Higenamine inhibits apoptosis and maintains survival of gastric smooth muscle cells in diabetic gastroparesis rat model via activating the β2-AR/PI3K/AKT pathway
Diabetic gastroparesis (DGP) is a common complication of diabetes mellitus (DM). The numerous clinical symptoms of DGP and the great cost on the treatment of DGP seriously lowered the patients’ life quality. However, the pathogenic mechanism of DGP is still elusive till now. In this study, we aimed...
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| Veröffentlicht in: | Biomedicine & pharmacotherapy 2017-11, Vol.95, p.1710-1717 |
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| creator | An, Xiaoxia Long, Chunli Deng, Xiaomin Tang, Aihua Xie, Junyan Chen, Li Wang, Zhengang |
| description | Diabetic gastroparesis (DGP) is a common complication of diabetes mellitus (DM). The numerous clinical symptoms of DGP and the great cost on the treatment of DGP seriously lowered the patients’ life quality. However, the pathogenic mechanism of DGP is still elusive till now. In this study, we aimed to explore the effect of higenamine on the proliferation and apoptosis of gastric smooth muscle cells (SMCs) in DGP rat model. The DGP rat model was built by intraperitoneal injection of Streptozotocin (STZ) into male Sprague-Dawley (SD) rats. Compared with the healthy control group, the level of DGP indicator c-kit was strongly suppressed and the level of Gsα was largely elevated in the STZ-induced model group. By contrast, the addition of higenamine obviously counteracted the effect of STZ on the expression of c-kit and Gsα. Besides that, higenamine improved the decreased emptying ability of the stomach. In addition, the number of gastric SMCs was strongly decreased and cell morphology became irregular in STZ-induced model group. The treatment of higenamine weakened the harm of STZ on the number and morphology of gastric SMCs. Beyond that, higenamine promoted gastric SMCs proliferation and inhibited gastric SMCs apoptosis in DGP model. Further research revealed that higenamine regulated cell proliferation and apoptosis via activating the β2-AR/PI3K/AKT pathway. Taken together, our research revealed that higenamine maintained the survival of gastric SMCs in DGP rat model via the β2-AR/PI3K/AKT pathway, providing a new sight for the treatment of DGP. |
| doi_str_mv | 10.1016/j.biopha.2017.08.112 |
| format | Article |
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The numerous clinical symptoms of DGP and the great cost on the treatment of DGP seriously lowered the patients’ life quality. However, the pathogenic mechanism of DGP is still elusive till now. In this study, we aimed to explore the effect of higenamine on the proliferation and apoptosis of gastric smooth muscle cells (SMCs) in DGP rat model. The DGP rat model was built by intraperitoneal injection of Streptozotocin (STZ) into male Sprague-Dawley (SD) rats. Compared with the healthy control group, the level of DGP indicator c-kit was strongly suppressed and the level of Gsα was largely elevated in the STZ-induced model group. By contrast, the addition of higenamine obviously counteracted the effect of STZ on the expression of c-kit and Gsα. Besides that, higenamine improved the decreased emptying ability of the stomach. In addition, the number of gastric SMCs was strongly decreased and cell morphology became irregular in STZ-induced model group. The treatment of higenamine weakened the harm of STZ on the number and morphology of gastric SMCs. Beyond that, higenamine promoted gastric SMCs proliferation and inhibited gastric SMCs apoptosis in DGP model. Further research revealed that higenamine regulated cell proliferation and apoptosis via activating the β2-AR/PI3K/AKT pathway. Taken together, our research revealed that higenamine maintained the survival of gastric SMCs in DGP rat model via the β2-AR/PI3K/AKT pathway, providing a new sight for the treatment of DGP.</description><identifier>ISSN: 0753-3322</identifier><identifier>EISSN: 1950-6007</identifier><identifier>DOI: 10.1016/j.biopha.2017.08.112</identifier><identifier>PMID: 28958133</identifier><language>eng</language><publisher>France: Elsevier Masson SAS</publisher><subject>Adrenergic beta-Agonists - pharmacology ; Alkaloids - pharmacology ; Animals ; Apoptosis ; Apoptosis - drug effects ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - drug therapy ; Diabetic gastroparesis ; Gastric Emptying - drug effects ; Gastric smooth muscle cells ; Gastroparesis - drug therapy ; Gastroparesis - etiology ; Higenamine ; Male ; Myocytes, Smooth Muscle - drug effects ; Myocytes, Smooth Muscle - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta-2 - metabolism ; Signal Transduction - drug effects ; Streptozocin ; Survival ; Tetrahydroisoquinolines - pharmacology ; β2-AR/PI3K/AKT pathway</subject><ispartof>Biomedicine & pharmacotherapy, 2017-11, Vol.95, p.1710-1717</ispartof><rights>2017</rights><rights>Copyright © 2017. Published by Elsevier Masson SAS.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c343t-dd7355c5e585314ea621bb97abfb0e908c036cd9b428816e4f4780475759bb1b3</citedby><cites>FETCH-LOGICAL-c343t-dd7355c5e585314ea621bb97abfb0e908c036cd9b428816e4f4780475759bb1b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.biopha.2017.08.112$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28958133$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>An, Xiaoxia</creatorcontrib><creatorcontrib>Long, Chunli</creatorcontrib><creatorcontrib>Deng, Xiaomin</creatorcontrib><creatorcontrib>Tang, Aihua</creatorcontrib><creatorcontrib>Xie, Junyan</creatorcontrib><creatorcontrib>Chen, Li</creatorcontrib><creatorcontrib>Wang, Zhengang</creatorcontrib><title>Higenamine inhibits apoptosis and maintains survival of gastric smooth muscle cells in diabetic gastroparesis rat model via activating the β2-AR/PI3K/AKT pathway</title><title>Biomedicine & pharmacotherapy</title><addtitle>Biomed Pharmacother</addtitle><description>Diabetic gastroparesis (DGP) is a common complication of diabetes mellitus (DM). The numerous clinical symptoms of DGP and the great cost on the treatment of DGP seriously lowered the patients’ life quality. However, the pathogenic mechanism of DGP is still elusive till now. In this study, we aimed to explore the effect of higenamine on the proliferation and apoptosis of gastric smooth muscle cells (SMCs) in DGP rat model. The DGP rat model was built by intraperitoneal injection of Streptozotocin (STZ) into male Sprague-Dawley (SD) rats. Compared with the healthy control group, the level of DGP indicator c-kit was strongly suppressed and the level of Gsα was largely elevated in the STZ-induced model group. By contrast, the addition of higenamine obviously counteracted the effect of STZ on the expression of c-kit and Gsα. Besides that, higenamine improved the decreased emptying ability of the stomach. In addition, the number of gastric SMCs was strongly decreased and cell morphology became irregular in STZ-induced model group. The treatment of higenamine weakened the harm of STZ on the number and morphology of gastric SMCs. Beyond that, higenamine promoted gastric SMCs proliferation and inhibited gastric SMCs apoptosis in DGP model. Further research revealed that higenamine regulated cell proliferation and apoptosis via activating the β2-AR/PI3K/AKT pathway. Taken together, our research revealed that higenamine maintained the survival of gastric SMCs in DGP rat model via the β2-AR/PI3K/AKT pathway, providing a new sight for the treatment of DGP.</description><subject>Adrenergic beta-Agonists - pharmacology</subject><subject>Alkaloids - pharmacology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Diabetes Mellitus, Experimental - complications</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetic gastroparesis</subject><subject>Gastric Emptying - drug effects</subject><subject>Gastric smooth muscle cells</subject><subject>Gastroparesis - drug therapy</subject><subject>Gastroparesis - etiology</subject><subject>Higenamine</subject><subject>Male</subject><subject>Myocytes, Smooth Muscle - drug effects</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Adrenergic, beta-2 - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Streptozocin</subject><subject>Survival</subject><subject>Tetrahydroisoquinolines - pharmacology</subject><subject>β2-AR/PI3K/AKT pathway</subject><issn>0753-3322</issn><issn>1950-6007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9u1DAQhy0EokvhDRDykUuy_hMnzgVpVQGtWgmEytmyncnGqyQOtrOor8Mj8CA8E162cOQw8kj-5jcafQi9pqSkhNbbQ2mcXwZdMkKbksiSUvYEbWgrSFET0jxFG9IIXnDO2AV6EeOBECJqLp-jCyZbISnnG_Tj2u1h1pObAbt5cMaliPXil-Sjy93c4Um7OeWKOK7h6I56xL7Hex1TcBbHyfs04GmNdgRsYRxjDsKd0wZS_v_D-UUHOOUFnfDkOxjx0Wmsbcpxyc17nAbAv36yYvdl-_mG3253t_d40Wn4rh9eome9HiO8enwv0dcP7--vrou7Tx9vrnZ3heUVT0XXNVwIK0BIwWkFumbUmLbRpjcEWiIt4bXtWlMxKWkNVV81klSNaERrDDX8Er095y7Bf1shJjW5eDpIz-DXqGhbCUYFr0lGqzNqg48xQK-W4CYdHhQl6mRHHdTZjjrZUUSqbCePvXncsJoJun9Df3Vk4N0ZgHzn0UFQ0TqYLXQugE2q8-7_G34D_Nqliw</recordid><startdate>201711</startdate><enddate>201711</enddate><creator>An, Xiaoxia</creator><creator>Long, Chunli</creator><creator>Deng, Xiaomin</creator><creator>Tang, Aihua</creator><creator>Xie, Junyan</creator><creator>Chen, Li</creator><creator>Wang, Zhengang</creator><general>Elsevier Masson SAS</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201711</creationdate><title>Higenamine inhibits apoptosis and maintains survival of gastric smooth muscle cells in diabetic gastroparesis rat model via activating the β2-AR/PI3K/AKT pathway</title><author>An, Xiaoxia ; Long, Chunli ; Deng, Xiaomin ; Tang, Aihua ; Xie, Junyan ; Chen, Li ; Wang, Zhengang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c343t-dd7355c5e585314ea621bb97abfb0e908c036cd9b428816e4f4780475759bb1b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adrenergic beta-Agonists - pharmacology</topic><topic>Alkaloids - pharmacology</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Diabetes Mellitus, Experimental - complications</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetic gastroparesis</topic><topic>Gastric Emptying - drug effects</topic><topic>Gastric smooth muscle cells</topic><topic>Gastroparesis - drug therapy</topic><topic>Gastroparesis - etiology</topic><topic>Higenamine</topic><topic>Male</topic><topic>Myocytes, Smooth Muscle - drug effects</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Adrenergic, beta-2 - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Streptozocin</topic><topic>Survival</topic><topic>Tetrahydroisoquinolines - pharmacology</topic><topic>β2-AR/PI3K/AKT pathway</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>An, Xiaoxia</creatorcontrib><creatorcontrib>Long, Chunli</creatorcontrib><creatorcontrib>Deng, Xiaomin</creatorcontrib><creatorcontrib>Tang, Aihua</creatorcontrib><creatorcontrib>Xie, Junyan</creatorcontrib><creatorcontrib>Chen, Li</creatorcontrib><creatorcontrib>Wang, Zhengang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biomedicine & pharmacotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>An, Xiaoxia</au><au>Long, Chunli</au><au>Deng, Xiaomin</au><au>Tang, Aihua</au><au>Xie, Junyan</au><au>Chen, Li</au><au>Wang, Zhengang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Higenamine inhibits apoptosis and maintains survival of gastric smooth muscle cells in diabetic gastroparesis rat model via activating the β2-AR/PI3K/AKT pathway</atitle><jtitle>Biomedicine & pharmacotherapy</jtitle><addtitle>Biomed Pharmacother</addtitle><date>2017-11</date><risdate>2017</risdate><volume>95</volume><spage>1710</spage><epage>1717</epage><pages>1710-1717</pages><issn>0753-3322</issn><eissn>1950-6007</eissn><abstract>Diabetic gastroparesis (DGP) is a common complication of diabetes mellitus (DM). The numerous clinical symptoms of DGP and the great cost on the treatment of DGP seriously lowered the patients’ life quality. However, the pathogenic mechanism of DGP is still elusive till now. In this study, we aimed to explore the effect of higenamine on the proliferation and apoptosis of gastric smooth muscle cells (SMCs) in DGP rat model. The DGP rat model was built by intraperitoneal injection of Streptozotocin (STZ) into male Sprague-Dawley (SD) rats. Compared with the healthy control group, the level of DGP indicator c-kit was strongly suppressed and the level of Gsα was largely elevated in the STZ-induced model group. By contrast, the addition of higenamine obviously counteracted the effect of STZ on the expression of c-kit and Gsα. Besides that, higenamine improved the decreased emptying ability of the stomach. In addition, the number of gastric SMCs was strongly decreased and cell morphology became irregular in STZ-induced model group. The treatment of higenamine weakened the harm of STZ on the number and morphology of gastric SMCs. Beyond that, higenamine promoted gastric SMCs proliferation and inhibited gastric SMCs apoptosis in DGP model. Further research revealed that higenamine regulated cell proliferation and apoptosis via activating the β2-AR/PI3K/AKT pathway. Taken together, our research revealed that higenamine maintained the survival of gastric SMCs in DGP rat model via the β2-AR/PI3K/AKT pathway, providing a new sight for the treatment of DGP.</abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>28958133</pmid><doi>10.1016/j.biopha.2017.08.112</doi><tpages>8</tpages></addata></record> |
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| subjects | Adrenergic beta-Agonists - pharmacology Alkaloids - pharmacology Animals Apoptosis Apoptosis - drug effects Cell Proliferation - drug effects Cell Survival - drug effects Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - drug therapy Diabetic gastroparesis Gastric Emptying - drug effects Gastric smooth muscle cells Gastroparesis - drug therapy Gastroparesis - etiology Higenamine Male Myocytes, Smooth Muscle - drug effects Myocytes, Smooth Muscle - metabolism Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Sprague-Dawley Receptors, Adrenergic, beta-2 - metabolism Signal Transduction - drug effects Streptozocin Survival Tetrahydroisoquinolines - pharmacology β2-AR/PI3K/AKT pathway |
| title | Higenamine inhibits apoptosis and maintains survival of gastric smooth muscle cells in diabetic gastroparesis rat model via activating the β2-AR/PI3K/AKT pathway |
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