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Article(id=1317115206266897202, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317115107243573307, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2026.04.038, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1791954335991, onlineDateStr=2026-10-14, pubDate=1775750400000, pubDateStr=2026-04-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791954335991, onlineIssueDateStr=2026-10-14, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791954335991, creator=13701087609, updateTime=1791954335991, updator=13701087609, issue=Issue{id=1317115107243573307, tenantId=1146029695717560320, journalId=1255847919539208197, year='2026', volume='44', issue='4', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1775750400000', pubDateStr='2026-04-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1791954312382, creator='13701087609', updateTime=1791958738709, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1317133672680116252, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317115107243573307, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1317133672680116253, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317115107243573307, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=196, endPage=200, ext={EN=ArticleExt(id=1317115206447252275, articleId=1317115206266897202, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Protective Mechanism of Cardiomyocytes by Yiqi Wenyang Huoxue Lishui Recipe（益气温阳活血利水方）Through Regulating MLK3-Mediated Mitochondrial Unfolded Protein Response, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=
Objective

The study aimed to observe the cardioprotective effects of Yiqi Wenyang Huoxue Lishui Recipe（益气温阳活血利水方, YWHLR）by regulating the mixed lineage kinase 3（MLK3）mediated mitochondrial unfolded protein response（UPRmt）and to explore the mechanism of YWHLR in preventing and treating heart failure.

Method

The mouse HL-1 cardiomyocyte model was prepared using angiotensin Ⅱ（AngⅡ）, followed by interventions with URMC-099, Oligomycin A and YWHLR medicated serum. The mice were divided into control, AngⅡ, AngⅡ + URMC-099, AngⅡ + Oligomycin and AngⅡ + YWHLR groups. Cell viability and proliferation were assessed using the CCK-8 assay. RT-PCR measured the levels of MLK3 and UPRmt mRNA（MLK3, CHOP, LONP1, HSP60, HSP70）, and Western blot analyzed the protein levels related to MLK3 and UPRmt（MLK3, CHOP, LONP1, HSP60, HSP70）. Immunofluorescence double staining was employed to detect the expressions of HSP70 and MLK3 proteins.

Results

Compared to the control group, the AngⅡ group showed a significant increase in MLK3 expression（P<0.01）and a significant decrease in the levels of CHOP, LONP1, HSP60 and HSP70（P<0.01）. The AngⅡ + URMC-099 group exhibited a significant decrease in MLK3 expression（P<0.01）and a significant increase in the levels of CHOP, LONP1, HSP60 and HSP70（P<0.01）compared to the AngⅡ group. The AngⅡ + Oligomycin group showed no significant difference in MLK3 expression（P>0.05）but a significant increase in the levels of CHOP, LONP1, HSP60 and HSP70（P<0.01）. The AngⅡ + YWHLR group demonstrated a significant decrease in MLK3 expression（P<0.01）and a significant increase in the levels of CHOP, LONP1, HSP60 and HSP70（P<0.01）compared to the AngⅡ group.

Conclusion

YWHLR medicated serum may exert its therapeutic effects by modulating the MLK3-mediated mitochondrial unfolded protein response.

, authors=Zhennan LI1, 2, Zhongzheng ZHANG2, Kang XIE3, Haowen ZHUANG3, Junyan WANG2, 3, authorsList=Zhennan LI, Zhongzheng ZHANG, Kang XIE, Haowen ZHUANG, Junyan WANG, authorCompany=null, correspAuthors=Junyan WANG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1317115206782796596, articleId=1317115206266897202, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=益气温阳活血利水方调控MLK3介导的线粒体未折叠蛋白反应保护心肌细胞作用机制研究, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=
目的

观察益气温阳活血利水方（Yiqi Wenyang Huoxue Lishui Recipe，YWHLR）调控混合谱系酶3（mixed lineage kinase 3，MLK3）介导的线粒体未折叠蛋白反应（mitochondrial unfolded protein response，UPRmt）对心肌细胞的保护作用，探讨益气温阳活血利水方防治心力衰竭的作用机制。

方法

采用血管紧张素2（angiotensin Ⅱ，AngⅡ）制备小鼠HL-1心肌细胞损伤模型，分别给予URMC-099、寡霉素A（Oligomycin A）、益气温阳活血利水方干预，分为对照组（Control）、AngⅡ组、AngⅡ + URMC-099组、AngⅡ + Oligomycin组、AngⅡ + YWHLR组，收集上述细胞，采用CCK-8法检测细胞活性；RT-qPCR法检测各组HL-1细胞MLK3及UPRmt mRNA水平[MLK3、C/EBP同源蛋白（C/EBP-homologous protein，CHOP）、线粒体离子肽酶1（lon peptidase 1，mitochondrial，LONP1）、热休克蛋白60（heat shock protein 60，HSP60）、热休克蛋白70（heat shock protein 70，HSP70）]；Western blot检测各组HL-1细胞MLK3及UPRmt相关蛋白水平（MLK3、CHOP、LONP1、HSP60、HSP70）；免疫荧光双标法检测HSP70、MLK3蛋白的表达情况。

结果

与对照组相比，AngⅡ组的MLK3表达水平显著上升（P<0.05），CHOP、LONP1、HSP60、HSP70表达水平显著下降（P<0.05）；与AngⅡ组相比，AngⅡ + URMC-099组MLK3表达水平显著下降（P<0.05），CHOP、LONP1、HSP60、HSP70表达水平显著上升（P<0.05）；与AngⅡ组相比，AngⅡ + Oligomycin组MLK3表达水平差异无统计学意义（P>0.05），CHOP、LONP1、HSP60、HSP70表达水平显著上升（P<0.05）；与AngⅡ组相比，AngⅡ + YWHLR组MLK3表达水平显著下降（P<0.05），CHOP、LONP1、HSP60、HSP70表达水平显著上升（P<0.05）。

结论

益气温阳活血利水方可能通过调控MLK3介导的线粒体未折叠蛋白反应发挥保护心肌细胞作用。

, authors=李镇南1, 2, 张中正2, 谢抗3, 庄皓文3, 王俊岩2, 3, authorsList=李镇南, 张中正, 谢抗, 庄皓文, 王俊岩, authorCompany=null, correspAuthors=王俊岩, authorNote=

李镇南（2002-），男，广东广州人，硕士在读，研究方向：中医药防治心血管疾病。

, correspAuthorsNote=
王俊岩（1992-），男，辽宁营口人，副研究员，博士研究生导师，博士，研究方向：中医药防治心力衰竭。E-mail: 。
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李镇南（2002-），男，广东广州人，硕士在读，研究方向：中医药防治心血管疾病。

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李镇南（2002-），男，广东广州人，硕士在读，研究方向：中医药防治心血管疾病。

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益气温阳活血利水方调控MLK3介导的线粒体未折叠蛋白反应保护心肌细胞作用机制研究
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李镇南 1, 2 , 张中正 2 , 谢抗 3 , 庄皓文 3 , 王俊岩 2, 3
中华中医药学刊 | 国家项目点击 2026,44(4): 196-200
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中华中医药学刊 |国家项目点击 2026 , 44 (4) : 196 -200
益气温阳活血利水方调控MLK3介导的线粒体未折叠蛋白反应保护心肌细胞作用机制研究
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2.广州中医药大学中药学院，广东 广州 510006, bio={"content":"

李镇南（2002-），男，广东广州人，硕士在读，研究方向：中医药防治心血管疾病。

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李镇南（2002-），男，广东广州人，硕士在读，研究方向：中医药防治心血管疾病。

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李镇南1, 2, 张中正2, 谢抗3, 庄皓文3, 王俊岩2, 3
作者信息
  • 1.浙江大学药学院，浙江 杭州 310058
  • 2.广州中医药大学中药学院，广东 广州 510006
  • 3.广州中医药大学第一临床医学院，广东 广州 510405
通讯作者:
王俊岩（1992-），男，辽宁营口人，副研究员，博士研究生导师，博士，研究方向：中医药防治心力衰竭。E-mail: 。
作者简介:

李镇南（2002-），男，广东广州人，硕士在读，研究方向：中医药防治心血管疾病。

Protective Mechanism of Cardiomyocytes by Yiqi Wenyang Huoxue Lishui Recipe（益气温阳活血利水方）Through Regulating MLK3-Mediated Mitochondrial Unfolded Protein Response
Zhennan LI1, 2, Zhongzheng ZHANG2, Kang XIE3, Haowen ZHUANG3, Junyan WANG2, 3
Affiliations
  • 1.College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, Zhejiang, China
  • 2.College of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong, China
  • 3.The First Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, China
出版时间: 2026-04-10 doi: 10.13193/j.issn.1673-7717.2026.04.038
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摘要
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目的

观察益气温阳活血利水方（Yiqi Wenyang Huoxue Lishui Recipe，YWHLR）调控混合谱系酶3（mixed lineage kinase 3，MLK3）介导的线粒体未折叠蛋白反应（mitochondrial unfolded protein response，UPRmt）对心肌细胞的保护作用，探讨益气温阳活血利水方防治心力衰竭的作用机制。

方法

采用血管紧张素2（angiotensin Ⅱ，AngⅡ）制备小鼠HL-1心肌细胞损伤模型，分别给予URMC-099、寡霉素A（Oligomycin A）、益气温阳活血利水方干预，分为对照组（Control）、AngⅡ组、AngⅡ + URMC-099组、AngⅡ + Oligomycin组、AngⅡ + YWHLR组，收集上述细胞，采用CCK-8法检测细胞活性；RT-qPCR法检测各组HL-1细胞MLK3及UPRmt mRNA水平[MLK3、C/EBP同源蛋白（C/EBP-homologous protein，CHOP）、线粒体离子肽酶1（lon peptidase 1，mitochondrial，LONP1）、热休克蛋白60（heat shock protein 60，HSP60）、热休克蛋白70（heat shock protein 70，HSP70）]；Western blot检测各组HL-1细胞MLK3及UPRmt相关蛋白水平（MLK3、CHOP、LONP1、HSP60、HSP70）；免疫荧光双标法检测HSP70、MLK3蛋白的表达情况。

结果

与对照组相比，AngⅡ组的MLK3表达水平显著上升（P<0.05），CHOP、LONP1、HSP60、HSP70表达水平显著下降（P<0.05）；与AngⅡ组相比，AngⅡ + URMC-099组MLK3表达水平显著下降（P<0.05），CHOP、LONP1、HSP60、HSP70表达水平显著上升（P<0.05）；与AngⅡ组相比，AngⅡ + Oligomycin组MLK3表达水平差异无统计学意义（P>0.05），CHOP、LONP1、HSP60、HSP70表达水平显著上升（P<0.05）；与AngⅡ组相比，AngⅡ + YWHLR组MLK3表达水平显著下降（P<0.05），CHOP、LONP1、HSP60、HSP70表达水平显著上升（P<0.05）。

结论

益气温阳活血利水方可能通过调控MLK3介导的线粒体未折叠蛋白反应发挥保护心肌细胞作用。

线粒体未折叠蛋白反应  /  益气温阳活血利水方  /  心力衰竭  /  MLK3
Objective

The study aimed to observe the cardioprotective effects of Yiqi Wenyang Huoxue Lishui Recipe（益气温阳活血利水方, YWHLR）by regulating the mixed lineage kinase 3（MLK3）mediated mitochondrial unfolded protein response（UPRmt）and to explore the mechanism of YWHLR in preventing and treating heart failure.

Method

The mouse HL-1 cardiomyocyte model was prepared using angiotensin Ⅱ（AngⅡ）, followed by interventions with URMC-099, Oligomycin A and YWHLR medicated serum. The mice were divided into control, AngⅡ, AngⅡ + URMC-099, AngⅡ + Oligomycin and AngⅡ + YWHLR groups. Cell viability and proliferation were assessed using the CCK-8 assay. RT-PCR measured the levels of MLK3 and UPRmt mRNA（MLK3, CHOP, LONP1, HSP60, HSP70）, and Western blot analyzed the protein levels related to MLK3 and UPRmt（MLK3, CHOP, LONP1, HSP60, HSP70）. Immunofluorescence double staining was employed to detect the expressions of HSP70 and MLK3 proteins.

Results

Compared to the control group, the AngⅡ group showed a significant increase in MLK3 expression（P<0.01）and a significant decrease in the levels of CHOP, LONP1, HSP60 and HSP70（P<0.01）. The AngⅡ + URMC-099 group exhibited a significant decrease in MLK3 expression（P<0.01）and a significant increase in the levels of CHOP, LONP1, HSP60 and HSP70（P<0.01）compared to the AngⅡ group. The AngⅡ + Oligomycin group showed no significant difference in MLK3 expression（P>0.05）but a significant increase in the levels of CHOP, LONP1, HSP60 and HSP70（P<0.01）. The AngⅡ + YWHLR group demonstrated a significant decrease in MLK3 expression（P<0.01）and a significant increase in the levels of CHOP, LONP1, HSP60 and HSP70（P<0.01）compared to the AngⅡ group.

Conclusion

YWHLR medicated serum may exert its therapeutic effects by modulating the MLK3-mediated mitochondrial unfolded protein response.

mitochondrial unfolded protein response  /  Yiqi Wenyang Huoxue Lishui Recipe（益气温阳活血利水方）  /  heart failure  /  MLK3
李镇南, 张中正, 谢抗, 庄皓文, 王俊岩. 益气温阳活血利水方调控MLK3介导的线粒体未折叠蛋白反应保护心肌细胞作用机制研究. 中华中医药学刊, 2026 , 44 (4) : 196 -200 . DOI: 10.13193/j.issn.1673-7717.2026.04.038
Zhennan LI, Zhongzheng ZHANG, Kang XIE, Haowen ZHUANG, Junyan WANG. Protective Mechanism of Cardiomyocytes by Yiqi Wenyang Huoxue Lishui Recipe（益气温阳活血利水方）Through Regulating MLK3-Mediated Mitochondrial Unfolded Protein Response[J]. Chinese Archives of Traditional Chinese Medicine, 2026 , 44 (4) : 196 -200 . DOI: 10.13193/j.issn.1673-7717.2026.04.038
基金
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  • 国家自然科学基金项目(8220150462)
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doi: 10.13193/j.issn.1673-7717.2026.04.038
  • 首发时间：2026-10-14
  • 出版时间：2026-04-10
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国家自然科学基金项目(8220150462)
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    1.浙江大学药学院，浙江 杭州 310058
    2.广州中医药大学中药学院，广东 广州 510006
    3.广州中医药大学第一临床医学院，广东 广州 510405

通讯作者:

王俊岩（1992-），男，辽宁营口人，副研究员，博士研究生导师，博士，研究方向：中医药防治心力衰竭。E-mail: 。
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2种不同金属材料的力学参数
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Family		 属数
Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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