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Article: Pro-angiogenesis effect and transcriptome profile of Shuxinyin formula in zebrafish

TitlePro-angiogenesis effect and transcriptome profile of Shuxinyin formula in zebrafish
Authors
KeywordsAngiogenesis
Coronary heart disease
Traditional Chinese medicine
Transcriptome
VEGF
Zebrafish
Issue Date2019
Citation
Phytomedicine, 2019, v. 65, article no. 153083 How to Cite?
AbstractBackground: Angiogenesis plays a critical role in ischemia disease like coronary heart disease. Shunxinyin formula has been developed for treating coronary heart disease according to the principle of traditional Chinese medicine while its underlying mechanism is not fully elucidated. Purpose: Here, we hypothesize Shuxinyin formula could promote angiogenesis and microcirculation, and the underlying mechanism is also investigated. Methods: We established the chemical profile of Shuxinyin (SXY) extract utilizing a UHPLC-Q/Exactive analysis system and evaluated its pro-angiogenesis effect in zebrafish model. The underlying mechanisms were investigated by combination of pharmacological experiments with transcriptome analysis in zebrafish. Zebrafish treated with VEGF was served as the positive control in present study. Results: We found SXY significantly enhanced the sub-intestinal vessel plexus (SIVs) growth in zebrafish. Co-treatment and post-treatment SXY attenuated VEGF receptor tyrosine kinase inhibitor II (VRI)-induced deficiency of intersegmental vessels (ISVs) in a concentration dependent manner. Post-treatment VEGF, which is a well-known angiogenesis driver, also partially ameliorated VRI-induced ISVs deficiency. In addition, SXY inhibited the down-regulation of VEGF receptors, including kdr, flt1 and kdrl, induced by VRI in zebrafish. The pro-angiogenesis effect of SXY on VRI-induced ISVs deficiency was suppressed by PI3K and JNK inhibitors, and Akt inhibitor abolished the pro-angiogenesis effect of SXY. The transcriptome profile of SXY preventing from VRI-induced vascular growth deficiency revealed that the underlying mechanisms were also co-related to cell junction, apoptosis and autophagy. Conclusion: We could conclude that SXY presented pro-angiogenesis effect and the action mechanisms were involved in VEGF/PI3K/Akt/MAPK signaling pathways, cell junction, apoptosis and autophagy.
Persistent Identifierhttp://hdl.handle.net/10722/335841
ISSN
2023 Impact Factor: 6.7
2023 SCImago Journal Rankings: 1.267
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhou, Zhong Yan-
dc.contributor.authorXiao, Ying-
dc.contributor.authorZhao, Wai Rong-
dc.contributor.authorZhang, Jing-
dc.contributor.authorShi, Wen Ting-
dc.contributor.authorMa, Zi Lin-
dc.contributor.authorYe, Qing-
dc.contributor.authorChen, Xin Lin-
dc.contributor.authorTang, Nuo-
dc.contributor.authorTang, Jing Yi-
dc.date.accessioned2023-12-28T08:49:09Z-
dc.date.available2023-12-28T08:49:09Z-
dc.date.issued2019-
dc.identifier.citationPhytomedicine, 2019, v. 65, article no. 153083-
dc.identifier.issn0944-7113-
dc.identifier.urihttp://hdl.handle.net/10722/335841-
dc.description.abstractBackground: Angiogenesis plays a critical role in ischemia disease like coronary heart disease. Shunxinyin formula has been developed for treating coronary heart disease according to the principle of traditional Chinese medicine while its underlying mechanism is not fully elucidated. Purpose: Here, we hypothesize Shuxinyin formula could promote angiogenesis and microcirculation, and the underlying mechanism is also investigated. Methods: We established the chemical profile of Shuxinyin (SXY) extract utilizing a UHPLC-Q/Exactive analysis system and evaluated its pro-angiogenesis effect in zebrafish model. The underlying mechanisms were investigated by combination of pharmacological experiments with transcriptome analysis in zebrafish. Zebrafish treated with VEGF was served as the positive control in present study. Results: We found SXY significantly enhanced the sub-intestinal vessel plexus (SIVs) growth in zebrafish. Co-treatment and post-treatment SXY attenuated VEGF receptor tyrosine kinase inhibitor II (VRI)-induced deficiency of intersegmental vessels (ISVs) in a concentration dependent manner. Post-treatment VEGF, which is a well-known angiogenesis driver, also partially ameliorated VRI-induced ISVs deficiency. In addition, SXY inhibited the down-regulation of VEGF receptors, including kdr, flt1 and kdrl, induced by VRI in zebrafish. The pro-angiogenesis effect of SXY on VRI-induced ISVs deficiency was suppressed by PI3K and JNK inhibitors, and Akt inhibitor abolished the pro-angiogenesis effect of SXY. The transcriptome profile of SXY preventing from VRI-induced vascular growth deficiency revealed that the underlying mechanisms were also co-related to cell junction, apoptosis and autophagy. Conclusion: We could conclude that SXY presented pro-angiogenesis effect and the action mechanisms were involved in VEGF/PI3K/Akt/MAPK signaling pathways, cell junction, apoptosis and autophagy.-
dc.languageeng-
dc.relation.ispartofPhytomedicine-
dc.subjectAngiogenesis-
dc.subjectCoronary heart disease-
dc.subjectTraditional Chinese medicine-
dc.subjectTranscriptome-
dc.subjectVEGF-
dc.subjectZebrafish-
dc.titlePro-angiogenesis effect and transcriptome profile of Shuxinyin formula in zebrafish-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.phymed.2019.153083-
dc.identifier.pmid31600690-
dc.identifier.scopuseid_2-s2.0-85072858344-
dc.identifier.volume65-
dc.identifier.spagearticle no. 153083-
dc.identifier.epagearticle no. 153083-
dc.identifier.eissn1618-095X-
dc.identifier.isiWOS:000500561700002-

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