Effect of Tongxinluo on Podocyte Apoptosis via Inhibition of Oxidative Stress and P38 Pathway in Diabetic Rats
Diabetic nephropathy (DN) has been the leading cause of end-stage renal disease (ESRD). Podocyte apoptosis is a main mechanism of progression of DN. It has been demonstrated that activated P38 and caspase-3 induced by oxidative stress mainly account for increased podocyte apoptosis and proteinuria i...
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| Veröffentlicht in: | Evidence-based complementary and alternative medicine 2016-01, Vol.2016 (2016), p.1-10 |
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| creator | Tong, Yu Liu, Jing Tian, Nianxiu Wu, Xiaoming Zhu, Zhi-Yao Zou, Dawei Zhao, Wenjing Gao, Yanbin Cui, Fangqiang Wang, Xiaolei |
| description | Diabetic nephropathy (DN) has been the leading cause of end-stage renal disease (ESRD). Podocyte apoptosis is a main mechanism of progression of DN. It has been demonstrated that activated P38 and caspase-3 induced by oxidative stress mainly account for increased podocyte apoptosis and proteinuria in DN. Meanwhile, Tongxinluo (TXL) can ameliorate renal structure disruption and dysfunction in DN patients in our clinical practice. However, the effect of TXL on podocyte apoptosis and P38 pathway remains unclear. To explore the effect of TXL on podocyte apoptosis and its molecular mechanism in DN, our in vivo and in vitro studies were performed. TXL attenuated oxidative stress in podocyte in DN in our in vivo and in vitro studies. Moreover, TXL inhibited the activation of P38 and caspase-3. Bcl-2 and Bax expression was partially restored by TXL treatment in our in vivo and in vitro studies. More importantly, TXL decreased podocyte apoptosis in diabetic rats and high glucose cultured podocyte. In conclusion, TXL protects podocyte from apoptosis in DN, partially through its antioxidant effect and inhibiting of the activation of P38 and caspase-3. |
| doi_str_mv | 10.1155/2016/5957423 |
| format | Article |
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Podocyte apoptosis is a main mechanism of progression of DN. It has been demonstrated that activated P38 and caspase-3 induced by oxidative stress mainly account for increased podocyte apoptosis and proteinuria in DN. Meanwhile, Tongxinluo (TXL) can ameliorate renal structure disruption and dysfunction in DN patients in our clinical practice. However, the effect of TXL on podocyte apoptosis and P38 pathway remains unclear. To explore the effect of TXL on podocyte apoptosis and its molecular mechanism in DN, our in vivo and in vitro studies were performed. TXL attenuated oxidative stress in podocyte in DN in our in vivo and in vitro studies. Moreover, TXL inhibited the activation of P38 and caspase-3. Bcl-2 and Bax expression was partially restored by TXL treatment in our in vivo and in vitro studies. More importantly, TXL decreased podocyte apoptosis in diabetic rats and high glucose cultured podocyte. In conclusion, TXL protects podocyte from apoptosis in DN, partially through its antioxidant effect and inhibiting of the activation of P38 and caspase-3.</description><identifier>ISSN: 1741-427X</identifier><identifier>EISSN: 1741-4288</identifier><identifier>DOI: 10.1155/2016/5957423</identifier><identifier>PMID: 27672400</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Antioxidants ; Apoptosis ; Chinese medicine ; Chronic kidney failure ; Clinical medicine ; Dextrose ; Diabetes ; Diabetic nephropathies ; FDA approval ; Glucose ; Laboratory animals ; Medical research ; Oxidative stress ; Rodents ; Studies</subject><ispartof>Evidence-based complementary and alternative medicine, 2016-01, Vol.2016 (2016), p.1-10</ispartof><rights>Copyright © 2016 Fangqiang Cui et al.</rights><rights>COPYRIGHT 2016 John Wiley & Sons, Inc.</rights><rights>Copyright © 2016 Fangqiang Cui et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2016 Fangqiang Cui et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-26a386dff0e3711cf8cff08dd72116676fd2ca1cf99cb6be79365cfae1d7f1b73</citedby><cites>FETCH-LOGICAL-c499t-26a386dff0e3711cf8cff08dd72116676fd2ca1cf99cb6be79365cfae1d7f1b73</cites><orcidid>0000-0001-8030-5450 ; 0000-0003-3635-1040</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5031883/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5031883/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27672400$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Ohta, Yoshiji</contributor><creatorcontrib>Tong, Yu</creatorcontrib><creatorcontrib>Liu, Jing</creatorcontrib><creatorcontrib>Tian, Nianxiu</creatorcontrib><creatorcontrib>Wu, Xiaoming</creatorcontrib><creatorcontrib>Zhu, Zhi-Yao</creatorcontrib><creatorcontrib>Zou, Dawei</creatorcontrib><creatorcontrib>Zhao, Wenjing</creatorcontrib><creatorcontrib>Gao, Yanbin</creatorcontrib><creatorcontrib>Cui, Fangqiang</creatorcontrib><creatorcontrib>Wang, Xiaolei</creatorcontrib><title>Effect of Tongxinluo on Podocyte Apoptosis via Inhibition of Oxidative Stress and P38 Pathway in Diabetic Rats</title><title>Evidence-based complementary and alternative medicine</title><addtitle>Evid Based Complement Alternat Med</addtitle><description>Diabetic nephropathy (DN) has been the leading cause of end-stage renal disease (ESRD). Podocyte apoptosis is a main mechanism of progression of DN. It has been demonstrated that activated P38 and caspase-3 induced by oxidative stress mainly account for increased podocyte apoptosis and proteinuria in DN. Meanwhile, Tongxinluo (TXL) can ameliorate renal structure disruption and dysfunction in DN patients in our clinical practice. However, the effect of TXL on podocyte apoptosis and P38 pathway remains unclear. To explore the effect of TXL on podocyte apoptosis and its molecular mechanism in DN, our in vivo and in vitro studies were performed. TXL attenuated oxidative stress in podocyte in DN in our in vivo and in vitro studies. Moreover, TXL inhibited the activation of P38 and caspase-3. Bcl-2 and Bax expression was partially restored by TXL treatment in our in vivo and in vitro studies. More importantly, TXL decreased podocyte apoptosis in diabetic rats and high glucose cultured podocyte. In conclusion, TXL protects podocyte from apoptosis in DN, partially through its antioxidant effect and inhibiting of the activation of P38 and caspase-3.</description><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Chinese medicine</subject><subject>Chronic kidney failure</subject><subject>Clinical medicine</subject><subject>Dextrose</subject><subject>Diabetes</subject><subject>Diabetic nephropathies</subject><subject>FDA approval</subject><subject>Glucose</subject><subject>Laboratory animals</subject><subject>Medical research</subject><subject>Oxidative stress</subject><subject>Rodents</subject><subject>Studies</subject><issn>1741-427X</issn><issn>1741-4288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqN0c1rFDEYB-AgFlurN88S8CLotvmYSTIXYamtFgpdtIK3kMnHbspssk4y2-5_3wy7bm1PnvKSPPm9CS8A7zA6wbiuTwnC7LRual4R-gIcYV7hSUWEeLmv-e9D8DqlW4RIwzl_BQ4JZ5xUCB2BcO6c1RlGB29imN_70A0RxgBn0US9yRZOV3GVY_IJrr2Cl2HhW599EeXK9b03Kvu1hT9zb1OCKhg4owLOVF7cqQ30AX71qrXZa_hD5fQGHDjVJft2tx6DXxfnN2ffJ1fX3y7PplcTXTVNnhCmqGDGOWQpx1g7oUstjOEEY8Y4c4ZoVfabRrestbyhrNZOWWy4wy2nx-DLNnc1tEtrtA25V51c9X6p-o2MysunJ8Ev5DyuZY0oFoKWgI-7gD7-GWzKcumTtl2ngo1DkliQihBGyNjrwzN6G4c-lO-NCjFSF_So5qqz0gcXS189hsopw6Ur4w0q6vNW6T6m1Fu3fzJGchy3HMctd-Mu_P2_39zjv_Mt4NMWLHww6s7_Z5wtxjr1qDGqSCXoA90nvBk</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Tong, Yu</creator><creator>Liu, Jing</creator><creator>Tian, Nianxiu</creator><creator>Wu, Xiaoming</creator><creator>Zhu, Zhi-Yao</creator><creator>Zou, Dawei</creator><creator>Zhao, Wenjing</creator><creator>Gao, Yanbin</creator><creator>Cui, Fangqiang</creator><creator>Wang, Xiaolei</creator><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M2M</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8030-5450</orcidid><orcidid>https://orcid.org/0000-0003-3635-1040</orcidid></search><sort><creationdate>20160101</creationdate><title>Effect of Tongxinluo on Podocyte Apoptosis via Inhibition of Oxidative Stress and P38 Pathway in Diabetic Rats</title><author>Tong, Yu ; 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Podocyte apoptosis is a main mechanism of progression of DN. It has been demonstrated that activated P38 and caspase-3 induced by oxidative stress mainly account for increased podocyte apoptosis and proteinuria in DN. Meanwhile, Tongxinluo (TXL) can ameliorate renal structure disruption and dysfunction in DN patients in our clinical practice. However, the effect of TXL on podocyte apoptosis and P38 pathway remains unclear. To explore the effect of TXL on podocyte apoptosis and its molecular mechanism in DN, our in vivo and in vitro studies were performed. TXL attenuated oxidative stress in podocyte in DN in our in vivo and in vitro studies. Moreover, TXL inhibited the activation of P38 and caspase-3. Bcl-2 and Bax expression was partially restored by TXL treatment in our in vivo and in vitro studies. More importantly, TXL decreased podocyte apoptosis in diabetic rats and high glucose cultured podocyte. 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| subjects | Antioxidants Apoptosis Chinese medicine Chronic kidney failure Clinical medicine Dextrose Diabetes Diabetic nephropathies FDA approval Glucose Laboratory animals Medical research Oxidative stress Rodents Studies |
| title | Effect of Tongxinluo on Podocyte Apoptosis via Inhibition of Oxidative Stress and P38 Pathway in Diabetic Rats |
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