Article(id=1292126480692179846, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.01.007, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1746633600000, receivedDateStr=2025-05-08, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996559545, onlineDateStr=2026-08-06, pubDate=1768579200000, pubDateStr=2026-01-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996559545, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996559545, creator=13701087609, updateTime=1785996559545, updator=13701087609, issue=Issue{id=1292126377440989952, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='1', pageStart='1', pageEnd='147', issueExtLink='null', onlineDate='null', pubDate='1768579200000', pubDateStr='2026-01-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785996534929, creator='13701087609', updateTime=1786014708731, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292202603945947673, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292202603950141978, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=40, endPage=46, ext={EN=ArticleExt(id=1292126482126631816, articleId=1292126480692179846, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of corilagin alleviating diabetic nephropathy by influencing podocyte oxidative stress and apoptosis by transcription factor 7, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective

To explore the possible mechanisms through which corilagin affects high-glucose-induced oxidative stress and apoptosis in podocytes to alleviate diabetic nephropathy (DN).

Methods

MPC5 cells in the logarithmic growth phase were divided into 5 groups: control group (5 mmol·L-1 glucose), model group (30 mmol·L-1 glucose), corilagin group (30 mmol·L-1 glucose plus 50 μM corilagin treatment), corilagin + pcDNA3.1 group (30 mmol·L-1 glucose plus corilagin 50 μM treatment after transfection with pcDNA3.1), and corilagin + pcDNA3.1-transcription factor 7 (TCF7) group (30 mmol·L-1 glucose plus corilagin 50 μM treatment after transfection with pcDNA3.1-TCF7). Real-time quantitative polymerase chain reaction (qPCR) was used to detect the expression of long non-coding RNA (LncRNA) TCF7; terminal deoxynucleotidyl transferase dUTP nick-end labeling was employed to assess the apoptosis rate; Western blot was used to analyze the expression of Cleaved caspase-9, Cleaved caspase-3, and proteins related to the glycogen synthase kinase 3 beta (GSK3β)/nuclear factor erythroid-2-related factor2 (Nrf2) signaling pathway; 2′,7′-dichlorofluorescein diacetate fluorescent probe was utilized to measure reactive oxygen species (ROS) levels; and immunofluorescence was used to examine the expression of nephrin and podocin.

Results

The apoptosis rates for the control, model, corilagin, corilagin + pcDNA3.1 and corilagin + pcDNA3.1-TCF7 groups were (5.72±0.49)%, (31.14±5.46)%, (17.01±2.75)%, (16.21±2.83)% and (25.80±3.42)%, respectively; the relative expression levels of Cleaved caspase-9 were 1.00±0.11, 3.91±0.41, 2.43±0.29, 2.49±0.33 and 3.88±0.37, respectively; the relative expression levels for Cleaved caspase-3 were 1.00±0.08, 5.04±0.63, 3.35±0.48, 3.29±0.45 and 4.78±0.56, respectively; the ROS levels were 1.00±0.14, 6.27±1.16, 2.29±0.32, 2.41±0.38 and 5.17±1.08, respectively; malondialdehyde (MDA) levels were (2.33±0.35), (9.26±2.23), (4.80±0.86), (4.47±0.74) and (7.52±1.36) nmol·mg-1, respectively; superoxide dismutase (SOD) levels were (41.34±6.13), (12.15±1.99), (33.38±4.55), (30.01±4.70) and (24.16±3.71) U·mg-1, respectively; and catalase (CAT) levels were (68.22±5.45), (28.27±3.48), (52.13±6.06), (50.24±7.43) and (41.91±5.39) U·mg-1, respectively. When the above indicators in control group compared with those in model group, the above indicators in model group compared with those in the corilagin group, and the above indicators in the corilagin+pcDNA3.1 group compared with those in the corilagin+pcDNA3.1-TCF7 group, all differences showed statistically significant (P<0.05, P<0.01, P<0.001).

Conclusion

Corilagin can inhibit high-glucose-induced oxidative stress and apoptosis in podocytes, thereby alleviating DN, possibly related to its regulation of the GSK3β/Nrf2 signaling pathway by LncRNA TCF7.

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目的

探讨柯里拉京(corilagin)影响高糖诱导足细胞氧化应激及凋亡缓解糖尿病肾病(DN)的可能作用机制。

方法

将对数生长期MPC5细胞分为5组:对照组(5 mmol·L-1葡萄糖)、模型组(30 mmol·L-1葡萄糖)、corilagin组(30 mmol·L-1葡萄糖和50 μM的corilagin处理)、corilagin+pcDNA3.1组(转染pcDNA3.1后30 mmol·L-1葡萄糖和50 μM的corilagin处理)和corilagin+pcDNA3.1-转录因子7(TCF7)组(转染pcDNA3.1-TCF7后30 mmol·L-1葡萄糖和corilagin 50 μM处理)。用实时荧光定量聚合酶链反应法检测长链非编码RNA(LncRNATCF7的表达;用末端脱氧核苷酸转移酶dUTP缺口末端标记法检测凋亡率;用蛋白质印迹法检测切割型半胱天冬酶(Cleaved caspase)-9、Cleaved caspase-3、糖原合成酶激酶3β(GSK3β)/核因子E2相关因子2(Nrf2)信号通路相关蛋白的表达;用2′,7′-二氯荧光素二乙酸酯荧光探针法检测活性氧(ROS)的水平;用免疫荧光法检测肾病蛋白(Nephrin)和足突蛋白(Podocin)的表达。

结果

对照组、模型组、corilagin组、corilagin+pcDNA3.1组和corilagin+pcDNA3.1-TCF7组的细胞凋亡率分别为(5.72±0.49)%、(31.14±5.46)%、(17.01±2.75)%、(16.21±2.83)%和(25.80±3.42)%,Cleaved caspase-9相对表达水平分别为1.00±0.11、3.91±0.41、2.43±0.29、2.49±0.33和3.88±0.37,Cleaved caspase-3相对表达水平分别为1.00±0.08、5.04±0.63、3.35±0.48、3.29±0.45和4.78±0.56,ROS相对表达水平分别为1.00±0.14、6.27±1.16、2.29±0.32、2.41±0.38和5.17±1.08,丙二醛(MDA)水平分别为(2.33±0.35)、(9.26±2.23)、(4.80±0.86)、(4.47±0.74)和(7.52±1.36)nmol·mg-1,超氧化物歧化酶(SOD)水平分别为(41.34±6.13)、(12.15±1.99)、(33.38±4.55)、(30.01±4.70)和(24.16±3.71)U·mg-1,过氧化氢酶(CAT)水平分别为(68.22±5.45)、(28.27±3.48)、(52.13±6.06)、(50.24±7.43)和(41.91±5.39)U·mg-1。对照组的上述指标与模型组比较、模型组的上述指标与corilagin组比较、corilagin+pcDNA3.1组的上述指标与corilagin+pcDNA3.1-TCF7组比较,在统计学上差异均有统计学意义(P<0.05,P<0.01,P<0.001)。

结论

corilagin能够抑制高糖诱导足细胞氧化应激及凋亡从而缓解DN,可能与其通过LncRNA TCF7调控GSK3β/Nrf2信号通路有关。

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桑乾才让(1983-),男,副主任医师,主要从事藏医特色诊疗与优势病种防治研究

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李先加,教授,博士生导师 MP: 13519704087 E-mail:
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柯里拉京通过转录因子7影响足细胞氧化应激及凋亡缓解糖尿病肾病的研究
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桑乾才让 1a, 2a , 扎西措 2b , 慕晓旭 2b , 才让吉 3 , 李先加 1b
中国临床药理学杂志 | 临床与基础桥接研究 2026,42(1): 40-46
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中国临床药理学杂志 |临床与基础桥接研究 2026 , 42 (1) : 40 -46
柯里拉京通过转录因子7影响足细胞氧化应激及凋亡缓解糖尿病肾病的研究
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桑乾才让1a, 2a, 扎西措2b, 慕晓旭2b, 才让吉3, 李先加1b
作者信息
  • 1a.青海大学 藏医学院,青海 西宁 810016
  • 1b.青海大学 藏医药教研室,青海 西宁 810016
  • 2a.青海省藏医院 内科,青海 西宁 810016
  • 2b.青海省藏医院 药剂科,青海 西宁 810016
  • 3.成都中医药大学 民族医药学院,四川 成都 611137
通讯作者:
李先加,教授,博士生导师 MP: 13519704087 E-mail:
作者简介:

桑乾才让(1983-),男,副主任医师,主要从事藏医特色诊疗与优势病种防治研究

Research of corilagin alleviating diabetic nephropathy by influencing podocyte oxidative stress and apoptosis by transcription factor 7
Qian-cairang SANG1a, 2a, Xi-cuo ZHA2b, Xiao-xu MU2b, Rang-ji CAI3, Xian-jia LI1b
Affiliations
  • 1a.College of Tibetan Medicine, Qinghai University, Xining 810016, Qinghai Province, China
  • 1b.Department of Tibetan Medicine, Qinghai University, Xining 810016, Qinghai Province, China
  • 2a.Department of Internal Medicine, Qinghai Tibetan Hospital, Xining 810016, Qinghai Province, China
  • 2b.Department of Pharmacy, Qinghai Tibetan Hospital, Xining 810016, Qinghai Province, China
  • 3.College of Ethnic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, Sichuan Province, China
出版时间: 2026-01-17 doi: 10.13699/j.cnki.1001-6821.2026.01.007
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目的

探讨柯里拉京(corilagin)影响高糖诱导足细胞氧化应激及凋亡缓解糖尿病肾病(DN)的可能作用机制。

方法

将对数生长期MPC5细胞分为5组:对照组(5 mmol·L-1葡萄糖)、模型组(30 mmol·L-1葡萄糖)、corilagin组(30 mmol·L-1葡萄糖和50 μM的corilagin处理)、corilagin+pcDNA3.1组(转染pcDNA3.1后30 mmol·L-1葡萄糖和50 μM的corilagin处理)和corilagin+pcDNA3.1-转录因子7(TCF7)组(转染pcDNA3.1-TCF7后30 mmol·L-1葡萄糖和corilagin 50 μM处理)。用实时荧光定量聚合酶链反应法检测长链非编码RNA(LncRNATCF7的表达;用末端脱氧核苷酸转移酶dUTP缺口末端标记法检测凋亡率;用蛋白质印迹法检测切割型半胱天冬酶(Cleaved caspase)-9、Cleaved caspase-3、糖原合成酶激酶3β(GSK3β)/核因子E2相关因子2(Nrf2)信号通路相关蛋白的表达;用2′,7′-二氯荧光素二乙酸酯荧光探针法检测活性氧(ROS)的水平;用免疫荧光法检测肾病蛋白(Nephrin)和足突蛋白(Podocin)的表达。

结果

对照组、模型组、corilagin组、corilagin+pcDNA3.1组和corilagin+pcDNA3.1-TCF7组的细胞凋亡率分别为(5.72±0.49)%、(31.14±5.46)%、(17.01±2.75)%、(16.21±2.83)%和(25.80±3.42)%,Cleaved caspase-9相对表达水平分别为1.00±0.11、3.91±0.41、2.43±0.29、2.49±0.33和3.88±0.37,Cleaved caspase-3相对表达水平分别为1.00±0.08、5.04±0.63、3.35±0.48、3.29±0.45和4.78±0.56,ROS相对表达水平分别为1.00±0.14、6.27±1.16、2.29±0.32、2.41±0.38和5.17±1.08,丙二醛(MDA)水平分别为(2.33±0.35)、(9.26±2.23)、(4.80±0.86)、(4.47±0.74)和(7.52±1.36)nmol·mg-1,超氧化物歧化酶(SOD)水平分别为(41.34±6.13)、(12.15±1.99)、(33.38±4.55)、(30.01±4.70)和(24.16±3.71)U·mg-1,过氧化氢酶(CAT)水平分别为(68.22±5.45)、(28.27±3.48)、(52.13±6.06)、(50.24±7.43)和(41.91±5.39)U·mg-1。对照组的上述指标与模型组比较、模型组的上述指标与corilagin组比较、corilagin+pcDNA3.1组的上述指标与corilagin+pcDNA3.1-TCF7组比较,在统计学上差异均有统计学意义(P<0.05,P<0.01,P<0.001)。

结论

corilagin能够抑制高糖诱导足细胞氧化应激及凋亡从而缓解DN,可能与其通过LncRNA TCF7调控GSK3β/Nrf2信号通路有关。

柯里拉京  /  糖尿病肾病  /  转录因子7  /  糖原合成酶激酶3β  /  核因子E2相关因子2  /  足细胞  /  氧化应激  /  凋亡
Objective

To explore the possible mechanisms through which corilagin affects high-glucose-induced oxidative stress and apoptosis in podocytes to alleviate diabetic nephropathy (DN).

Methods

MPC5 cells in the logarithmic growth phase were divided into 5 groups: control group (5 mmol·L-1 glucose), model group (30 mmol·L-1 glucose), corilagin group (30 mmol·L-1 glucose plus 50 μM corilagin treatment), corilagin + pcDNA3.1 group (30 mmol·L-1 glucose plus corilagin 50 μM treatment after transfection with pcDNA3.1), and corilagin + pcDNA3.1-transcription factor 7 (TCF7) group (30 mmol·L-1 glucose plus corilagin 50 μM treatment after transfection with pcDNA3.1-TCF7). Real-time quantitative polymerase chain reaction (qPCR) was used to detect the expression of long non-coding RNA (LncRNA) TCF7; terminal deoxynucleotidyl transferase dUTP nick-end labeling was employed to assess the apoptosis rate; Western blot was used to analyze the expression of Cleaved caspase-9, Cleaved caspase-3, and proteins related to the glycogen synthase kinase 3 beta (GSK3β)/nuclear factor erythroid-2-related factor2 (Nrf2) signaling pathway; 2′,7′-dichlorofluorescein diacetate fluorescent probe was utilized to measure reactive oxygen species (ROS) levels; and immunofluorescence was used to examine the expression of nephrin and podocin.

Results

The apoptosis rates for the control, model, corilagin, corilagin + pcDNA3.1 and corilagin + pcDNA3.1-TCF7 groups were (5.72±0.49)%, (31.14±5.46)%, (17.01±2.75)%, (16.21±2.83)% and (25.80±3.42)%, respectively; the relative expression levels of Cleaved caspase-9 were 1.00±0.11, 3.91±0.41, 2.43±0.29, 2.49±0.33 and 3.88±0.37, respectively; the relative expression levels for Cleaved caspase-3 were 1.00±0.08, 5.04±0.63, 3.35±0.48, 3.29±0.45 and 4.78±0.56, respectively; the ROS levels were 1.00±0.14, 6.27±1.16, 2.29±0.32, 2.41±0.38 and 5.17±1.08, respectively; malondialdehyde (MDA) levels were (2.33±0.35), (9.26±2.23), (4.80±0.86), (4.47±0.74) and (7.52±1.36) nmol·mg-1, respectively; superoxide dismutase (SOD) levels were (41.34±6.13), (12.15±1.99), (33.38±4.55), (30.01±4.70) and (24.16±3.71) U·mg-1, respectively; and catalase (CAT) levels were (68.22±5.45), (28.27±3.48), (52.13±6.06), (50.24±7.43) and (41.91±5.39) U·mg-1, respectively. When the above indicators in control group compared with those in model group, the above indicators in model group compared with those in the corilagin group, and the above indicators in the corilagin+pcDNA3.1 group compared with those in the corilagin+pcDNA3.1-TCF7 group, all differences showed statistically significant (P<0.05, P<0.01, P<0.001).

Conclusion

Corilagin can inhibit high-glucose-induced oxidative stress and apoptosis in podocytes, thereby alleviating DN, possibly related to its regulation of the GSK3β/Nrf2 signaling pathway by LncRNA TCF7.

corilagin  /  diabetic nephropathy  /  transcription factor 7  /  glycogen synthase kinase 3 beta  /  nuclear factor erythroid-2-related factor2  /  podocyte  /  oxidative stress  /  apoptosis
桑乾才让, 扎西措, 慕晓旭, 才让吉, 李先加. 柯里拉京通过转录因子7影响足细胞氧化应激及凋亡缓解糖尿病肾病的研究. 中国临床药理学杂志, 2026 , 42 (1) : 40 -46 . DOI: 10.13699/j.cnki.1001-6821.2026.01.007
Qian-cairang SANG, Xi-cuo ZHA, Xiao-xu MU, Rang-ji CAI, Xian-jia LI. Research of corilagin alleviating diabetic nephropathy by influencing podocyte oxidative stress and apoptosis by transcription factor 7[J]. Chinese Journal of Clinical Pharmacology, 2026 , 42 (1) : 40 -46 . DOI: 10.13699/j.cnki.1001-6821.2026.01.007
  • 第七批全国老中医药专家学术经验继承工作基金资助项目(2022-2408)
  • 2023年青海‘昆仑英才’中青年科技人才托举工程基金资助项目(2023QHSKXRCTJ42)
  • 青海省藏医院院级科研基金资助项目(ZYKY-2024-10)
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doi: 10.13699/j.cnki.1001-6821.2026.01.007
  • 接收时间:2025-05-08
  • 首发时间:2026-08-06
  • 出版时间:2026-01-17
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  • 收稿日期:2025-05-08
基金
第七批全国老中医药专家学术经验继承工作基金资助项目(2022-2408)
2023年青海‘昆仑英才’中青年科技人才托举工程基金资助项目(2023QHSKXRCTJ42)
青海省藏医院院级科研基金资助项目(ZYKY-2024-10)
作者信息
    1a.青海大学 藏医学院,青海 西宁 810016
    1b.青海大学 藏医药教研室,青海 西宁 810016
    2a.青海省藏医院 内科,青海 西宁 810016
    2b.青海省藏医院 药剂科,青海 西宁 810016
    3.成都中医药大学 民族医药学院,四川 成都 611137

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李先加,教授,博士生导师 MP: 13519704087 E-mail:
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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
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红菇属 Russula 17 8.13
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