Apoptosis induction and inhibition of hyperplasia formation by 2-[piperidinoethoxyphenyl]-3-[4-hydroxyphenyl]- 2H-benzo(b)pyran in rat uterus

Vishal Chandra, Iram Fatima, Ruchi Saxena, Shakti Kitchlu, Sharad Sharma, Mohammad Kamil Hussain, Kanchan Hajela, Preeti Bajpai, Anila Dwivedi

Research output: Contribution to journalArticle

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Abstract

OBJECTIVE: The study was undertaken to explore the antiproliferative mechanism of action of 2-[piperidinoethoxyphenyl]-3-[4-hydroxyphenyl]- 2H-benzo(b)pyran (K-1) in estradiol-induced rat uterine hyperplasia. STUDY DESIGN: Adult ovariectomized rats received vehicle or estradiol alone (20μg/kg) or estradiol along with K-1 (100 or 200μg/kg) for 14 days. Uterine histomorphometric analysis and immunoblotting were performed. Caspase-3 activity and terminal deoxynucleotidyl transferase- mediated nick end-labeling staining were performed to analyze the apoptotic potential of compound. RESULTS: Compound inhibited estradiol-induced uterine weight and histomorphometric changes pertaining to endometrial growth and down-regulated the expression of estrogen response element and activator protein-1 regulated genes and transcription factors. The compound significantly induced apoptosis, interfered with Akt activation, decreased X-linked inhibitor of apoptosis protein expression leading to an increased cleavage of caspase-9, caspase-3, poly(adenosine diphosphate- ribose) polymerase, increased Bax/Bcl2 ratio, and caspase-3 activity. CONCLUSION: K-1 inhibits endometrial proliferation via nonclassical estrogen receptor signaling mechanisms. It interfered with Akt activation and induced apoptosis via the intrinsic pathway and inhibited estradiol- induced hyperplasia formation in rat uterus.

Original languageEnglish (US)
Pages (from-to)362.e1-362.e11
JournalAmerican Journal of Obstetrics and Gynecology
Volume205
Issue number4
DOIs
StatePublished - Jan 1 2011

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Uterus
Hyperplasia
Estradiol
Apoptosis
Caspase 3
X-Linked Inhibitor of Apoptosis Protein
Poly Adenosine Diphosphate Ribose
DNA Nucleotidylexotransferase
Caspase 9
Transcription Factor AP-1
Response Elements
Immunoblotting
Estrogen Receptors
Estrogens
Transcription Factors
2-(piperidinoethoxyphenyl)-3-(4-hydroxyphenyl)-2H-benzo(b)pyran
Staining and Labeling
Weights and Measures
Growth
Genes

All Science Journal Classification (ASJC) codes

  • Obstetrics and Gynecology

Cite this

Apoptosis induction and inhibition of hyperplasia formation by 2-[piperidinoethoxyphenyl]-3-[4-hydroxyphenyl]- 2H-benzo(b)pyran in rat uterus. / Chandra, Vishal; Fatima, Iram; Saxena, Ruchi; Kitchlu, Shakti; Sharma, Sharad; Hussain, Mohammad Kamil; Hajela, Kanchan; Bajpai, Preeti; Dwivedi, Anila.

In: American Journal of Obstetrics and Gynecology, Vol. 205, No. 4, 01.01.2011, p. 362.e1-362.e11.

Research output: Contribution to journalArticle

Chandra, Vishal ; Fatima, Iram ; Saxena, Ruchi ; Kitchlu, Shakti ; Sharma, Sharad ; Hussain, Mohammad Kamil ; Hajela, Kanchan ; Bajpai, Preeti ; Dwivedi, Anila. / Apoptosis induction and inhibition of hyperplasia formation by 2-[piperidinoethoxyphenyl]-3-[4-hydroxyphenyl]- 2H-benzo(b)pyran in rat uterus. In: American Journal of Obstetrics and Gynecology. 2011 ; Vol. 205, No. 4. pp. 362.e1-362.e11.
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abstract = "OBJECTIVE: The study was undertaken to explore the antiproliferative mechanism of action of 2-[piperidinoethoxyphenyl]-3-[4-hydroxyphenyl]- 2H-benzo(b)pyran (K-1) in estradiol-induced rat uterine hyperplasia. STUDY DESIGN: Adult ovariectomized rats received vehicle or estradiol alone (20μg/kg) or estradiol along with K-1 (100 or 200μg/kg) for 14 days. Uterine histomorphometric analysis and immunoblotting were performed. Caspase-3 activity and terminal deoxynucleotidyl transferase- mediated nick end-labeling staining were performed to analyze the apoptotic potential of compound. RESULTS: Compound inhibited estradiol-induced uterine weight and histomorphometric changes pertaining to endometrial growth and down-regulated the expression of estrogen response element and activator protein-1 regulated genes and transcription factors. The compound significantly induced apoptosis, interfered with Akt activation, decreased X-linked inhibitor of apoptosis protein expression leading to an increased cleavage of caspase-9, caspase-3, poly(adenosine diphosphate- ribose) polymerase, increased Bax/Bcl2 ratio, and caspase-3 activity. CONCLUSION: K-1 inhibits endometrial proliferation via nonclassical estrogen receptor signaling mechanisms. It interfered with Akt activation and induced apoptosis via the intrinsic pathway and inhibited estradiol- induced hyperplasia formation in rat uterus.",
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AU - Fatima, Iram

AU - Saxena, Ruchi

AU - Kitchlu, Shakti

AU - Sharma, Sharad

AU - Hussain, Mohammad Kamil

AU - Hajela, Kanchan

AU - Bajpai, Preeti

AU - Dwivedi, Anila

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N2 - OBJECTIVE: The study was undertaken to explore the antiproliferative mechanism of action of 2-[piperidinoethoxyphenyl]-3-[4-hydroxyphenyl]- 2H-benzo(b)pyran (K-1) in estradiol-induced rat uterine hyperplasia. STUDY DESIGN: Adult ovariectomized rats received vehicle or estradiol alone (20μg/kg) or estradiol along with K-1 (100 or 200μg/kg) for 14 days. Uterine histomorphometric analysis and immunoblotting were performed. Caspase-3 activity and terminal deoxynucleotidyl transferase- mediated nick end-labeling staining were performed to analyze the apoptotic potential of compound. RESULTS: Compound inhibited estradiol-induced uterine weight and histomorphometric changes pertaining to endometrial growth and down-regulated the expression of estrogen response element and activator protein-1 regulated genes and transcription factors. The compound significantly induced apoptosis, interfered with Akt activation, decreased X-linked inhibitor of apoptosis protein expression leading to an increased cleavage of caspase-9, caspase-3, poly(adenosine diphosphate- ribose) polymerase, increased Bax/Bcl2 ratio, and caspase-3 activity. CONCLUSION: K-1 inhibits endometrial proliferation via nonclassical estrogen receptor signaling mechanisms. It interfered with Akt activation and induced apoptosis via the intrinsic pathway and inhibited estradiol- induced hyperplasia formation in rat uterus.

AB - OBJECTIVE: The study was undertaken to explore the antiproliferative mechanism of action of 2-[piperidinoethoxyphenyl]-3-[4-hydroxyphenyl]- 2H-benzo(b)pyran (K-1) in estradiol-induced rat uterine hyperplasia. STUDY DESIGN: Adult ovariectomized rats received vehicle or estradiol alone (20μg/kg) or estradiol along with K-1 (100 or 200μg/kg) for 14 days. Uterine histomorphometric analysis and immunoblotting were performed. Caspase-3 activity and terminal deoxynucleotidyl transferase- mediated nick end-labeling staining were performed to analyze the apoptotic potential of compound. RESULTS: Compound inhibited estradiol-induced uterine weight and histomorphometric changes pertaining to endometrial growth and down-regulated the expression of estrogen response element and activator protein-1 regulated genes and transcription factors. The compound significantly induced apoptosis, interfered with Akt activation, decreased X-linked inhibitor of apoptosis protein expression leading to an increased cleavage of caspase-9, caspase-3, poly(adenosine diphosphate- ribose) polymerase, increased Bax/Bcl2 ratio, and caspase-3 activity. CONCLUSION: K-1 inhibits endometrial proliferation via nonclassical estrogen receptor signaling mechanisms. It interfered with Akt activation and induced apoptosis via the intrinsic pathway and inhibited estradiol- induced hyperplasia formation in rat uterus.

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