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Study of the protective effect of Astragaloside Ⅳ mediated by HO-1 against hypoxia/reoxygenation induced cell injury in primary cardiomyocytes |
Hits 1666 Download times 1193 Received:August 13, 2018 |
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DOI
10.11656/j.issn.1672-1519.2019.01.21 |
Key Words
Astragaloside Ⅳ;heme oxygenase-1;cardiomyocytes;hypoxia/reoxygenation;CoPP;ZnPP |
Author Name | Affiliation | YANG Ping | School of Nursing, Ningbo College of Health Sciences, Ningbo 315100, China | ZHOU Yuping | Affiliated Hospital of Medical College of Ningbo University, Ningbo 315020, China | XIA Qing | School of Nursing, Ningbo College of Health Sciences, Ningbo 315100, China | YAO Lipeng | School of Nursing, Ningbo College of Health Sciences, Ningbo 315100, China | LI Gaowen | School of Nursing, Ningbo College of Health Sciences, Ningbo 315100, China | CHANG Xiuchun | School of Nursing, Ningbo College of Health Sciences, Ningbo 315100, China | WANG Feng | School of Nursing, Ningbo College of Health Sciences, Ningbo 315100, China |
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Abstract
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[Objective] To study the protective effect and mechanism of Astragaloside Ⅳ(AS-Ⅳ) against hypoxia/reoxygenation (H/R) induced cell injury in primary cardiomyocytes.[Methods] Neonatal rat primary cardiomyocytes were cultured, then H/R injury model was established by hypoxia followed by reoxygenation for 4 h respectively. Cell viability was measured by MTT method. Besides, different treatment factors impacts on cTnT, LDH and inflammatory cytokine hs-CRP and TNF-α level in cell culture medium was examined. Protein level of HO-1 was detected by Western blot analysis, and mRNA level was detected by RT-PCR.[Results] Compared with H/R group, both AS-Ⅳ and CoPP, HO-1 inducer, could significantly protect cells from damage induced by H/R, and inhibit inflammatory cytokine hs-CRP and TNF-α level(P<0.01). While ZnPP, HO-1 inhibitor, showed a remarkable effect of cell damage based on H/R injury. AS-Ⅳ showed a similar effect to CoPP, which could further increased HO-1 mRNA and protein expression(P<0.01).[Conclusion] AS-Ⅳ could inhibit cell damage caused by H/R by induction of HO-1 expression. |
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