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Casticin, a flavonoid isolated from Vitex rotundifolia, inhibits prolactin release in vivo and in vitro
Aim: To investigate the anti-hyperprolactinemia activity of casticin, a flavonoid isolated from Vitex rotundifolia, and elucidate its molecular mechanism. Methods: Hyperprolactinemia (MIHP) was induced by administration of metoclopramide dihydrochloride (50 mg/kg, tid, ip, for 10 d) in SD rats and t...
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Published in: | Acta pharmacologica Sinica 2010-12, Vol.31 (12), p.1564-1568 |
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description | Aim: To investigate the anti-hyperprolactinemia activity of casticin, a flavonoid isolated from Vitex rotundifolia, and elucidate its molecular mechanism. Methods: Hyperprolactinemia (MIHP) was induced by administration of metoclopramide dihydrochloride (50 mg/kg, tid, ip, for 10 d) in SD rats and the primary pituitary cells were prepared from the pituitary glands of the SD rats. Prolactin concentrations were measured using a radioimmunoassay. Cell viability was measured using an MTT assay. The mRNA expression of estrogen receptor alpha and beta in rat pituitary cells was measured using semi-quantitative RT-PCR analysis. Results: The level of serum prolactin in the MIHP model group was 2.1 fold higher than that in the untreated control group (P〈0.01). Casticin (10, 20, and 40 mg/kg, ip, for 7 d) reduced serum prolactin levels by 33.9%, 54.3%, and 64.7%, respectively (P〈0.01). The positive control drug bromocriptine 1 mg/kg decreased the serum prolactin concentration in MIHP rats by 44.9%. 1713-Estradiol (E2) significantly increased the proliferation of pituitary cells and casticin (1 and 10 μmol/L) markedly inhibited E2-induced pituitary cell proliferation by 27.7% and 42.1%, respectively. Stimulation of pituitary cells with E2 increased prolactin secretion into the cell culture supernatants, and casticin (0.1, 1, and 10 μmol/L) significantly inhibited the prolactin release stimulated by E2 in a concentration-dependent manner. Casticin (1 and 10 μmol/L) significantly inhibited ERa mRNA expression in pituitary cells stimulated with E2 (P〈O.01) but increased ERI3 mRNA expression at a concentration of 10 μmol/L (P〈0.01). However, casticin had no effects on proliferation and prolectin release of the unstimulated primary pituitary cells in vitro. Conclusion: Casticin inhibited the release of prolactin from pituitary cells of SD rats stimulated with E2 in vivo and in vitro. These effects might be related with inhibiting the ERα mRNA expression and increasing the ERβ mRNA expression. |
doi_str_mv | 10.1038/aps.2010.178 |
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fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4002951</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>36071327</cqvip_id><sourcerecordid>2203390731</sourcerecordid><originalsourceid>FETCH-LOGICAL-c503t-1dfce1d521e1a3fd497374584c19d40651cecf62eba93e8e41fec5bdb00e2a473</originalsourceid><addsrcrecordid>eNpVkc9vVCEQx4mxaWvtzbMhnve1DPB-XUzMxlaTJl7UK-HBsEt9C1tgN_W_l83WVk8MmU--M5MPIe-AXQETw7Xe5ivODr9-eEXOoZdt0_NWvq5110Mj2SDOyJuc7xkTXMB4Ss44MMn5MJyT1VLn4o0PC6qpm_U-hugt9TnOuqClLsUN_ekLPtIUyy5Y7-Ls9YL6sPaTL5luU0VN8YEmnFFnrC269_tIdbDHuqT4lpw4PWe8fHovyI-bz9-XX5q7b7dfl5_uGtMyURqwziDYlgOCFs7KsRf1oEEaGK1kXQsGjes4TnoUOKAEh6ad7MQYci17cUE-HnO3u2mD1mAoSc9qm_xGp98qaq_-7wS_Vqu4V5IxPrZQAz48BaT4sMNc1H3cpVB3VgN0MLKOdxVaHCGTYs4J3fMAYOpgRVUr6mBFVSsVf__vUs_wXw0vQ806htWDDys1afPL-RmV6FgPgvfiD3kullE</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>816190626</pqid></control><display><type>article</type><title>Casticin, a flavonoid isolated from Vitex rotundifolia, inhibits prolactin release in vivo and in vitro</title><source>PubMed Central</source><creator>YE, Qi ; ZHANG, Qiao-yan ; ZHENG, Cheng-jian ; WANG, Yang ; QIN, Lu-ping</creator><creatorcontrib>YE, Qi ; ZHANG, Qiao-yan ; ZHENG, Cheng-jian ; WANG, Yang ; QIN, Lu-ping</creatorcontrib><description>Aim: To investigate the anti-hyperprolactinemia activity of casticin, a flavonoid isolated from Vitex rotundifolia, and elucidate its molecular mechanism. Methods: Hyperprolactinemia (MIHP) was induced by administration of metoclopramide dihydrochloride (50 mg/kg, tid, ip, for 10 d) in SD rats and the primary pituitary cells were prepared from the pituitary glands of the SD rats. Prolactin concentrations were measured using a radioimmunoassay. Cell viability was measured using an MTT assay. The mRNA expression of estrogen receptor alpha and beta in rat pituitary cells was measured using semi-quantitative RT-PCR analysis. Results: The level of serum prolactin in the MIHP model group was 2.1 fold higher than that in the untreated control group (P〈0.01). Casticin (10, 20, and 40 mg/kg, ip, for 7 d) reduced serum prolactin levels by 33.9%, 54.3%, and 64.7%, respectively (P〈0.01). The positive control drug bromocriptine 1 mg/kg decreased the serum prolactin concentration in MIHP rats by 44.9%. 1713-Estradiol (E2) significantly increased the proliferation of pituitary cells and casticin (1 and 10 μmol/L) markedly inhibited E2-induced pituitary cell proliferation by 27.7% and 42.1%, respectively. Stimulation of pituitary cells with E2 increased prolactin secretion into the cell culture supernatants, and casticin (0.1, 1, and 10 μmol/L) significantly inhibited the prolactin release stimulated by E2 in a concentration-dependent manner. Casticin (1 and 10 μmol/L) significantly inhibited ERa mRNA expression in pituitary cells stimulated with E2 (P〈O.01) but increased ERI3 mRNA expression at a concentration of 10 μmol/L (P〈0.01). However, casticin had no effects on proliferation and prolectin release of the unstimulated primary pituitary cells in vitro. Conclusion: Casticin inhibited the release of prolactin from pituitary cells of SD rats stimulated with E2 in vivo and in vitro. These effects might be related with inhibiting the ERα mRNA expression and increasing the ERβ mRNA expression.</description><identifier>ISSN: 1671-4083</identifier><identifier>EISSN: 1745-7254</identifier><identifier>DOI: 10.1038/aps.2010.178</identifier><identifier>PMID: 21042288</identifier><language>eng</language><publisher>United States: Nature Publishing Group</publisher><subject>Animals ; Cells, Cultured ; Dose-Response Relationship, Drug ; Estradiol - metabolism ; Estrogen Receptor alpha - metabolism ; Estrogen Receptor beta - metabolism ; Female ; Flavonoids - isolation & purification ; Flavonoids - pharmacology ; Flavonoids - therapeutic use ; Fruit - chemistry ; Hyperprolactinemia - chemically induced ; Hyperprolactinemia - physiopathology ; Hyperprolactinemia - prevention & control ; Metoclopramide ; Original ; Phytotherapy ; Pituitary Gland - metabolism ; Plant Extracts - administration & dosage ; Plant Extracts - pharmacology ; Plant Extracts - therapeutic use ; Prolactin - secretion ; Rats ; Rats, Sprague-Dawley ; Vitex - chemistry ; 体外释放 ; 催乳素 ; 垂体细胞 ; 类黄酮 ; 雌激素受体α</subject><ispartof>Acta pharmacologica Sinica, 2010-12, Vol.31 (12), p.1564-1568</ispartof><rights>Copyright Nature Publishing Group Dec 2010</rights><rights>Copyright © 2010 CPS and SIMM 2010 CPS and SIMM</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-1dfce1d521e1a3fd497374584c19d40651cecf62eba93e8e41fec5bdb00e2a473</citedby><cites>FETCH-LOGICAL-c503t-1dfce1d521e1a3fd497374584c19d40651cecf62eba93e8e41fec5bdb00e2a473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/95561A/95561A.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4002951/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4002951/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,733,786,790,891,27957,27958,53827,53829</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21042288$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YE, Qi</creatorcontrib><creatorcontrib>ZHANG, Qiao-yan</creatorcontrib><creatorcontrib>ZHENG, Cheng-jian</creatorcontrib><creatorcontrib>WANG, Yang</creatorcontrib><creatorcontrib>QIN, Lu-ping</creatorcontrib><title>Casticin, a flavonoid isolated from Vitex rotundifolia, inhibits prolactin release in vivo and in vitro</title><title>Acta pharmacologica Sinica</title><addtitle>Acta Pharmacologica Sinica</addtitle><description>Aim: To investigate the anti-hyperprolactinemia activity of casticin, a flavonoid isolated from Vitex rotundifolia, and elucidate its molecular mechanism. Methods: Hyperprolactinemia (MIHP) was induced by administration of metoclopramide dihydrochloride (50 mg/kg, tid, ip, for 10 d) in SD rats and the primary pituitary cells were prepared from the pituitary glands of the SD rats. Prolactin concentrations were measured using a radioimmunoassay. Cell viability was measured using an MTT assay. The mRNA expression of estrogen receptor alpha and beta in rat pituitary cells was measured using semi-quantitative RT-PCR analysis. Results: The level of serum prolactin in the MIHP model group was 2.1 fold higher than that in the untreated control group (P〈0.01). Casticin (10, 20, and 40 mg/kg, ip, for 7 d) reduced serum prolactin levels by 33.9%, 54.3%, and 64.7%, respectively (P〈0.01). The positive control drug bromocriptine 1 mg/kg decreased the serum prolactin concentration in MIHP rats by 44.9%. 1713-Estradiol (E2) significantly increased the proliferation of pituitary cells and casticin (1 and 10 μmol/L) markedly inhibited E2-induced pituitary cell proliferation by 27.7% and 42.1%, respectively. Stimulation of pituitary cells with E2 increased prolactin secretion into the cell culture supernatants, and casticin (0.1, 1, and 10 μmol/L) significantly inhibited the prolactin release stimulated by E2 in a concentration-dependent manner. Casticin (1 and 10 μmol/L) significantly inhibited ERa mRNA expression in pituitary cells stimulated with E2 (P〈O.01) but increased ERI3 mRNA expression at a concentration of 10 μmol/L (P〈0.01). However, casticin had no effects on proliferation and prolectin release of the unstimulated primary pituitary cells in vitro. Conclusion: Casticin inhibited the release of prolactin from pituitary cells of SD rats stimulated with E2 in vivo and in vitro. These effects might be related with inhibiting the ERα mRNA expression and increasing the ERβ mRNA expression.</description><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Dose-Response Relationship, Drug</subject><subject>Estradiol - metabolism</subject><subject>Estrogen Receptor alpha - metabolism</subject><subject>Estrogen Receptor beta - metabolism</subject><subject>Female</subject><subject>Flavonoids - isolation & purification</subject><subject>Flavonoids - pharmacology</subject><subject>Flavonoids - therapeutic use</subject><subject>Fruit - chemistry</subject><subject>Hyperprolactinemia - chemically induced</subject><subject>Hyperprolactinemia - physiopathology</subject><subject>Hyperprolactinemia - prevention & control</subject><subject>Metoclopramide</subject><subject>Original</subject><subject>Phytotherapy</subject><subject>Pituitary Gland - metabolism</subject><subject>Plant Extracts - administration & dosage</subject><subject>Plant Extracts - pharmacology</subject><subject>Plant Extracts - therapeutic use</subject><subject>Prolactin - secretion</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Vitex - chemistry</subject><subject>体外释放</subject><subject>催乳素</subject><subject>垂体细胞</subject><subject>类黄酮</subject><subject>雌激素受体α</subject><issn>1671-4083</issn><issn>1745-7254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNpVkc9vVCEQx4mxaWvtzbMhnve1DPB-XUzMxlaTJl7UK-HBsEt9C1tgN_W_l83WVk8MmU--M5MPIe-AXQETw7Xe5ivODr9-eEXOoZdt0_NWvq5110Mj2SDOyJuc7xkTXMB4Ss44MMn5MJyT1VLn4o0PC6qpm_U-hugt9TnOuqClLsUN_ekLPtIUyy5Y7-Ls9YL6sPaTL5luU0VN8YEmnFFnrC269_tIdbDHuqT4lpw4PWe8fHovyI-bz9-XX5q7b7dfl5_uGtMyURqwziDYlgOCFs7KsRf1oEEaGK1kXQsGjes4TnoUOKAEh6ad7MQYci17cUE-HnO3u2mD1mAoSc9qm_xGp98qaq_-7wS_Vqu4V5IxPrZQAz48BaT4sMNc1H3cpVB3VgN0MLKOdxVaHCGTYs4J3fMAYOpgRVUr6mBFVSsVf__vUs_wXw0vQ806htWDDys1afPL-RmV6FgPgvfiD3kullE</recordid><startdate>20101201</startdate><enddate>20101201</enddate><creator>YE, Qi</creator><creator>ZHANG, Qiao-yan</creator><creator>ZHENG, Cheng-jian</creator><creator>WANG, Yang</creator><creator>QIN, 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a flavonoid isolated from Vitex rotundifolia, inhibits prolactin release in vivo and in vitro</title><author>YE, Qi ; ZHANG, Qiao-yan ; ZHENG, Cheng-jian ; WANG, Yang ; QIN, Lu-ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-1dfce1d521e1a3fd497374584c19d40651cecf62eba93e8e41fec5bdb00e2a473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Dose-Response Relationship, Drug</topic><topic>Estradiol - metabolism</topic><topic>Estrogen Receptor alpha - metabolism</topic><topic>Estrogen Receptor beta - metabolism</topic><topic>Female</topic><topic>Flavonoids - isolation & purification</topic><topic>Flavonoids - pharmacology</topic><topic>Flavonoids - therapeutic use</topic><topic>Fruit - chemistry</topic><topic>Hyperprolactinemia - chemically induced</topic><topic>Hyperprolactinemia - physiopathology</topic><topic>Hyperprolactinemia - prevention & control</topic><topic>Metoclopramide</topic><topic>Original</topic><topic>Phytotherapy</topic><topic>Pituitary Gland - metabolism</topic><topic>Plant Extracts - administration & dosage</topic><topic>Plant Extracts - pharmacology</topic><topic>Plant Extracts - therapeutic use</topic><topic>Prolactin - secretion</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Vitex - chemistry</topic><topic>体外释放</topic><topic>催乳素</topic><topic>垂体细胞</topic><topic>类黄酮</topic><topic>雌激素受体α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YE, Qi</creatorcontrib><creatorcontrib>ZHANG, Qiao-yan</creatorcontrib><creatorcontrib>ZHENG, Cheng-jian</creatorcontrib><creatorcontrib>WANG, Yang</creatorcontrib><creatorcontrib>QIN, 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Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>YE, Qi</au><au>ZHANG, Qiao-yan</au><au>ZHENG, Cheng-jian</au><au>WANG, Yang</au><au>QIN, Lu-ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Casticin, a flavonoid isolated from Vitex rotundifolia, inhibits prolactin release in vivo and in vitro</atitle><jtitle>Acta pharmacologica Sinica</jtitle><addtitle>Acta Pharmacologica Sinica</addtitle><date>2010-12-01</date><risdate>2010</risdate><volume>31</volume><issue>12</issue><spage>1564</spage><epage>1568</epage><pages>1564-1568</pages><issn>1671-4083</issn><eissn>1745-7254</eissn><notes>casticin; premenstrual syndrome; prolactin; estrogen; estrogen receptors</notes><notes>estrogen</notes><notes>prolactin</notes><notes>Q575.13</notes><notes>premenstrual syndrome</notes><notes>estrogen receptors</notes><notes>casticin</notes><notes>31-1347/R</notes><notes>TQ920</notes><abstract>Aim: To investigate the anti-hyperprolactinemia activity of casticin, a flavonoid isolated from Vitex rotundifolia, and elucidate its molecular mechanism. Methods: Hyperprolactinemia (MIHP) was induced by administration of metoclopramide dihydrochloride (50 mg/kg, tid, ip, for 10 d) in SD rats and the primary pituitary cells were prepared from the pituitary glands of the SD rats. Prolactin concentrations were measured using a radioimmunoassay. Cell viability was measured using an MTT assay. The mRNA expression of estrogen receptor alpha and beta in rat pituitary cells was measured using semi-quantitative RT-PCR analysis. Results: The level of serum prolactin in the MIHP model group was 2.1 fold higher than that in the untreated control group (P〈0.01). Casticin (10, 20, and 40 mg/kg, ip, for 7 d) reduced serum prolactin levels by 33.9%, 54.3%, and 64.7%, respectively (P〈0.01). The positive control drug bromocriptine 1 mg/kg decreased the serum prolactin concentration in MIHP rats by 44.9%. 1713-Estradiol (E2) significantly increased the proliferation of pituitary cells and casticin (1 and 10 μmol/L) markedly inhibited E2-induced pituitary cell proliferation by 27.7% and 42.1%, respectively. Stimulation of pituitary cells with E2 increased prolactin secretion into the cell culture supernatants, and casticin (0.1, 1, and 10 μmol/L) significantly inhibited the prolactin release stimulated by E2 in a concentration-dependent manner. Casticin (1 and 10 μmol/L) significantly inhibited ERa mRNA expression in pituitary cells stimulated with E2 (P〈O.01) but increased ERI3 mRNA expression at a concentration of 10 μmol/L (P〈0.01). However, casticin had no effects on proliferation and prolectin release of the unstimulated primary pituitary cells in vitro. Conclusion: Casticin inhibited the release of prolactin from pituitary cells of SD rats stimulated with E2 in vivo and in vitro. These effects might be related with inhibiting the ERα mRNA expression and increasing the ERβ mRNA expression.</abstract><cop>United States</cop><pub>Nature Publishing Group</pub><pmid>21042288</pmid><doi>10.1038/aps.2010.178</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Cells, Cultured Dose-Response Relationship, Drug Estradiol - metabolism Estrogen Receptor alpha - metabolism Estrogen Receptor beta - metabolism Female Flavonoids - isolation & purification Flavonoids - pharmacology Flavonoids - therapeutic use Fruit - chemistry Hyperprolactinemia - chemically induced Hyperprolactinemia - physiopathology Hyperprolactinemia - prevention & control Metoclopramide Original Phytotherapy Pituitary Gland - metabolism Plant Extracts - administration & dosage Plant Extracts - pharmacology Plant Extracts - therapeutic use Prolactin - secretion Rats Rats, Sprague-Dawley Vitex - chemistry 体外释放 催乳素 垂体细胞 类黄酮 雌激素受体α |
title | Casticin, a flavonoid isolated from Vitex rotundifolia, inhibits prolactin release in vivo and in vitro |
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