Induction of HT-29 Colon Cancer Cells Apoptosis by Pyrogallol with Growth Inhibiting Efficacy Against Drug Resistant Helicobacter Pylori

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Abstract

Background: Colon cancer is the most aggressive form of cancers, that causes 0.5 million deaths per year around the globe. Targeting colon cancer by conventional therapeutic options elicits toxicity. Traditional medicines take lead to alleviate the existing clinical challenges.

Objective: To investigate anti bacterial activity against Helicobacter Pylori and in vitro anti colon cancer activity by Acacia nilotica extract (ACE) and its active constituent pyrogallol.
Methods: Pyrogallol isolated from A. nilotica by column chromatography and HPLC and structure was elucidated by spectral analysis. Antibacterial activity was done by flow cytometry. Cyto-toxicity was measured by MTT assay. Apoptotic morphology and nuclear fragmentation was assessed with AO/ethidium bromide and DAPI staining. Western blot used to analyze the molecular mechanism of apoptosis. Cell cycle arrest was determined using flow cytometry of propidium iodide stained cells. Cell migration was determined by wound healing assay.
Results: ACE (20 μg/ml) and pyrogallol (10 μg/ml) treatment reduced the survival of H.pylori at 61% and 62%, respectively. MTT results showed that HT-29 cells are more sensitive to pyrogallol with an IC50 value of 35μg/ml compare to ACE. Pyrogallol treated HT-29 cells reached a dead state i.e. late apoptotic state with severe nuclear fragmentation. Pyrogallol induced apoptosis by simultaneous down regulation of Bcl-2 and up regulation of BAX and cytochrome c. Pyrogallol arrested HT-29 cells in S and G2/M phase of cell cycle. Further, pyrogallol exhibited marked anti metastatic potential by inhibiting the migration of HT-29 cells dose dependently.
Conclusion: Both ACE and pyrogallol repressed the growth of H.pylori and as significant anti colon cancer agent.
LanguageEnglish
Pages1875-1884
Number of pages10
JournalAnti-Cancer Agents in Medicinal Chemistry
Volume18
Issue number13
Early online dateSep 2018
DOIs
Publication statusPublished - 2018

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Pyrogallol
Helicobacter pylori
Colonic Neoplasms
Apoptosis
Acacia
HT29 Cells
Growth
Pharmaceutical Preparations
Pylorus
Flow Cytometry
Ethidium
Propidium
G2 Phase
Traditional Medicine
Cell Cycle Checkpoints
Cytochromes c
Cell Division
Wound Healing
Inhibitory Concentration 50
Cell Movement

Cite this

@article{31d2979853bd4c1b87c300a1af0c1571,
title = "Induction of HT-29 Colon Cancer Cells Apoptosis by Pyrogallol with Growth Inhibiting Efficacy Against Drug Resistant Helicobacter Pylori",
abstract = "Background: Colon cancer is the most aggressive form of cancers, that causes 0.5 million deaths per year around the globe. Targeting colon cancer by conventional therapeutic options elicits toxicity. Traditional medicines take lead to alleviate the existing clinical challenges.Objective: To investigate anti bacterial activity against Helicobacter Pylori and in vitro anti colon cancer activity by Acacia nilotica extract (ACE) and its active constituent pyrogallol.Methods: Pyrogallol isolated from A. nilotica by column chromatography and HPLC and structure was elucidated by spectral analysis. Antibacterial activity was done by flow cytometry. Cyto-toxicity was measured by MTT assay. Apoptotic morphology and nuclear fragmentation was assessed with AO/ethidium bromide and DAPI staining. Western blot used to analyze the molecular mechanism of apoptosis. Cell cycle arrest was determined using flow cytometry of propidium iodide stained cells. Cell migration was determined by wound healing assay.Results: ACE (20 μg/ml) and pyrogallol (10 μg/ml) treatment reduced the survival of H.pylori at 61{\%} and 62{\%}, respectively. MTT results showed that HT-29 cells are more sensitive to pyrogallol with an IC50 value of 35μg/ml compare to ACE. Pyrogallol treated HT-29 cells reached a dead state i.e. late apoptotic state with severe nuclear fragmentation. Pyrogallol induced apoptosis by simultaneous down regulation of Bcl-2 and up regulation of BAX and cytochrome c. Pyrogallol arrested HT-29 cells in S and G2/M phase of cell cycle. Further, pyrogallol exhibited marked anti metastatic potential by inhibiting the migration of HT-29 cells dose dependently.Conclusion: Both ACE and pyrogallol repressed the growth of H.pylori and as significant anti colon cancer agent.",
keywords = "Acacia nilotica, pyrogallol, Helicobacter pylori, colon cancer, apoptosis, HT-29 cells",
author = "Farideh Javid",
year = "2018",
doi = "10.2174/1871520618666180806104902",
language = "English",
volume = "18",
pages = "1875--1884",
journal = "Anti-Cancer Agents in Medicinal Chemistry",
issn = "1871-5206",
publisher = "Bentham Science Publishers B.V.",
number = "13",

}

TY - JOUR

T1 - Induction of HT-29 Colon Cancer Cells Apoptosis by Pyrogallol with Growth Inhibiting Efficacy Against Drug Resistant Helicobacter Pylori

AU - Javid, Farideh

PY - 2018

Y1 - 2018

N2 - Background: Colon cancer is the most aggressive form of cancers, that causes 0.5 million deaths per year around the globe. Targeting colon cancer by conventional therapeutic options elicits toxicity. Traditional medicines take lead to alleviate the existing clinical challenges.Objective: To investigate anti bacterial activity against Helicobacter Pylori and in vitro anti colon cancer activity by Acacia nilotica extract (ACE) and its active constituent pyrogallol.Methods: Pyrogallol isolated from A. nilotica by column chromatography and HPLC and structure was elucidated by spectral analysis. Antibacterial activity was done by flow cytometry. Cyto-toxicity was measured by MTT assay. Apoptotic morphology and nuclear fragmentation was assessed with AO/ethidium bromide and DAPI staining. Western blot used to analyze the molecular mechanism of apoptosis. Cell cycle arrest was determined using flow cytometry of propidium iodide stained cells. Cell migration was determined by wound healing assay.Results: ACE (20 μg/ml) and pyrogallol (10 μg/ml) treatment reduced the survival of H.pylori at 61% and 62%, respectively. MTT results showed that HT-29 cells are more sensitive to pyrogallol with an IC50 value of 35μg/ml compare to ACE. Pyrogallol treated HT-29 cells reached a dead state i.e. late apoptotic state with severe nuclear fragmentation. Pyrogallol induced apoptosis by simultaneous down regulation of Bcl-2 and up regulation of BAX and cytochrome c. Pyrogallol arrested HT-29 cells in S and G2/M phase of cell cycle. Further, pyrogallol exhibited marked anti metastatic potential by inhibiting the migration of HT-29 cells dose dependently.Conclusion: Both ACE and pyrogallol repressed the growth of H.pylori and as significant anti colon cancer agent.

AB - Background: Colon cancer is the most aggressive form of cancers, that causes 0.5 million deaths per year around the globe. Targeting colon cancer by conventional therapeutic options elicits toxicity. Traditional medicines take lead to alleviate the existing clinical challenges.Objective: To investigate anti bacterial activity against Helicobacter Pylori and in vitro anti colon cancer activity by Acacia nilotica extract (ACE) and its active constituent pyrogallol.Methods: Pyrogallol isolated from A. nilotica by column chromatography and HPLC and structure was elucidated by spectral analysis. Antibacterial activity was done by flow cytometry. Cyto-toxicity was measured by MTT assay. Apoptotic morphology and nuclear fragmentation was assessed with AO/ethidium bromide and DAPI staining. Western blot used to analyze the molecular mechanism of apoptosis. Cell cycle arrest was determined using flow cytometry of propidium iodide stained cells. Cell migration was determined by wound healing assay.Results: ACE (20 μg/ml) and pyrogallol (10 μg/ml) treatment reduced the survival of H.pylori at 61% and 62%, respectively. MTT results showed that HT-29 cells are more sensitive to pyrogallol with an IC50 value of 35μg/ml compare to ACE. Pyrogallol treated HT-29 cells reached a dead state i.e. late apoptotic state with severe nuclear fragmentation. Pyrogallol induced apoptosis by simultaneous down regulation of Bcl-2 and up regulation of BAX and cytochrome c. Pyrogallol arrested HT-29 cells in S and G2/M phase of cell cycle. Further, pyrogallol exhibited marked anti metastatic potential by inhibiting the migration of HT-29 cells dose dependently.Conclusion: Both ACE and pyrogallol repressed the growth of H.pylori and as significant anti colon cancer agent.

KW - Acacia nilotica

KW - pyrogallol

KW - Helicobacter pylori

KW - colon cancer

KW - apoptosis

KW - HT-29 cells

U2 - 10.2174/1871520618666180806104902

DO - 10.2174/1871520618666180806104902

M3 - Article

VL - 18

SP - 1875

EP - 1884

JO - Anti-Cancer Agents in Medicinal Chemistry

T2 - Anti-Cancer Agents in Medicinal Chemistry

JF - Anti-Cancer Agents in Medicinal Chemistry

SN - 1871-5206

IS - 13

ER -