[1]郭艳杰,刘乃溶,于心悦,等.和厚朴酚对缺氧心肌细胞的保护作用及机制研究[J].陕西医学杂志,2022,51(6):647-653.[doi:DOI:10.3969/j.issn.1000-7377.2022.06.002]
　GUO Yanjie,LIU Nairong,YU Xinyue,et al.Protective effect and mechanism of honokiol on hypoxic cardiomyocytes[J].,2022,51(6):647-653.[doi:DOI:10.3969/j.issn.1000-7377.2022.06.002]
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和厚朴酚对缺氧心肌细胞的保护作用及机制研究
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
51
期数:
2022年6期
页码:
647-653
栏目:
基础研究
出版日期:
2022-06-05

文章信息/Info

Title:
Protective effect and mechanism of honokiol on hypoxic cardiomyocytes
作者:
郭艳杰1; 刘乃溶1; 于心悦2; 王梦柳2; 王 博3
(1.西安国际医学中心医院心脏内科,陕西 西安 710100; 2.西安国际医学中心医院医教部,陕西 西安 710100; 3.空军军医大学西京医院心脏内科,陕西 西安 710032)
Author(s):
GUO Yanjie; LIU Nairong; YU Xinyue; WANG Mengliu; WANG Bo
(Department of Cardiology,Xi'an International Medical Center Hospital,Xi'an 710100,China)
关键词:
心肌细胞;  缺氧;  和厚朴酚;  凋亡;  细胞活力;  沉默信息调节因子3
Keywords:
Cardiomyocytes;  Anoxia;  Honokiol;  Apoptosis;  Cell viability;  SIRT3
分类号:
R 542.2
DOI:
DOI:10.3969/j.issn.1000-7377.2022.06.002
文献标志码:
A
摘要:
目的:探究和厚朴酚(HK)对缺氧心肌细胞的保护作用及机制。方法:对大鼠新生鼠原代心肌细胞进行提取并培养。在HK对缺氧心肌细胞保护作用的实验中,原代心肌细胞分为常氧组(Nor+DMSO组)、对照+HK组(Nor+HK组)、缺氧组(Hypo+DMSO组)、缺氧+HK组(Hypo+HK组)。在验证去乙酰化酶沉默信息调节因子3(SIRT3)是HK保护缺氧心肌细胞关键信号分子的实验中,原代心肌细胞分为缺氧+对照病毒组(Hypo+Scramble+DMSO组)、缺氧+对照病毒+HK组(Hypo+Scramble+HK组)、缺氧+SIRT3干扰慢病毒组(Hypo+ShRNA+DMSO组)、缺氧+SIRT3干扰慢病毒+HK组(Hypo+ShRNA+HK组)。原代心肌细胞置于无糖无氧培养基中建立缺氧模型。采用CCK-8实验检测心肌细胞活力。采用TUNEL染色检测心肌细胞凋亡率。采用蛋白免疫印记检测关键分子及凋亡相关分子的表达。结果:给予HK后,缺氧原代心肌细胞的细胞活力升高,乳酸脱氢酶(LDH)释放增加,凋亡率下降,半胱氨酸蛋白酶-3(Caspase-3)活性下降,Bcl-2/Bax比值上升(均P<0.01)。进一步实验表明,HK降低了锰超氧化物歧化酶(SOD2)乙酰化水平,提高了SIRT3表达水平(均P<0.05)。慢病毒干扰SIRT3表达以后,再给予HK与未给予HK相比,在细胞活力、LDH释放、凋亡率、Caspase-3活性、Bcl-2/Bax比值及SOD2乙酰化水平等方面比较差异均无统计学意义(均P<0.05))。结论:HK通过SIRT3对缺氧心肌细胞发挥保护作用。
Abstract:
Objective:To explore the protective effect and mechanism of honokiol(HK)on hypoxic cardiomyocytes.Methods:Rat neonatal rat primary cardiomyocytes were isolated and cultured.In the part of protective effect of HK on cardiomyocytes,the primary cardiomyocytes were divided into normoxia group(Nor+DMSO group),control+HK group(Nor+HK group),hypoxia group(Hypo+DMSO group)and hypoxia+HK group(Hypo+HK group).In the experiment to verify that deacetylase silence information regulator 3(SIRT3)was a key signaling molecule of HK to protect hypoxic cardiomyocytes,primary cardiomyocytes were divided into hypoxia+control virus group(Hypo+Scramble+DMSO group),hypoxia+control virus+HK group(Hypo+Scramble+HK group),hypoxia+SIRT3 interference lentivirus group(Hypo+ShRNA+DMSO group),hypoxia+SIRT3 interference lentivirus+HK group(Hypo+ShRNA+HK group).Primary cardiomyocytes were placed in glucose-free medium to establish a hypoxia model.Cell vitality was measured by CCK-8 assay.TUNEL staining was used to detect the rate of cardiomyocyte apoptosis.Protein immunoblotting was used to detect the expression of key molecules and apoptosis-related molecules.Results:After administration of HK,the cell viability of simulated ischemic primary cardiomyocytes increased, the release of LDH increased, the apoptotic ratio decreased, the activity of Caspase-3 decreased,and the ratio of Bcl-2/Bax increased(all P<0.01).Further results showed that HK decreased the acetylation level of SOD2 and increased the expression level of SIRT3(both P<0.05).After lentivirus interfered with SIRT3 expression,there was no significant difference in cell viability,LDH release,apoptosis rate,Caspase-3 activity,Bcl-2/Bax ratio and SOD2 acetylation level between HK-treated and HK-untreated groups(all P<0.05).Conclusion:HK exerts a protective effect on hypoxic cardiomyocytes through SIRT3.

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金青年科学基金资助项目(81800229); 陕西省重点研发计划项目(2022SF-317); 西安国际医学中心医院院级重点课题(2021ZD001)
更新日期/Last Update: 2022-06-06