. The data indicate that curcumin can cause cell damage by inactivating the Akt-related cell survival pathway and release of cytochrome c, providing a new mechanism for curcumin-induced cytotoxicity.
––Woo JH, Kim YH, Choi YJ, Kim DG, Lee KS, Bae JH, Min do S, Chang JS, Jeong YJ, Lee YH, Park JW, Kwon TK. Carcinogenesis. 2003 Jul;24(7):1199-208. Epub 2003 May 09.
1. Antimicrobial activities of naphthazarins from Arnebia euchroma.
Bioassay-directed fractionation of extract of Arnebia euchroma led to the isolation of alkannin (1), shikonin (2), and their derivatives (3-8) as the active principles against methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococci (VRE). The stereochemistry of alpha-methylbutyryl alkannin (8) is revealed for the first time, and the antimicrobial activity of 8 was compared with its corresponding diastereomer (9). The derivatives 3-9 showed stronger anti-MRSA activity [minimum inhibitory concentrations (MICs) ranged from 1.56 to 3.13 microg/mL] than alkannin or shikonin (MIC = 6.25 microg/mL). Anti-MRSA activity of derivatives was bactericidal with minimum bactericidal concentration (MBC)/MIC < or = 2. In a time-kill assay, the bactericidal activity against MRSA was achieved as rapidly as 2 h. The derivatives 3-9 were also active against vancomycin-resistant Enterococcus faecium (F935) and vancomycin-resistant Enterococcus faecalis (CKU-17) with MICs similar to those with MRSA. Aromatic ester derivatives were also synthesized for antimicrobial activity comparison. None of these compounds were active against Gram-negative bacteria tested. Their cytotoxicity was also evaluated on selected cancer cell lines, and they expressed their activity in the range 0.6-5.4 microg/mL (CD(50)). Our results indicate that the ester derivatives of alkannin are potential candidates of anti-MRSA and anti-VRE agents with antitumor activity.
––Shen CC, Syu WJ, Li SY, Lin CH, Lee GH, Sun CM. J Nat Prod. 2002 Dec;65(12):1857-62.
2. Beta-hydroxyisovalerylshikonin induces apoptosis in human leukemia cells by inhibiting the activity of a polo-like kinase 1 (PLK1).
beta-Hydroxyisovalerylshikonin (beta-HIVS), which was isolated from the plant, Lithospermum radix, induces apoptosis in various lines of human tumor cells. To identify genes involved in beta-HIVS-induced apoptotic process, we performed cDNA array analysis and found that beta-HIVS suppresses the expression of the gene for a polo-like kinase 1 (PLK1) that is involved in control of the cell cycle. When U937 and HL60 cells were treated with 10(-6) M beta-HIVS for 0.5 h, both the amount of PLK1 itself and the kinase activity of this enzyme were decreased. By contrast, Bcr-Abl-positive K562 cells were resistant to the induction of apoptosis by beta-HIVS and this compound did not suppress the kinase activity of PLK1 in these cells. However, simultaneous treatment of K562 cells with both beta-HIVS and STI571, which selectively inhibits the protein tyrosine kinase (PTK) activity of Bcr-Abl, strongly induced apoptosis. Moreover, beta-HIVS increased the inhibitory effect of STI571 on PTK activity. Treatment of K562 cells with antisense oligodeoxynucleotides (ODNs) specific for PLK1 sensitized these cells to the beta-HIVS-induced fragmentation of DNA. These results suggest that suppression of the activity of PLK1 via inhibition of tyrosine kinase activity by beta-HIVS might play a critical role in the induction of apoptosis.
––Masuda Y, Nishida A, Hori K, Hirabayashi T, Kajimoto S, Nakajo S, Kondo T, Asaka M, Nakaya K. Oncogene. 2003 Feb 20;22(7):1012-23.
1. Treatment of intestinal metaplasia and atypical hyperplasia of gastric mucosa with xiao wei yan powder
138 cases of intestinal metaplasia (IM) and 104 cases of atypical hyperplasia (AH) of the gastric mucosa of chronic gastritis treated with Xiao Wei Yan Powder (XWYP) were reported. The diagnoses were based on the pathological examination of gastric antrum biopsy specimens. The cases were randomly divided into treated group and control group. The XWYP contained Smilax glabrae, Hedyotis diffusae, Taraxacum mongolicum, Caesalpinia sappan, Paeonia alba, Cyperus rotundus, Bletilla striata, Glycyrrhiza uralensis etc., and was prepared in powder form, taken orally 5-7g tid. After 2-4 months of administration, gastroscopic and pathological examinations were repeated. Results: In treated group, the total effective rate of IM was 91.3% and that of the AH was 92.16%, while in control group, they were 21.3% and 14.46% respectively (P < 0.01). It denoated that XWYP had marked therapeutic effects for IM and AH. The animal experiments revealed no toxic effect, so safety guarantee was provided for its clinical application.
Liu XR, Han WQ, Sun DR. Zhongguo Zhong Xi Yi Jie He Za Zhi. 1992 Oct;12(10):602-3, 580.
2. Anti-carcinogenic activity of Taraxacum plant. II.
Eleven triterpenoids (1-11) from the roots of Taraxacum japonicum (Compositae) were examined for their inhibitory effects on Epstein-Barr virus early antigen (EBV-EA) induced by the tumor promoter, 12-O-tetrade-canoylphorbol-13-acetate (TPA), in Raji cells as a primary screening test for anti-tumor-promoters (cancer chemopreventive agents). Of these triterpenoids, taraxasterol (1) and taraxerol (7) exhibited significant inhibitory effects on EBV-EA induction, but the inhibitory effects of their acetates 2 and 8 were weaker than those of 1 and 7. Furthermore, 1 and 7 exhibited potent anti-tumor-promoting activity in the two-stage carcinogenesis tests of mouse skin using 7,12-dimethylbenz[a]anthracene (DMBA) as an initiator and TPA as a promoter, and 1 showed a remarkable inhibitory effect on mouse spontaneous mammary tumors using C3H/OuJ mouse. These results strongly suggested that taraxasterol (1) could be a valuable chemopreventive agent.
––Takasaki M, Konoshima T, Tokuda H, Masuda K, Arai Y, Shiojima K, Ageta H. Biol Pharm Bull. 1999 Jun;22(6):606-10.
3. Studies on immunopotentiating activities of antitumor polysaccharide from aerial parts of Taraxacum platycarpum.
The polysaccharide fraction from Taraxii Herba showed potent immunopotentiating activities with antitumor activities. The fraction having small amount of protein inhibited the growth of solid tumor and increased peritoneal exudate cells and immunoorgan weights in normal mice, and also increased hypersensitivities in tumor bearing mice.
––Jeong JY, Chung YB, Lee CC, Park SW, Lee CK. Arch Pharm Res. 1991 Mar;14(1):68-72.
1. In vitro anti-hepatoma activity of fifteen natural medicines from Canada.
Fifteen crude drugs, Stellaria media Cyrill. (Caryophyllaceae), Calendula officinalis L. (Compositae), Achillea millefolium L. (Compositae), Verbascum thapsus L. (Scrophulariaceae), Plantago major L. (Plantaginaceae), Borago officinalis L. (Boraginaceae), Satureja hortensis L. (Labiatae), Coptis groenlandica Salisb. (Ranunculaceae), Cassia angustifolia Vahl. (Leguminosae), Origanum majorana L. (Labiatae), Centella asiatica L. (Umbelliferae), Caulophyllum thalictroides Mich. (Berberidaceae), Picea rubens Sargent. (Pinaceae), Rhamnus purshiana D.C. (Rhamnaceae) and Hibiscus sabdariffa L. (Malvaceae), which have been used as folk medicine in Canada, were evaluated for their anti-hepatoma activity on five human liver-cancer cell lines, i.e. HepG2/C3A, SK-HEP-1, HA22T/VGH, Hep3B and PLC/PRF/5. The samples were examined by in vitro evaluation for their cytotoxicity. The results showed that the effects of crude drugs on hepatitis B virus genome-containing cell lines were different from those against non hepatitis B virus genome-containing cell lines. C. groenlandica was observed to be the most effective against the growth of all five cell lines and its chemotherapeutic values will be of interest for further studies.
––Lin LT, Liu LT, Chiang LC, Lin CC. Phytother Res. 2002 Aug;16(5):440-4.
No related research.
1. Apoptosis of human gastric cancer cell line MGC-803 induced by glycyrrhiza uralensis extract
OBJECTIVE: To study the apoptosis in human gastric cancer cell MGC-803 induced by the extract of glycyrrhiza uralensis Fisch. METHODS: Apoptosis was detected by laser scanning confocal microscope, agarose gel electrophoresis and flow cytometry. The p53 gene expression was analyzed by double immunolabelling and immunohistochemistry technique. RESULTS: Chromatin condensation of different phases of apoptotic cells were observed by laser scanning confocal microscope, the percentage of apoptosis determined by flow cytometry was time- and dose-dependent, agarose gel electrophoresis of DNA exhibited obvious "ladder" in the cells treated with higher concentration of the extract of glycyrrhiza uralensis. The p53 gene expression was unchanged after treatment. CONCLUSION: Glycyrrhiza can induce human gastric cancer cell line MGC-803 to apoptosis by p53-independent pathway and can be used as a potential, natural apoptosis-inducing agent for gastric cancer therapy.
––Ma J, Peng W, Liang D. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2000 Dec;20(12):928-30.
2. Differential regulation of activator protein 1 activity by glycyrrhizin.
Glycyrrhizin, a major component of Glycyrrhiza uralensis (licorice) root, is a saponin and exhibits a number of pharmacological effects, including anti-inflammation, anti-ulcer, anti-allergy, and anticarcinogenesis. Activator protein I (AP-1), a nuclear transcription factor, consists of Jun/Fos heterodimers or Jun/Jun homodimers, and blocking of tumor promoter-induced AP-1 activity could inhibit induced cellular transformation. In order to elucidate the molecular mechanism of glycyrrhizin-induced anticarcinogenesis, effect of glycyrrhizin on the AP-1 activity in untreated and tumor promoter-12-O-tetradecanoylphorbol-13-acetate (TPA)-treated conditions was analyzed in this study. Glycyrrhizin induced the AP-1/TATA reporter activity in a dose-dependent fashion, which was judged by chloramphenicol acetyltransferase assay and electrophoretic mobility-shift assay. Similar results were observed in HepG2 and Vero cells, suggested that glycyrrhizin effect was cell type-independent. In addition, the cis element responsible for glycyrrhizin activity was AP-1 responsive element. Further analysis indicated that glycyrrhizin exhibited a different regulation on the AP-1 activity in untreated and TPA-treated cells. Glycyrrhizin induced the AP-1 activity in untreated cells, while it inhibited the TPA-induced AP-1 activation in TPA-treated cells. These results provide insight into the biological actions of glycyrrhizin and the molecular basis for the development of new chemoprotective agents for cancer.
––Hsiang CY, Lai IL, Chao DC, Ho TY. Life Sci. 2002 Feb 22;70(14):1643-56.
1. Oesophagus cancer, rectal cancer
30~60g fresh shi zhu (qu mai) root (or 20~30 dried one), water decoction, or combined with ren shen, fu ling, bai zhu, gan cao. It had certain therapeutic effect on oesophagus cancer and rectal cancer.
No related research.
1. Inhibition of protein kinase C and proto-oncogene expression by crocetin in NIH/3T3 cells.
Crocetin, a carotenoid isolated from the seeds of Gardenia jasminoides, was found to be a potent inhibitor of tumor promotion induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) in mouse skin. When mouse fibroblast NIH/3T3 cells were treated with TPA alone, protein kinase C (PKC) translocated from the cytosolic fraction to the particulate fraction. Pretreatment with 60 and 120 microM crocetin for 15 min inhibited the TPA-induced PKC activity in the particulate fraction by 50% and 66%, respectively, but did not affect the level of PKC protein. Crocetin also reduced the level of TPA-stimulated phosphorylation of cellular proteins. Cells pretreated with crocetin (120 microM) had 55% less PKC [3H]phorbol dibutyrate-binding capacity. Suppression of TPA (100 ng/mL)-induced c-jun and c-fos gene expression was also observed in the mouse fibroblast cells pretreated with crocetin (30, 60, and 120 microM). Our results provided a basis for understanding the inhibitory effect of crocetin on TPA-mediated tumor promotion.
––Wang CJ, Cheng TC, Liu JY, Chou FP, Kuo ML, Lin JK. Mol Carcinog. 1996 Dec;17(4):235-40.
2. Inhibitory effect of crocetin on benzo(a)pyrene genotoxicity and neoplastic transformation in C3H10T1/2 cells.
Crocetin is a major component in the fruit of Gardenia jasminoides Ellis, a Chinese herbal medicine. In the work, we investigate the protective action and mechanism against benzo(a)pyrene [B(a)P]-induced genotoxicity and neoplastic transformation with a non-toxic dose of crocetin (0.01-0.10 mM) for 1 hour prior to the administration of 0.1 mM B(a)P. B(a)P genotoxicity was inhibited significantly by crocetin in a dose responsive manner. Pretreating C3H10T1/2 cells with crocetin (0.1 mM) also caused a decrease in the covalent binding of B(a)P-diol-epoxide to DNA, to about half that of cells without crocetin treatment. Crocetin also inhibited B(a)P-induced transformations. When the culture was treated with crocetin (0.01, 0.05 and 0.10 mM) for 7 days, the transformation frequencies were lower than that of the culture without crocetin treatment. Furthermore, pretreating cells with crocetin (0.01-0.10 mM) also caused an increase in the activity of GSH S-transferase (GST) to 18-71% that of the cells without crocetin treatment. These results suggest that the inhibition by crocetin of B(a)P-induced genotoxicity and neoplastic transformation in C3H10T1/2 cells is due to a mechanism that increases the activity of GST and decreases the formation of a B(a)P-DNA adduct.
––Chang WC, Lin YL, Lee MJ, Shiow SJ, Wang CJ. Anticancer Res. 1996 Nov-Dec;16(6B):3603-8.
1. Perineal application of cosmetic talc and risk of invasive epithelial ovarian cancer: a meta-analysis of 11,933 subjects from sixteen observational studies.
OBJECTIVE: Prior epidemiological studies suggest an association between perineal cosmetic talc use and increased risk of epithelial ovarian cancer. A meta-analysis was performed to evaluate this suspected association. MATERIALS AND METHODS: Using previously described methods, a protocol was developed for a meta-analysis examining the association between perineal talc use versus non-use and the development of invasive epithelial ovarian cancer. Literature search techniques, study inclusion criteria and statistical procedures were prospectively defined. Data from observational studies were pooled using a general variance based meta-analytic method employing confidence intervals previously described by Greenland. The outcome of interest was a summary relative risk (RRs) reflecting the risk of ovarian cancer development associated with perineal talc use versus non-use. Sensitivity analyses were performed when necessary to explain any observed statistical heterogeneity. RESULTS: Sixteen observational studies meeting protocol specified inclusion criteria were located via a comprehensive literature search. These studies enrolled a total of 11,933 subjects. Analysis for heterogeneity demonstrated that the data were homogenous (p = 0.17) and could be combined in a meta-analysis. Pooling all sixteen studies yielded a RRs of 1.33 (CI = 1.16-1.45), a statistically significant result suggesting a 33% increased risk of ovarian cancer with perineal talc use. Despite this finding, the data showed a lack of a clear dose-response relationship making the RRs of questionable validity. Further sensitivity analyses showed that hospital-based studies showed no relationship between talc use and ovarian cancer risk, i.e. RRs 1.19 (0.99-1.41) versus population-based studies (RRs = 1.38, CI = 1.25-1.52). This suggests that selection bias and/or uncontrolled confouding may result in a spurious positive association between talc use and ovarian cancer risk in population-based studies. CONCLUSION: The available observational data do not support the existence of a causal relationship between perineal talc exposure and an increased risk of epithelial ovarian cancer. Selection bias and uncontrolled confouding may account for the positive associations seen in prior epidemiological studies.
––Huncharek M, Geschwind JF, Kupelnick B. Anticancer Res. 2003 Mar-Apr;23(2C):1955-60.
No related research.