Boswellic acid disables signal transduction of IL-6–STAT-3 in Ehrlich ascites tumor bearing irradiated mice

2016 ◽  
Vol 94 (4) ◽  
pp. 307-313 ◽  
Author(s):  
Enas Mahmoud Moustafa ◽  
Noura Magdy Thabet ◽  
Khaled Shaaban Azab
Keyword(s):  
Signal Transduction ◽  
Caspase 3 ◽  
Tumor Tissue ◽  
Ehrlich Ascites Carcinoma ◽  
Boswellic Acid ◽  
Over Expression ◽  
Radiation Data ◽  
Tumor Bearing ◽  
Ehrlich Ascites ◽  
Specific Impact

Boswellic acid (BA) is known for its ability to trigger apoptosis as well as to inhibit angiogenesis in tumor tissue. In this study, we investigated the effect of BA on the IL-6–STAT-3 signalling pathway in irradiated mice bearing solid tumors of Ehrlich ascites carcinoma (EAC). For this, we administered BA (25 mg·(kg body mass)–1·day–1, by intraperitoneal injection) to mice with EAC, and then exposed them to 4 Gy of gamma radiation. Data analyses of the results revealed a specific impact from BA on IL-6R mRNA and survivin mRNA in EACs and irradiated EAC-bearing mice. Also, significant improvements were observed in the protein expression of JAK-1, P-JAK-1, STAT-3, P-STAT-3, and caspase-3, as well as VEGF and IL-6 levels. We propose that BA interfered with IL-6–STAT-3 signal transduction, thereby preventing the activation of caspase-3 and subsequently triggering the process of apoptosis. However, the alternative angiogenesis pathway, which includes the over-expression of VEGF and which depends on IL-6–STAT-3 signalling, was inhibited by the action of BA. Thus, we recommend that therapeutic strategies for cancer should include treatment with BA.

scholarly journals Fuzheng Qingjie Granules Inhibit Growth of Hepatoma Cells via Inducing Mitochondria-Mediated Apoptosis and Enhancing Immune Function

2016 ◽  
Vol 16 (3) ◽  
pp. 329-338 ◽  
Author(s):  
Xuzheng Chen ◽  
Zhiyun Cao ◽  
Youquan Zhang ◽  
Jinnong Li ◽  
Suqing Wang ◽  
...  
Keyword(s):  
T Cells ◽  
Cytochrome C ◽  
Immune Function ◽  
Nk Cells ◽  
Hepg2 Cells ◽  
Caspase 3 ◽  
Tumor Tissue ◽  
Hepatoma Cells ◽  
Tumor Bearing ◽  
Tnf Α

Fuzheng Qingjie (FZQJ) granules, a compound Chinese medicine, have been used as an adjuvant therapy for alimentary tract cancers. However, the underlying anticancer mechanisms are still not well understood. In the present study, HepG2 cells were treated with FZQJ-containing serum. Cell proliferation was evaluated using MTT assay. Apoptosis was analyzed using a flow cytometer. Cell ultrastructure was observed under a transmission electron microscope. The mitochondrial membrane potential (Δψ) was examined with JC-1 dye. In H22 tumor–bearing mice, CD4+ T cells, CD8+ T cells, CD3+ T cells, and natural killer (NK) cells in peripheral blood were evaluated cytometrically. Interleukin (IL)-2 and tumor necrosis factor (TNF)-α levels were measured using radioimmunoassay.The mRNA levels of Bax and Bcl-2 were examined by reverse transcription–polymerase chain reaction. The protein levels of Bax, Bcl-2, cytochrome C, caspase 3 and 9, PARP, and CD69 were examined by Western blotting. The apoptotic cells in tissues were observed using TUNEL method. Alanine transaminase (ALT), aspartate transaminase (AST), blood urea nitrogen (BUN), and creatinine (CRE) were detected by an automatic biochemical analyzer. The results showed that FZQJ-containing serum remarkably inhibited proliferation of HepG2 cells in dose- and time-dependent manners, induced HepG2 cell apoptosis and caused a decrease of Δψ. Analysis of tumor tissue showed that FZQJ-induced apoptosis was accompanied by downregulation of Bcl-2 and upregulation of Bax, release of cytochrome c, activation of caspase 3 and 9, and cleavage of PARP. In addition, FZQJ increased the percentages of CD4+ T and NK cells, the ratio of CD4+/CD8+ T cells as well as the levels of serum TNF-α. FZQJ also increased CD69 expression in tumor tissue. No hepatorenal toxicity was observed in H22 tumor–bearing mice. These results indicated that FZQJ could inhibit the growth of hepatoma cells via regulating immune function and inducing mitochondria mediated apoptosis.

scholarly journals Gan-Qing-Ning Formula Inhibits the Growth of Hepatocellular Carcinoma by Promoting Apoptosis and Inhibiting Angiogenesis in H22 Tumor-Bearing Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Fan-Yan Zeng ◽  
Kai-Li Zhao ◽  
Le-Zhen Lin ◽  
Ying Deng ◽  
Si Qin ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Antitumor Effect ◽  
Caspase 3 ◽  
Tumor Tissue ◽  
Mitochondrial Apoptosis ◽  
Apoptosis Pathway ◽  
Expression Levels ◽  
Mitochondrial Apoptosis Pathway ◽  
Tumor Bearing ◽  
Mrna Expression Levels

Objective. Gang-Qing-Ning (GQN) is a traditional Chinese medicine formula that has been used in the treatment of hepatocellular carcinoma (HCC) in the folk population for decades. However, scientific validation is still necessary to lend credibility to the traditional use of GQN against HCC. This study investigates the antitumor effect of GQN on H22 tumor-bearing mice and its possible mechanism. Methods. Fifty H22 tumor-bearing mice were randomly assigned to five groups. Three groups were treated with high, medium, and low dosages of GQN (27.68, 13.84, and 6.92 g/kg, respectively); the positive control group was treated with cytoxan (CTX) (20 mg/kg) and the model group was treated with normal saline. After 10 days’ treatment, the tumor inhibitory rates were calculated. Pathological changes in tumor tissue were observed, and the key proteins and genes of the mitochondrial apoptosis pathway were measured, as well as the mRNA expression levels of VEGF in tumor tissue. Results. The tumor inhibitory rates of high, medium, and low dosages of GQN groups were 47.39%, 38.26%, and 22.17%, respectively. The high dosage of the GQN group significantly increased the protein and mRNA expression levels of Bax, Cyt-C, and cleaved Caspase 3 (or Caspase 3) (P<0.01) but decreased the expression levels of Bcl-2, VEGF, and microvessel density (MVD) (P<0.01). Conclusions. The high dosage of GQN can significantly inhibit the tumor growth in H22 tumor-bearing mice. It exerts the antitumor effect by enhancing proapoptotic factors and inhibiting the antiapoptotic factor of the mitochondrial apoptosis pathway and inhibiting tumor angiogenesis.

Tube Leukocyte Adherence-Inhibition Response to Related and Unrelated Tumor Antigens in Mammary Tumor-Bearing Mice

1983 ◽  
Vol 69 (4) ◽  
pp. 299-303 ◽  
Author(s):  
Utpala Chattopadhyay ◽  
Surajit Guha
Keyword(s):  
Mammary Tumor ◽  
Tumor Antigens ◽  
Ehrlich Ascites Carcinoma ◽  
Tumor Burden ◽  
Leukocyte Adherence ◽  
Tumor Bearing ◽  
Inhibition Response ◽  
Ehrlich Ascites ◽  
Leukocyte Adherence Inhibition ◽  
Adherence Inhibition

Tube leukocyte adherence-inhibition response to syngeneic mammary tumor antigens and alloantigens from Ehrlich ascites carcinoma and fibrosarcoma was studied in spontaneous mammary tumor-bearing C3H/Jax mice. The mice with limited tumor burden responded significantly to the mammary tumor antigen and the Ehrlich ascites carcinoma antigen. The reactivity disappeared with increased tumor load. Oscillatory responses in leukocyte adherence inhibition to the reactive antigens was observed with increasing tumor weight. There was no response to the alloantigen of fibrosarcoma.

Effects of ethanol extract of Pisonia aculeata Linn. on ehrlich ascites carcinoma tumor bearing mice

2008 ◽  
Vol 2 (1) ◽  
pp. 50 ◽  
Author(s):  
Raju Senthilkumar ◽  
Rangasamy Manivannan ◽  
Ayyasamy Balasubramaniam ◽  
Thangavel Sivakumar ◽  
Balasubramanian Rajkapoor
Keyword(s):  
Ethanol Extract ◽  
Ehrlich Ascites Carcinoma ◽  
Tumor Bearing ◽  
Ehrlich Ascites ◽  
Carcinoma Tumor

THE MECHANISM OF PYRIDINE NUCLEOTIDE SYNTHESIS IN EHRLICH ASCITES CARCINOMA AND HOST LIVER

1967 ◽  
Vol 45 (2) ◽  
pp. 179-190 ◽  
Author(s):  
J. Purko ◽  
H. B. Stewart
Keyword(s):  
Nicotinic Acid ◽  
Ehrlich Ascites Carcinoma ◽  
Pyridine Nucleotide ◽  
Host Liver ◽  
Nucleotide Synthesis ◽  
Tumor Bearing ◽  
Ehrlich Ascites ◽  
Metabolic Products ◽  
Ehrlich Ascites Cells ◽  
Specific Activities

Labeled nicotinamide–adenine dinucleotide (NAD) and nicotinic acid–adenine dinucleotide (NacAD) were identified following Dowex 2 (formate) chromatography of extracts of Ehrlich ascites cells and of livers of mice 3 and 6 h after injection of nicotinamide (Nam) (500 mg/kg) containing Nam-7-14C, and 3 h after injection of nicotinic acid (Nac) (50 mg/kg) containing Nac-7-14C into tumor-bearing animals. Labeled Nac mononucleotide (NacMN) was also identified in the liver extracts. The urinary metabolic products of the precursors were separated and partially characterized. Liver appeared to be somewhat more active in synthesis of NAD than tumor; the more efficient amidation of NacAD to NAD in liver probably contributes to this difference. The results are consistent with NacAD being an intermediate in NAD biosynthesis. Investigations of extracts of acetone powders of tumor provided evidence for two possible routes of synthesis (via NMN, and NacMN–NacAD): (1) Extracts incubated with Nam mononucleotide (NMN) and ATP formed NAD. (2) Extracts incubated with Nac-14C or Nam-14C with suitable supplementation gave rise to labeled NacMN, NacAD and NAD. These substances were isolated and their specific activities determined. Glutamine appeared to enhance NAD formation at the expense of NacAD. Although a net accumulation of NAD did not occur, the formation of Nam-14C from Nac-14C and the demonstration of NADase in the preparations suggested that NAD was formed but rapidly degraded.

scholarly journals Antitumor Activity of Diospyros peregrina on Ehrlich Ascites Carcinoma in Mice

2011 ◽  
Vol 3 (2) ◽  
pp. 413-419 ◽  
Author(s):  
A. B. Raju ◽  
Venu Gopal Y ◽  
Ravindranath A ◽  
Kalpana G ◽  
Prabhakar Reddy V
Keyword(s):  
Antitumor Activity ◽  
Life Span ◽  
Tumor Volume ◽  
Methanol Extract ◽  
Viable Cell ◽  
Ehrlich Ascites Carcinoma ◽  
Tumor Inoculation ◽  
Tumor Bearing ◽  
Hematological Profile ◽  
Ehrlich Ascites

The methanol extract of Diospyros peregrina (Ebenaceae) bark (MEDP) were evaluated for antitumor activity against Ehrlich ascites carcinoma (EAC)-bearing swiss albino mice. The extract was administered at the doses of 200 and 400 mg/kg body weight per day for 14 days after 24 h of tumor inoculation. After the last dose and 18 h fasting, the mice were sacrificed. The present study deals with the effect of MEDP on the growth of transplantable murine tumor, life span of EAC-bearing hosts and hematological profile  MEDP caused significant (P < 0.01) decrease in tumor volume, packed cell volume, and viable cell count; and it prolonged the life span of EAC-tumor bearing mice. Hematological profile converted to more or less normal levels in extract-treated mice. The results indicate that MEDP exhibited significant antitumor activity in EAC-bearing mice. Keywords: Diospyros peregrina; Ehrlich ascites carcinoma; Antitumor. © 2011 JSR Publications. ISSN: 2070-0237 (Print); 2070-0245 (Online). All rights reserved. doi:10.3329/jsr.v3i2.6787                J. Sci. Res. 3 (2), 413-419 (2011)

scholarly journals Anticancer potential of Michelia champaca Linn. bark against Ehrlich ascites carcinoma (EAC) cells in Swiss albino mice

2019 ◽  
Vol 09 ◽  
Author(s):  
Ruksana Yesmin ◽  
Plabon Kumar Das ◽  
Hazrat Belal ◽  
Suraiya Aktar ◽  
Ayesha Siddika ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Ehrlich Ascites Carcinoma ◽  
Bark Extract ◽  
Tumor Cell Proliferation ◽  
Tumor Weight ◽  
Tumor Bearing ◽  
Ehrlich Ascites ◽  
Eac Cells

Background: Adverse side effects of currently available therapies against cancer, leads scientists to find effective compounds from natural sources. Objective: In the present study, stem-bark of Mycelia champaca is subjected to evaluate its anti-proliferative effect against Ehrlich ascites carcinoma (EAC) cells. To date, anti-proliferative effects of M. champaca bark extract against EAC cell line has not been reported elsewhere. Therefore, we intended to investigate the anti-proliferative potential of M. champaca bark extract against EAC cells in vivo. Methods: In vivo anticancer activity was evaluated against EAC cells bearing Swiss albino mice by monitoring parameters such as tumor cell proliferation, tumor weight measurement, and survival time etc. The mechanism of EAC killing was examined by observation of cell morphology and analysis the expression of certain cancer related genes. In vitro antioxidant potentiality was determined in terms of several common antioxidant assays. In addition, total phenolic and flavonoids contents were measured to insure the presence of phytochemicals. Results: M. champaca bark extract showed strong antioxidant activities which were found to be strongly correlated (P< 0.001) with phenolics and flavonoids contents. Furthermore, it was found that bark extract decreased tumor cell proliferation (77.46%; P< 0.01), tumor weight (42.13%; P< 0.001) and increased life span of tumor bearing mice (71.97%; P< 0.01) at the dose of 250mg/kg (intraperitoneal; i.p.). M. champaca bark also altered the depleted hematological parameters such as red blood cell, white blood cell, hemoglobin (Hb%) towards normal in tumor bearing mice. In addition, upregulation ofp53, Bax and downregulation Bcl-2 followed by treatmentindicated M. champacabark could induce apoptosis of EAC cells. Conclusion: These results indicated that MEMCB possesses significant cytotoxic activities against EAC cells and has a strong in vitro antioxidant capacity. Therefore, bark of M. champaca could be considered as a potential resource of anti-cancer agents, which might be used to formulate effective anticancer drugs.

Sign in / Sign up

Export Citation Format

Share Document