Skip to main content

Main menu

  • Home
  • Current Issue
  • Archive
  • Info for
    • Authors
    • Editorial Policies
    • Advertisers
    • Editorial Board
    • Special Issues 2025
  • Journal Metrics
  • Other Publications
    • Anticancer Research
    • Cancer Genomics & Proteomics
    • Cancer Diagnosis & Prognosis
  • More
    • IIAR
    • Conferences
  • About Us
    • General Policy
    • Contact
  • Other Publications
    • In Vivo
    • Anticancer Research
    • Cancer Genomics & Proteomics

User menu

  • Register
  • Subscribe
  • My alerts
  • Log in
  • My Cart

Search

  • Advanced search
In Vivo
  • Other Publications
    • In Vivo
    • Anticancer Research
    • Cancer Genomics & Proteomics
  • Register
  • Subscribe
  • My alerts
  • Log in
  • My Cart
In Vivo

Advanced Search

  • Home
  • Current Issue
  • Archive
  • Info for
    • Authors
    • Editorial Policies
    • Advertisers
    • Editorial Board
    • Special Issues 2025
  • Journal Metrics
  • Other Publications
    • Anticancer Research
    • Cancer Genomics & Proteomics
    • Cancer Diagnosis & Prognosis
  • More
    • IIAR
    • Conferences
  • About Us
    • General Policy
    • Contact
  • Visit iiar on Facebook
  • Follow us on Linkedin
Research ArticleExperimental Studies

Wogonin, a Natural and Biologically-active Flavonoid, Influences a Murine WEHI-3 Leukemia Model in Vivo Through Enhancing Populations of T- and B-Cells

CHIN-CHUNG LIN, JEN-JYH LIN, PING-PING WU, CHI-CHENG LU, JO-HUA CHIANG, CHAO-LIN KUO, BIN-CHUAN JI, MING-HUEI LEE, AN-CHENG HUANG and JING-GUNG CHUNG
In Vivo November 2013, 27 (6) 733-738;
CHIN-CHUNG LIN
1Department of Chinese Medicine, Fong-Yuan Hospital, Department of Health, Executive Yuan, Taichung, Taiwan, R.O.C.
2School of Medicine and Nursing, Hunkuang University, Taichung, Taiwan, R.O.C.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
JEN-JYH LIN
3School of Chinese Medicine, China Medical University, Taichung, Taiwan, R.O.C.
4Division of Cardiology, China Medical University, Taichung, Taiwan, R.O.C.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
PING-PING WU
5School of Pharmacy, China Medical University, Taichung, Taiwan, R.O.C.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
CHI-CHENG LU
6Department of Life Sciences, National Chung Hsing University, Taichung, Taiwan, R.O.C.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
JO-HUA CHIANG
6Department of Life Sciences, National Chung Hsing University, Taichung, Taiwan, R.O.C.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
CHAO-LIN KUO
7School of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, Taiwan, R.O.C.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
BIN-CHUAN JI
8Division of Chest Medicine, Department of Internal Medicine, Changhua Christian Hospital, Changhua, Taiwan, R.O.C.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
MING-HUEI LEE
9Department of Urology, Fong-Yuan Hospital, Department of Health, Executive Yuan, Taichung, Taiwan, R.O.C.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
AN-CHENG HUANG
10Department of St. Mary's Junior College of Medicine, Nursing and Management, Yilan, Taiwan, R.O.C.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • For correspondence: jgchung@mail.cmu.edu.tw haj@smc.edu.tw
JING-GUNG CHUNG
11Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, R.O.C.
12Department of Biotechnology, Asia University, Taichung, Taiwan, R.O.C.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • For correspondence: jgchung@mail.cmu.edu.tw haj@smc.edu.tw
  • Article
  • Figures & Data
  • Info & Metrics
  • PDF
Loading

Abstract

Wogonin, a natural and biologically-active flavonoid found in plants, has been reported to exhibit anticancer effects on several cancer cell types. However, there is no available information regarding the responses to wogonin in leukemia mouse models. At concentrations of 10-200 μM, wogonin reduced the percentage of viable WEHI-3 cells in a concentration-dependent manner. In an in vivo study, WEHI-3 cells were intraperitoneally injected into normal BALB/c mice for establishing leukemic BALB/c mice to determine the anti-leukemia activity of wogonin. Wogonin increased the survival rate and the body weight of leukemic mice when compared to vehicle (olive oil)-treated groups. Furthermore, the results also revealed that wogonin increased the percentage of cluster of differentiation-3 CD3 (T-cell marker) and CD19 (B-cell marker) but reduced that of Mac-3 (macrophages) and CD11b (monocytes) cell surface markers in treated mice as compared with the untreated leukemia group. Based on these observations, wogonin might exhibit anti-leukemia effects on murine WEHI-3 cell line-induced leukemia in vivo.

  • Wogonin
  • flavonoid
  • BALB/c mice
  • murine WEHI-3 leukemia model

Leukemia and lymphomas account for about half of all childhood cancers (1). Leukemia is the second most malignant disease in children (2) and is the most frequent type of cancer in children less than 14 years of age (3). So far, the treatments of patients with leukemia include radiotherapy, chemotherapy, or a combination of radiotherapy with chemotherapy, but treatments are still unsatisfactory. Reports have shown that increased consumption of a plant-based diet can reduce the risk of cancer development (4-6).

Wogonin (5,7-dihydroxy-8-methoxyflavone), a naturally-occurring flavonoid from the root of the Scutellaria baicalensis Georgi, has been used for treating allergic and inflammatory diseases (7, 8). Numerous studies have reported that wogonin induces apoptosis in many human cancer cell types such as osteosarcoma (9), leukemia (10), breast cancer (11) and glioma (12). Furthermore, reports have shown that wogonin induces cell differentiation, apoptosis and cell-cycle arrest (13-15) and also suppresses the growth of human cancer xenografts in vivo (11, 16). It was reported that wogonin improves functional outcomes and reduces activation of Toll-like receptor-4 (TLR4)/Nuclear Factor-Kappa B (NF-κB) signaling in experimental traumatic brain injury (17). Several studies also showed that wogonin has no or little toxicity towards normal cells and had no obvious toxicity in animals (11, 13, 18-20). More interestingly, in early clinical trials, Scutellaria extracts have been successfully tested in patients with advanced breast cancer (21, 22).

In the present study, we investigated whether wogonin can promote the survival rate of leukemic BALB/c mice in vivo.

Materials and Methods

Materials and reagents. Wogonin, dimethyl sulfoxide (DMSO), propidium iodide (PI), RNase A and Triton X-100 were purchased from Sigma-Aldrich Corp. (St. Louis, MO, USA). Fetal bovine serum (FBS), RPMI-1640 medium, L-glutamine and penicillin-streptomycin were obtained from Gibco Life Technologies (Carlsbad, CA, USA).

WEHI-3 murine leukemia cells. The WEHI-3 murine myelomonocytic leukemia cell line was obtained from the Food Industry Research and Development Institute (Hsinchu, Taiwan, ROC). The WEHI-3 cells were immediately placed in plastic culture flasks (75 cm2) in RPMI-1640 medium supplemented with 10% FBS, 2 mM L-glutamine, 100 U/ml penicillin and 100 μg/ml streptomycin under a humidified atmosphere with 5% CO2 at 37°C. Cells were then cultivated for two complete cycles in an incubator.

Viability determination. 2×105 WEHI-3 cells/well were placed into each well of 24-well plates for 24 and 48 h. Then wogonin (dissolved in DMSO) was individually added to the wells at final concentrations of 0, 10, 25, 50, 100 and 200 μM, and 0.1% of DMSO as a control group in culture medium for incubation for 24 and 48 h. At the end of incubation, cells from each well were harvested for the determination of viability by using a flow cytometric method as described previously (23).

Male BALB/c mice. Forty male BALB/c mice at the age of eight weeks, around 22-25 g in weight, were obtained from the Laboratory Animal Center, College of Medicine, National Taiwan University (Taipei, Taiwan, ROC) and kept in the Animal Center of China Medical University. The whole animal study was carried out following the institutional guidelines (Affidavit of Approval of Animal Use Protocol) which was approved by the Institutional Animal Care and Use Committee (IACUC) of China Medical University (Taichung, Taiwan, ROC).

Establishment of leukemic mice and wogonin treatment. A total of fourty BALB/c mice were used for the experiments. Thirty BALB/c mice were individually intraperitoneally (i.p.) injected with 1×105 WEHI-3 cells. After 2 weeks, they were randomly separated into three groups as a model of leukemia. Another ten mice were used as control without WEHI-3 cell injection. Group I mice were normal mice (10 animals) and were treated with normal diet only. Group II WEHI-3-injected mice were treated with olive oil (vehicle) as control (10 animals). Group III WEHI-3-injected mice were treated with wogonin (30 mg/kg) in olive oil (10 animals). Group IV WEHI-3-injected mice were treated with wogonin (10 mg/kg) in olive oil (10 animals). Wogonin was administered by oral gavage to the treatment groups at the above doses daily for two weeks before mice were weighed and sacrificed by euthanasia with CO2 (23).

Immunofluorescence staining for surface markers from leukemic mice. After all animals were treated for two weeks, in order to measure the surface markers, blood samples of 1 ml from all experimental mice were collected before mice were sacrificed. Each collected red blood cell sample from each animal was lysed with 1×Pharm Lyse™ lysing buffer (BD Biosciences Pharmingen Inc., San Diego, CA, USA). All samples were centrifuged for 15 min at 1500×g at 4°C to isolate white blood cells then all isolated cells were stained by the R-Phycoerythrin (PE)-labeled anti-mouse Mac-3 antibodies, Fluorescein isothiocyanate (FITC)-labeled anti-mouse CD11b, FITC-labeled anti-mouse CD3 and PE-labeled anti-mouse CD19 (BD Biosciences Pharmingen Inc.) for 30 min before being analyzed for cell markers by flow cytometry as previously described (23).

Results

Wogonin reduces the percentage of viable WEHI-3 cells. In order to examine whether or not wogonin induced cytotoxic effects on mouse leukemia cells, the WEHI-3 cells were treated with different concentrations of wogonin for 24 and 48 h before all cells were measured for the percentage of viable cells by flow cytometric assay. The results are shown in Figure 1, indicating that wogonin reduced the percentage of viable WEHI-3 cells in a dose-dependent manner.

Wogonin affects the growth of leukemic mice. In this experiment, thirty mice were used as a leukemia model and 10 mice were not i.p. injected with WEHI-3 cells, as a normal group (Group I). Thirty male BALB/c mice were i.p. injected with WEHI-3 cells before being randomly separated into three groups. Group II mice were treated with olive oil alone. Group III mice were treated with wogonin (30 mg/kg) in olive oil. Group IV mice were treated with wogonin (10 mg/kg) in olive oil. Animals were treated for two weeks and then were examined and measured for survival rate and body weight in all groups. The results shown in Figure 2A indicate that wogonin at both doses significantly increased the survival rate. Figure 2B shows that both doses of wogonin increased the body weight when compared to the olive oil-treated leukemic group.

Wogonin affected surface markers on whole blood cells from WEHI-3-leukemic BALB/c mice. For investigating whether wogonin affects the level of cell surface markers from leukemic mice, leukocytes from wogonin-treated and untreated (control) groups were isolated and levels of Mac-3, CD19, CD3, and CD11b were measured by a flow cytometric assay and results are shown in Figure 3. The data from each treatment indicate that wogonin significantly reduced the levels of Mac-3 (Figure 3A) and CD11b (Figure 3B) but increased the levels of CD3 (Figure 3C) and CD19 (Figure 3D) when compared to the control leukemic group.

Figure 1.
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 1.

Wogonin reduced the percentage of viable WEHI-3 cells. Cells in 24-well plates were treated with 0, 10, 25, 50, 100 and 200 μM of wogonin for 24 (A) and 48 (B) h. Cells were harvested for measuring the percentage of viability by flow cytometric assay as described in the Materials and Methods. Significantly different from the control at *p<0.05.

Discussion

Many studies have shown that wogonin induces cytotoxic effects on various cancer cells through cell-cycle arrest and apoptosis including breast cancer cells (24), malignant T-cells (13) and osteosarcoma (9). However, there are no cytotoxic effects on normal cells even at concentrations up to 100 μM (25, 26). Thus, wogonin may be a potential anticancer drug. Our previous studies also showed that reactive oxygen species play an important role in wogonin-induced apoptosis of bone osteosarcoma cells by AKT-modulated, BAX and BCL-2-related intrinsic apoptotic pathways (9). However, there is no available information to show the effect of wogonin on the growth of leukemic mice in vivo. Herein, we investigated the effect of wogonin on the growth and immune-associated cell markers in WEHI-3 cell-generated leukemic mice in vivo.

Figure 2.
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 2.

Wogonin affects the survival rate and growth of leukemic BALB/c mice. All mice except the normal group (Group I) were intraperitoneally injected with WEHI-3 cells then divided into three groups: group II was orally-treated with olive oil-alone; group III was treated with wogonin at 30 mg/kg and group IV was treated with wogonin at 10 mg/kg for two weeks. Survival rates were calculated (A) and body weights were measured (B). Significantly different at *p<0.05.

Our results indicate that wogonin reduced the percentage of total viable WEHI-3 cells and this effect was concentration-dependent (Figure 1). This is in agreement with a report from Lee et al., which indicated that wogonin induced cytotoxicity in human promyelo-leukemic cells (27). Results from Figure 2A indicate that wogonin at both doses significantly promoted the survival rate of leukemic mice; however, Figure 2B demonstrates that wogonin did not significantly affect the weights of animals, nor the weights of the liver and spleen (data not shown) in leukemic mice when compared to leukemic mice not treated with wogonin.

Figure 3.
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 3.

Wogonin affects the level of cell surface markers in white blood cells from leukemic BALB/c mice. All mice except the normal group were intraperitoneally injected with WEHI-3 cells, followed by oral treatment with or without wogonin for two weeks. Blood was collected from each animal and was analyzed for cell markers by flow cytometry as described in the Materials and Methods. A: Mac-3; B: CD11b; C: CD3 and D: CD19 The data are expressed as the mean±S.D. of four experiments (n=10). Significantly different at *p<0.05.

It was reported that B-cell development and humoral immune responses are controlled by signaling thresholds that are differentially regulated by the CD22 and CD19 cell surface receptors in vivo. The differential regulation of tyrosine phosphorylation by CD19 and CD22 may provide a molecular mechanism for adjusting B Cell Receptor (BCR) signaling thresholds (28). Furthermore, it is well-known that CD19 is an activated B-cell surface marker (29), and B-cell differentiation also requires the interaction of various cytokines that are secreted from macrophages or T-cells (4). Herein, our results indicate that wogonin promoted the population of CD19+ cells (Figure 3D). This finding indicates that wogonin may promote the B-cell population. Figure 3C shows that wogonin at the low concentration applied promoted the population of CD3+ cells but at higher concentration did not significantly induce increased T-cell population. Based on the results from Figure 3, we conclude that wogonin reduced the Mac-3+ population at both concentrations but only low concentrations showed a significantly reduced CD11b+ population.

Based on these observations, we may suggest that wogonin promotes an immune response through increasing B- and T-cells populations in WEHI-3-generated leukemic BALB/c mice in vivo. This is the first finding showing that oral treatment with wogonin increased the growth survival rate of leukemic mice. Wogonin may act as a potent immunological adjuvant in vivo in leukemia.

Acknowledgements

This study was supported by a Grant Research project 101 from the Department of Health, Executive Yuan, Taiwan, R.O.C..

  • Received April 15, 2013.
  • Revision received July 19, 2013.
  • Accepted July 23, 2013.
  • Copyright © 2013 The Author(s). Published by the International Institute of Anticancer Research.

References

  1. ↵
    1. O'Neill KA,
    2. Bunch KJ,
    3. Murphy MF
    : Intrauterine growth and childhood leukemia and lymphoma risk. Expert Rev Hematol 5: 559-576, 2012.
    OpenUrlPubMed
  2. ↵
    1. Chen X,
    2. Zhou M,
    3. Ning B,
    4. Song H,
    5. Yang S,
    6. Tang Y
    : Transfusion-associated HIV infection in pediatric leukemia patients (Two Case Reports). Iran J Pediatr 22: 417-420, 2012.
    OpenUrlPubMed
  3. ↵
    1. Diamantaras AA,
    2. Dessypris N,
    3. Sergentanis TN,
    4. Ntouvelis E,
    5. Athanasiadou-Piperopoulou F,
    6. Baka M,
    7. Fragandrea I,
    8. Moschovi M,
    9. Polychronopoulou S,
    10. Stiakaki E,
    11. Panagiotakos D,
    12. Petridou E
    : Nutrition in early life and risk of childhood leukemia: A case control study in Greece. Cancer Causes Control 24: 117-124, 2013.
    OpenUrlPubMed
  4. ↵
    1. Mahmoud NN,
    2. Carothers AM,
    3. Grunberger D,
    4. Bilinski RT,
    5. Churchill MR,
    6. Martucci C,
    7. Newmark HL,
    8. Bertagnolli MM
    : Plant phenolics decrease intestinal tumors in an animal model of familial adenomatous polyposis. Carcinogenesis 21: 921-927, 2000.
    OpenUrlAbstract/FREE Full Text
    1. Mutoh M,
    2. Takahashi M,
    3. Fukuda K,
    4. Komatsu H,
    5. Enya T,
    6. Matsushima-Hibiya Y,
    7. Mutoh H,
    8. Sugimura T,
    9. Wakabayashi K
    : Suppression by flavonoids of cyclooxygenase-2 promoter-dependent transcriptional activity in colon cancer cells: Structure activity relationship. Jpn J Cancer Res 91: 686-691, 2000.
    OpenUrlCrossRef
  5. ↵
    1. Wenzel U,
    2. Kuntz S,
    3. Brendel MD,
    4. Daniel H
    : Dietary flavone is a potent apoptosis inducer in human colon carcinoma cells. Cancer Res 60: 3823-3831, 2000.
    OpenUrlAbstract/FREE Full Text
  6. ↵
    1. Tai MC,
    2. Tsang SY,
    3. Chang LY,
    4. Xue H
    : Therapeutic potential of wogonin: A naturally occurring flavonoid. CNS drug reviews 11: 141-150, 2005.
    OpenUrlPubMed
  7. ↵
    1. Wakabayashi I,
    2. Yasui K
    : Wogonin inhibits inducible prostaglandin E(2) production in macrophages. Eur J Pharmacol 406: 477-481, 2000.
    OpenUrlCrossRefPubMed
  8. ↵
    1. Lin CC,
    2. Kuo CL,
    3. Lee MH,
    4. Lai KC,
    5. Lin JP,
    6. Yang JS,
    7. Yu CS,
    8. Lu CC,
    9. Chiang JH,
    10. Chueh FS,
    11. Chung JG
    : Wogonin triggers apoptosis in human osteosarcoma U-2 OS cells through the endoplasmic reticulum stress, mitochondrial dysfunction and caspase-3-dependent signaling pathways. Int J Oncol 39: 217-224, 2011.
    OpenUrlPubMed
  9. ↵
    1. Yu CS,
    2. Yu FS,
    3. Chuang YC,
    4. Lu HF,
    5. Lin SY,
    6. Chiu TH,
    7. Chung JG
    : Wogonin inhibits N-acetyltransferase activity and gene expression in human leukemia HL-60 cells. Anticancer Res 25: 127-132, 2005.
    OpenUrlAbstract/FREE Full Text
  10. ↵
    1. Chung H,
    2. Jung YM,
    3. Shin DH,
    4. Lee JY,
    5. Oh MY,
    6. Kim HJ,
    7. Jang KS,
    8. Jeon SJ,
    9. Son KH,
    10. Kong G
    : Anticancer effects of wogonin in both estrogen receptor-positive and -negative human breast cancer cell lines in vitro and in nude mice xenografts. Int J Cancer 122: 816-822, 2008.
    OpenUrlCrossRefPubMed
  11. ↵
    1. Parajuli P,
    2. Joshee N,
    3. Rimando AM,
    4. Mittal S,
    5. Yadav AK
    : In vitro antitumor mechanisms of various Scutellaria extracts and constituent flavonoids. Planta Med 75: 41-48, 2009.
    OpenUrlPubMed
  12. ↵
    1. Fas SC,
    2. Baumann S,
    3. Zhu JY,
    4. Giaisi M,
    5. Treiber MK,
    6. Mahlknecht U,
    7. Krammer PH,
    8. Li-Weber M
    : Wogonin sensitizes resistant malignant cells to TNF-α and TRAIL-induced apoptosis. Blood 108: 3700-3706, 2006.
    OpenUrlAbstract/FREE Full Text
    1. Lee SO,
    2. Jeong YJ,
    3. Yu MH,
    4. Lee JW,
    5. Hwangbo MH,
    6. Kim CH,
    7. Lee IS
    : Wogonin suppresses TNF-α-induced MMP-9 expression by blocking the NF-κB activation via MAPK signaling pathways in human aortic smooth muscle cells. Biochem Biophys Res Commun 351: 118-125, 2006.
    OpenUrlCrossRefPubMed
  13. ↵
    1. Yang L,
    2. Zhang HW,
    3. Hu R,
    4. Yang Y,
    5. Qi Q,
    6. Lu N,
    7. Liu W,
    8. Chu YY,
    9. You QD,
    10. Guo QL
    : Wogonin induces G1 phase arrest through inhibiting CDK4 and cyclin D1 concomitant with an elevation in p21CIP1 in human cervical carcinoma HeLa cells. Biochem Cell Biol 87: 933-942, 2009.
    OpenUrlPubMed
  14. ↵
    1. Polier G,
    2. Ding J,
    3. Konkimalla BV,
    4. Eick D,
    5. Ribeiro N,
    6. Kohler R,
    7. Giaisi M,
    8. Efferth T,
    9. Desaubry L,
    10. Krammer PH,
    11. Li-Weber M
    : Wogonin and related natural flavones are inhibitors of CDK9 that induce apoptosis in cancer cells by transcriptional suppression of MCL-1. Cell Death Dis 2: e182, 2011.
    OpenUrlCrossRefPubMed
  15. ↵
    1. Chen CC,
    2. Hung TH,
    3. Wang YH,
    4. Lin CW,
    5. Wang PY,
    6. Lee CY,
    7. Chen SF
    : Wogonin improves histological and functional outcomes, and reduces activation of TLR4/NF-κB signaling after experimental traumatic brain injury. PLoS One 7: e30294, 2012.
    OpenUrlPubMed
  16. ↵
    1. Wang W,
    2. Guo QL,
    3. You QD,
    4. Zhang K,
    5. Yang Y,
    6. Yu J,
    7. Liu W,
    8. Zhao L,
    9. Gu HY,
    10. Hu Y,
    11. Tan Z,
    12. Wang XT
    : The anticancer activities of wogonin in murine sarcoma S180 both in vitro and in vivo. Biol Pharm Bull 29: 1132-1137, 2006.
    OpenUrlCrossRefPubMed
    1. Baumann S,
    2. Fas SC,
    3. Giaisi M,
    4. Muller WW,
    5. Merling A,
    6. Gulow K,
    7. Edler L,
    8. Krammer PH,
    9. Li-Weber M
    : Wogonin preferentially kills malignant lymphocytes and suppresses T-cell tumor growth by inducing PLCγ1- and Ca2+-dependent apoptosis. Blood 111: 2354-2363, 2008.
    OpenUrlAbstract/FREE Full Text
  17. ↵
    1. Lu N,
    2. Gao Y,
    3. Ling Y,
    4. Chen Y,
    5. Yang Y,
    6. Gu HY,
    7. Qi Q,
    8. Liu W,
    9. Wang XT,
    10. You QD,
    11. Guo QL
    : Wogonin suppresses tumor growth in vivo and VEGF-induced angiogenesis through inhibiting tyrosine phosphorylation of VEGFR2. Life Sci 82: 956-963, 2008.
    OpenUrlCrossRefPubMed
  18. ↵
    1. Perez AT,
    2. Arun B,
    3. Tripathy D,
    4. Tagliaferri MA,
    5. Shaw HS,
    6. Kimmick GG,
    7. Cohen I,
    8. Shtivelman E,
    9. Caygill KA,
    10. Grady D,
    11. Schactman M,
    12. Shapiro CL
    : A phase 1B dose escalation trial of Scutellaria barbata (BZL101) for patients with metastatic breast cancer. Breast Cancer Res Treat 120: 111-118, 2010.
    OpenUrlPubMed
  19. ↵
    1. Rugo H,
    2. Shtivelman E,
    3. Perez A,
    4. Vogel C,
    5. Franco S,
    6. Tan Chiu E,
    7. Melisko M,
    8. Tagliaferri M,
    9. Cohen I,
    10. Shoemaker M,
    11. Tran Z,
    12. Tripathy D
    : Phase I trial and antitumor effects of BZL101 for patients with advanced breast cancer. Breast Cancer Res Treat 105: 17-28, 2007.
    OpenUrlCrossRefPubMed
  20. ↵
    1. Lin CC,
    2. Yu CS,
    3. Yang JS,
    4. Lu CC,
    5. Chiang JH,
    6. Lin JP,
    7. Kuo CL,
    8. Chung JG
    : Chrysin, a natural and biologically active flavonoid, influences a murine leukemia model in vivo through enhancing populations of T- and B-cells, and promoting macrophage phagocytosis and NK cell cytotoxicity. In Vivo 26: 665-670, 2012.
    OpenUrlAbstract/FREE Full Text
  21. ↵
    1. Yu JS,
    2. Kim AK
    : Wogonin induces apoptosis by activation of ERK and p38 MAPKs signaling pathways and generation of reactive oxygen species in human breast cancer cells. Mol Cells 31: 327-335, 2011.
    OpenUrlPubMed
  22. ↵
    1. Lee DH,
    2. Kim C,
    3. Zhang L,
    4. Lee YJ
    : Role of p53, PUMA, and BAX in wogonin-induced apoptosis in human cancer cells. Biochem Pharmacol 75: 2020-2033, 2008.
    OpenUrlCrossRefPubMed
  23. ↵
    1. Liu ZL,
    2. Tanaka S,
    3. Horigome H,
    4. Hirano T,
    5. Oka K
    : Induction of apoptosis in human lung fibroblasts and peripheral lymphocytes in vitro by Shosaiko-to derived phenolic metabolites. Biol Pharm Bull 25: 37-41, 2002.
    OpenUrlCrossRefPubMed
  24. ↵
    1. Lee WR,
    2. Shen SC,
    3. Lin HY,
    4. Hou WC,
    5. Yang LL,
    6. Chen YC
    : Wogonin and fisetin induce apoptosis in human promyeloleukemic cells, accompanied by a decrease of reactive oxygen species, and activation of caspase 3 and Ca(2+)-dependent endonuclease. Biochem Pharmacol 63: 225-236, 2002.
    OpenUrlCrossRefPubMed
  25. ↵
    1. Sato S,
    2. Jansen PJ,
    3. Tedder TF
    : CD19 and CD22 expression reciprocally regulates tyrosine phosphorylation of Vav protein during B-lymphocyte signaling. Proc Natl Acad Sci USA 94: 13158-13162, 1997.
    OpenUrlAbstract/FREE Full Text
  26. ↵
    1. Kwon SH,
    2. Nam JI,
    3. Kim SH,
    4. Kim JH,
    5. Yoon JH,
    6. Kim KS
    : Kaempferol and quercetin, essential ingredients in Ginkgo bilboa extract, inhibit interleukin-1β-induced MUC5AC gene expression in human airway epithelial cells. Phytother Res 23: 1708-1712, 2009.
    OpenUrlPubMed
PreviousNext
Back to top

In this issue

In Vivo
Vol. 27, Issue 6
November-December 2013
  • Table of Contents
  • Table of Contents (PDF)
  • Index by author
  • Back Matter (PDF)
  • Ed Board (PDF)
  • Front Matter (PDF)
Print
Download PDF
Article Alerts
Sign In to Email Alerts with your Email Address
Email Article

Thank you for your interest in spreading the word on In Vivo.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Wogonin, a Natural and Biologically-active Flavonoid, Influences a Murine WEHI-3 Leukemia Model in Vivo Through Enhancing Populations of T- and B-Cells
(Your Name) has sent you a message from In Vivo
(Your Name) thought you would like to see the In Vivo web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
1 + 0 =
Solve this simple math problem and enter the result. E.g. for 1+3, enter 4.
Citation Tools
Wogonin, a Natural and Biologically-active Flavonoid, Influences a Murine WEHI-3 Leukemia Model in Vivo Through Enhancing Populations of T- and B-Cells
CHIN-CHUNG LIN, JEN-JYH LIN, PING-PING WU, CHI-CHENG LU, JO-HUA CHIANG, CHAO-LIN KUO, BIN-CHUAN JI, MING-HUEI LEE, AN-CHENG HUANG, JING-GUNG CHUNG
In Vivo Nov 2013, 27 (6) 733-738;

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Reprints and Permissions
Share
Wogonin, a Natural and Biologically-active Flavonoid, Influences a Murine WEHI-3 Leukemia Model in Vivo Through Enhancing Populations of T- and B-Cells
CHIN-CHUNG LIN, JEN-JYH LIN, PING-PING WU, CHI-CHENG LU, JO-HUA CHIANG, CHAO-LIN KUO, BIN-CHUAN JI, MING-HUEI LEE, AN-CHENG HUANG, JING-GUNG CHUNG
In Vivo Nov 2013, 27 (6) 733-738;
Twitter logo Facebook logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Abstract
    • Materials and Methods
    • Results
    • Discussion
    • Acknowledgements
    • References
  • Figures & Data
  • Info & Metrics
  • PDF

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Cited By...

  • Ethanol Extract of Hedyotis diffusa Willd Affects Immune Responses in Normal Balb/c Mice In Vivo
  • Crude Extract of Polygonum Cuspidatum Promotes Immune Responses in Leukemic Mice Through Enhancing Phagocytosis of Macrophage and Natural Killer Cell Activities In Vivo
  • {alpha}-Phellandrene Alters Expression of Genes Associated with DNA Damage, Cell Cycle, and Apoptosis in Murine Leukemia WEHI-3 Cells
  • Google Scholar

More in this TOC Section

  • RXRG as a Novel Biomarker and its Correlation With Immune Infiltration in Thyroid Carcinoma
  • Treatment of Recurrent Aneurysmal Bone Cyst in a Dog Using Bone Morphogenetic Protein-2-loaded Alginate Microbeads
  • Association of MMP-11 Genotypes With Colorectal Cancer in Taiwan
Show more Experimental Studies

Similar Articles

Keywords

  • Wogonin
  • flavonoid
  • Balb/c mice
  • murine WEHI-3 leukemia model
In Vivo

© 2025 In Vivo

Powered by HighWire