Effect of pyridoxamine and telmisartan on tubular epithelial cells proliferation and its mechanism

Effect of pyridoxamine and telmisartan on tubular epithelial cells proliferation and its mechanism

Objective The purpose of this study was to explore the protective effects of telmisartan and pyridoxamine on tubular epithelial cells (HK-2) in early renal damage. Methods Cultured HK-2 cells were divided into HK-2 control, angiotensin II (10−6 mol/l) group (Ang II), telmisartan (10−6 mol/l, T) grou...

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Veröffentlicht in:Heart (British Cardiac Society) 2011-10, Vol.97 (Suppl 3), p.A34-A35
Hauptverfasser: Zhu, Pengli, Chen, Jiangkang, Yu, Huizhen, Lin, Fan, Lin, Hong, Sun, Chengai
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container_issue Suppl 3
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container_title Heart (British Cardiac Society)
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creator Zhu, Pengli
Chen, Jiangkang
Yu, Huizhen
Lin, Fan
Lin, Hong
Sun, Chengai
description Objective The purpose of this study was to explore the protective effects of telmisartan and pyridoxamine on tubular epithelial cells (HK-2) in early renal damage. Methods Cultured HK-2 cells were divided into HK-2 control, angiotensin II (10−6 mol/l) group (Ang II), telmisartan (10−6 mol/l, T) group, pyridoxamine group (1 mmol/l, P1), pyridoxamine group (10 mmol/l, P10), and T (10−6 mol/l)+P (10 mmol/l) group (T+P). Methyl thiazolyl tetrazolium (MTT) was used to measure for cell proliferation. Reactive oxygen species (ROS) generation in cellular supernatant was detected by flow cytometry. Real-time quantitative PCR was performed to measure the mRNA expression of transforming growth factor β1 (TGFβ1) and receptor for advanced glycation end-products (RAGE). Results The OD values of HK-2 were inhibited in Ang II (p
doi_str_mv 10.1136/heartjnl-2011-300867.97
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Methods Cultured HK-2 cells were divided into HK-2 control, angiotensin II (10−6 mol/l) group (Ang II), telmisartan (10−6 mol/l, T) group, pyridoxamine group (1 mmol/l, P1), pyridoxamine group (10 mmol/l, P10), and T (10−6 mol/l)+P (10 mmol/l) group (T+P). Methyl thiazolyl tetrazolium (MTT) was used to measure for cell proliferation. Reactive oxygen species (ROS) generation in cellular supernatant was detected by flow cytometry. Real-time quantitative PCR was performed to measure the mRNA expression of transforming growth factor β1 (TGFβ1) and receptor for advanced glycation end-products (RAGE). Results The OD values of HK-2 were inhibited in Ang II (p<0.05), 10 mmol/l P group and TP group (p<0.01) after both 24 h and 48 h intervention. Synergy of inhibition showed in TP group after 48 h intervention (p <0.01). The level of ROS was reduced in P1, P10 and TP group (p<0.01). There was no statistically significant difference among the three groups (p>0.05). Compared with the Ang II, mRNA expression of RAGE and TGFβ1 were decreased in T, P and TP group (p<0.05). Synergy decreased of TGFβ1 expression was showed in TP group (p<0.01). Conclusion There is a synergistic effect of inhibiting HK-2 cells proliferation by combined use of telmisartan and pyridoxamine. It may be related to reduce RAGE and TGFβ expression and alleviate oxidative stress on early renal damage.]]></description><identifier>ISSN: 1355-6037</identifier><identifier>EISSN: 1468-201X</identifier><identifier>DOI: 10.1136/heartjnl-2011-300867.97</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Cardiovascular Society</publisher><ispartof>Heart (British Cardiac Society), 2011-10, Vol.97 (Suppl 3), p.A34-A35</ispartof><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><rights>Copyright: 2011 Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://heart.bmj.com/content/97/Suppl_3/A34.2.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://heart.bmj.com/content/97/Suppl_3/A34.2.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,780,784,3194,23569,27922,27923,77370,77401</link.rule.ids></links><search><creatorcontrib>Zhu, Pengli</creatorcontrib><creatorcontrib>Chen, Jiangkang</creatorcontrib><creatorcontrib>Yu, Huizhen</creatorcontrib><creatorcontrib>Lin, Fan</creatorcontrib><creatorcontrib>Lin, Hong</creatorcontrib><creatorcontrib>Sun, Chengai</creatorcontrib><title>Effect of pyridoxamine and telmisartan on tubular epithelial cells proliferation and its mechanism</title><title>Heart (British Cardiac Society)</title><addtitle>Heart</addtitle><description><![CDATA[Objective The purpose of this study was to explore the protective effects of telmisartan and pyridoxamine on tubular epithelial cells (HK-2) in early renal damage. Methods Cultured HK-2 cells were divided into HK-2 control, angiotensin II (10−6 mol/l) group (Ang II), telmisartan (10−6 mol/l, T) group, pyridoxamine group (1 mmol/l, P1), pyridoxamine group (10 mmol/l, P10), and T (10−6 mol/l)+P (10 mmol/l) group (T+P). Methyl thiazolyl tetrazolium (MTT) was used to measure for cell proliferation. Reactive oxygen species (ROS) generation in cellular supernatant was detected by flow cytometry. Real-time quantitative PCR was performed to measure the mRNA expression of transforming growth factor β1 (TGFβ1) and receptor for advanced glycation end-products (RAGE). Results The OD values of HK-2 were inhibited in Ang II (p<0.05), 10 mmol/l P group and TP group (p<0.01) after both 24 h and 48 h intervention. Synergy of inhibition showed in TP group after 48 h intervention (p <0.01). The level of ROS was reduced in P1, P10 and TP group (p<0.01). There was no statistically significant difference among the three groups (p>0.05). Compared with the Ang II, mRNA expression of RAGE and TGFβ1 were decreased in T, P and TP group (p<0.05). Synergy decreased of TGFβ1 expression was showed in TP group (p<0.01). Conclusion There is a synergistic effect of inhibiting HK-2 cells proliferation by combined use of telmisartan and pyridoxamine. 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Methods Cultured HK-2 cells were divided into HK-2 control, angiotensin II (10−6 mol/l) group (Ang II), telmisartan (10−6 mol/l, T) group, pyridoxamine group (1 mmol/l, P1), pyridoxamine group (10 mmol/l, P10), and T (10−6 mol/l)+P (10 mmol/l) group (T+P). Methyl thiazolyl tetrazolium (MTT) was used to measure for cell proliferation. Reactive oxygen species (ROS) generation in cellular supernatant was detected by flow cytometry. Real-time quantitative PCR was performed to measure the mRNA expression of transforming growth factor β1 (TGFβ1) and receptor for advanced glycation end-products (RAGE). Results The OD values of HK-2 were inhibited in Ang II (p<0.05), 10 mmol/l P group and TP group (p<0.01) after both 24 h and 48 h intervention. Synergy of inhibition showed in TP group after 48 h intervention (p <0.01). The level of ROS was reduced in P1, P10 and TP group (p<0.01). There was no statistically significant difference among the three groups (p>0.05). Compared with the Ang II, mRNA expression of RAGE and TGFβ1 were decreased in T, P and TP group (p<0.05). Synergy decreased of TGFβ1 expression was showed in TP group (p<0.01). Conclusion There is a synergistic effect of inhibiting HK-2 cells proliferation by combined use of telmisartan and pyridoxamine. It may be related to reduce RAGE and TGFβ expression and alleviate oxidative stress on early renal damage.]]></abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Cardiovascular Society</pub><doi>10.1136/heartjnl-2011-300867.97</doi><oa>free_for_read</oa></addata></record>
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title Effect of pyridoxamine and telmisartan on tubular epithelial cells proliferation and its mechanism
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