Article(id=1291707076686930420, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291707004800750583, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.22.011, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1747670400000, receivedDateStr=2025-05-20, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896565762, onlineDateStr=2026-08-05, pubDate=1764259200000, pubDateStr=2025-11-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896565762, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896565762, creator=13701087609, updateTime=1785896565762, updator=13701087609, issue=Issue{id=1291707004800750583, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='22', pageStart='3151', pageEnd='3300', issueExtLink='null', onlineDate='null', pubDate='1764259200000', pubDateStr='2025-11-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896548700, creator='13701087609', updateTime=1785896693213, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291707610999316815, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291707004800750583, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291707610999316816, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291707004800750583, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=3221, endPage=3227, ext={EN=ArticleExt(id=1291707078050079222, articleId=1291707076686930420, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of mangiferin alleviating liver injury induced by high-fat and high-sugar diet in obese rats by regulating miR-195-3p based on oxidative stress signaling pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective

To study the mechanism of mangiferin alleviating liver injury induced by high-fat and high-sugar diet in obese rats based on oxidative stress signaling pathway.

Methods

Forty SD rats were divided into blank control group (NC) (raised normally and given the same amount of normal saline), model group (fed with high-fat and high-sugar diet and given the same amount of normal saline), the mangiferin administration group (MGF) (fed with high-fat and high-sugar diet), and mangiferin administration+miR-195-3p mimics group (MGF+miR-195-3p mimics) (fed with high-fat and high-sugar diet and administered 40 mg·kg-1 mangiferin suspension, in addition, recombinant lentiviruses containing miR-195-3p mimics were injected into the tail vein), with 10 rats in each group. After treatment, body mass, visceral fat mass and liver coefficient were measured, blood glucose, blood lipid, aminotransferase, liver glycogen and oxidative stress related factors were detected by kit, and histopathological status of liver was detected by hematoxylin-eosin (HE) staining. Real-time quantitative fluorescence polymerase chain reaction (qRT-PCR) and fluorescence in situ hybridization (FISH) were used to detect the levels of miR-195-3p, and protein Western blot (WB) was used to detect the expression levels of nuclear factor erythroidderived 2-like 2 (Nrf2) and heme oxygenase-1 (HO-1).

Results

After different treatment, the liver coefficients of NC group, Model group and MGF group were (2.20±0.29)%, (3.11±0.40)% and (2.75±0.32)%, respectively. Insulin was (310.63±38.06), (426.59±55.35) and (378.57±42.81) ng·L-1; glutamic pyruvic transaminase was (55.17±6.11), (137.57±17.45) and (106.85±12.66) U·L-1, respectively. The liver glycogen was (21.64±2.98), (7.96±1.03) and (15.52±2.16) mg·g-1, respectively. The malondialdehyde levels in Model group, MGF group and MGF+miR-195-3p mimics group were (9.63±1.22), (7.79±0.91) and (9.11±1.16) mmol·g-1, respectively, super oxide dismutase was (110.42±14.57), (251.36±36.26) and (181.45±20.95) U·g-1, and Nrf2 mRNA was 1.00±0.12, 1.97±0.20, 1.29±0.15, respectively. The mRNA of HO-1 was 1.00±0.14, 2.84±0.35 and 1.81±0.29, respectively. Comparison of Model group with NC group, MGF group with Model group and MGF+miR-195-3p mimics group with MGF group showed statistically significant differences in the above indexes (all P<0.05).

Conclusion

Mangiferin can reduce liver injury and regulate glucose and lipid metabolism in obese rats, and its mechanism may be related to the down-regulation of miR-195-3p expression and activation of Nrf2/HO-1 signaling pathway.

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目的

研究芒果苷基于氧化应激信号通路减轻高脂高糖饮食诱导肥胖大鼠肝损伤的机制。

方法

将40只SD大鼠分为空白对照组(NC)(正常饲养,并给予同等量的生理盐水)、模型组(Model)(高脂高糖饲料喂养,并给予同等量的生理盐水)、芒果苷给药组(MGF)(高脂高糖饲料喂养,并灌胃40 mg·kg-1芒果苷混悬液)和芒果苷给药+miR-195-3p模拟物组(MGF+miR-195-3p mimics)(高脂高糖饲料喂养,并灌胃40 mg·kg-1芒果苷混悬液,另尾静脉注射含有miR-195-3p模拟物的重组慢病毒),每组10只。经处理后的大鼠,测量体质量、内脏脂肪质量并计算肝脏系数,用试剂盒检测血糖、血脂、转氨酶、肝糖原及氧化应激相关因子水平,用苏木精-伊红(HE)染色法检测肝脏组织病理学状态,用实时荧光定量聚合酶链式反应(qRT-PCR)及荧光原位杂交法(FISH)检测miR-195-3p水平,用蛋白免疫印迹(WB)法检测核因子-E2相关因子2(Nrf2)、血红素加氧酶1(HO-1)蛋白表达水平。

结果

不同处理后,NC组、Model组和MGF组的肝脏系数分别为(2.20±0.29)%、(3.11±0.40)%和(2.75±0.32)%,胰岛素分别为(310.63±38.06)、(426.59±55.35)和(378.57±42.81)ng·L-1,谷丙转氨酶分别为(55.17±6.11)、(137.57±17.45)和(106.85±12.66)U·L-1,肝糖原分别为(21.64±2.98)、(7.96±1.03)和(15.52±2.16)mg·g-1。Model组、MGF组和MGF+miR-195-3p mimics组的丙二醛分别为(9.63±1.22)、(7.79±0.91)和(9.11±1.16)mmol·g-1,超氧化物歧化酶分别为(110.42±14.57)、(251.36±36.26)和(181.45±20.95)U·g-1Nrf2 mRNA分别为1.00±0.12、1.97±0.20和1.29±0.15,HO-1 mRNA分别为1.00±0.14、2.84±0.35和1.81±0.29。Model组与NC组比较,MGF组与Model组比较,MGF+miR-195-3p mimics组与MGF组比较,上述指标在统计学上差异均有统计学意义(均P<0.05)。

结论

芒果苷可减轻肥胖大鼠的肝损伤,调节糖脂代谢,其机制可能与下调miR-195-3p表达而激活Nrf2/HO-1信号通路有关。

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韩凤超(1985-),男,主治医师,主要从事动脉粥样硬化与受体方面的研究和工作

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高夏青,副主任医师 MP: 15132551417 E-mail:
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基于氧化应激信号通路探究芒果苷通过调节miR-195-3p减轻高脂高糖饮食诱导肥胖大鼠肝损伤的研究
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韩凤超 , 唐坤龙 , 代艳楠 , 高夏青
中国临床药理学杂志 | 临床与基础桥接研究 2025,41(22): 3221-3227
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中国临床药理学杂志 |临床与基础桥接研究 2025 , 41 (22) : 3221 -3227
基于氧化应激信号通路探究芒果苷通过调节miR-195-3p减轻高脂高糖饮食诱导肥胖大鼠肝损伤的研究
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韩凤超, 唐坤龙, 代艳楠, 高夏青
作者信息
  • 唐山工人医院 心内四科,河北 唐山 063000
通讯作者:
高夏青,副主任医师 MP: 15132551417 E-mail:
作者简介:

韩凤超(1985-),男,主治医师,主要从事动脉粥样硬化与受体方面的研究和工作

Research of mangiferin alleviating liver injury induced by high-fat and high-sugar diet in obese rats by regulating miR-195-3p based on oxidative stress signaling pathway
Feng-chao HAN, Kun-long TANG, Yan-nan DAI, Xia-qing GAO
Affiliations
  • Department of Cardiology Ⅳ, Tangshan Workers’ Hospital, Tangshan 063000, Hebei Province, China
出版时间: 2025-11-28 doi: 10.13699/j.cnki.1001-6821.2025.22.011
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目的

研究芒果苷基于氧化应激信号通路减轻高脂高糖饮食诱导肥胖大鼠肝损伤的机制。

方法

将40只SD大鼠分为空白对照组(NC)(正常饲养,并给予同等量的生理盐水)、模型组(Model)(高脂高糖饲料喂养,并给予同等量的生理盐水)、芒果苷给药组(MGF)(高脂高糖饲料喂养,并灌胃40 mg·kg-1芒果苷混悬液)和芒果苷给药+miR-195-3p模拟物组(MGF+miR-195-3p mimics)(高脂高糖饲料喂养,并灌胃40 mg·kg-1芒果苷混悬液,另尾静脉注射含有miR-195-3p模拟物的重组慢病毒),每组10只。经处理后的大鼠,测量体质量、内脏脂肪质量并计算肝脏系数,用试剂盒检测血糖、血脂、转氨酶、肝糖原及氧化应激相关因子水平,用苏木精-伊红(HE)染色法检测肝脏组织病理学状态,用实时荧光定量聚合酶链式反应(qRT-PCR)及荧光原位杂交法(FISH)检测miR-195-3p水平,用蛋白免疫印迹(WB)法检测核因子-E2相关因子2(Nrf2)、血红素加氧酶1(HO-1)蛋白表达水平。

结果

不同处理后,NC组、Model组和MGF组的肝脏系数分别为(2.20±0.29)%、(3.11±0.40)%和(2.75±0.32)%,胰岛素分别为(310.63±38.06)、(426.59±55.35)和(378.57±42.81)ng·L-1,谷丙转氨酶分别为(55.17±6.11)、(137.57±17.45)和(106.85±12.66)U·L-1,肝糖原分别为(21.64±2.98)、(7.96±1.03)和(15.52±2.16)mg·g-1。Model组、MGF组和MGF+miR-195-3p mimics组的丙二醛分别为(9.63±1.22)、(7.79±0.91)和(9.11±1.16)mmol·g-1,超氧化物歧化酶分别为(110.42±14.57)、(251.36±36.26)和(181.45±20.95)U·g-1Nrf2 mRNA分别为1.00±0.12、1.97±0.20和1.29±0.15,HO-1 mRNA分别为1.00±0.14、2.84±0.35和1.81±0.29。Model组与NC组比较,MGF组与Model组比较,MGF+miR-195-3p mimics组与MGF组比较,上述指标在统计学上差异均有统计学意义(均P<0.05)。

结论

芒果苷可减轻肥胖大鼠的肝损伤,调节糖脂代谢,其机制可能与下调miR-195-3p表达而激活Nrf2/HO-1信号通路有关。

芒果苷  /  氧化应激  /  高脂高糖  /  肥胖  /  肝损伤  /  核因子-E2相关因子2
Objective

To study the mechanism of mangiferin alleviating liver injury induced by high-fat and high-sugar diet in obese rats based on oxidative stress signaling pathway.

Methods

Forty SD rats were divided into blank control group (NC) (raised normally and given the same amount of normal saline), model group (fed with high-fat and high-sugar diet and given the same amount of normal saline), the mangiferin administration group (MGF) (fed with high-fat and high-sugar diet), and mangiferin administration+miR-195-3p mimics group (MGF+miR-195-3p mimics) (fed with high-fat and high-sugar diet and administered 40 mg·kg-1 mangiferin suspension, in addition, recombinant lentiviruses containing miR-195-3p mimics were injected into the tail vein), with 10 rats in each group. After treatment, body mass, visceral fat mass and liver coefficient were measured, blood glucose, blood lipid, aminotransferase, liver glycogen and oxidative stress related factors were detected by kit, and histopathological status of liver was detected by hematoxylin-eosin (HE) staining. Real-time quantitative fluorescence polymerase chain reaction (qRT-PCR) and fluorescence in situ hybridization (FISH) were used to detect the levels of miR-195-3p, and protein Western blot (WB) was used to detect the expression levels of nuclear factor erythroidderived 2-like 2 (Nrf2) and heme oxygenase-1 (HO-1).

Results

After different treatment, the liver coefficients of NC group, Model group and MGF group were (2.20±0.29)%, (3.11±0.40)% and (2.75±0.32)%, respectively. Insulin was (310.63±38.06), (426.59±55.35) and (378.57±42.81) ng·L-1; glutamic pyruvic transaminase was (55.17±6.11), (137.57±17.45) and (106.85±12.66) U·L-1, respectively. The liver glycogen was (21.64±2.98), (7.96±1.03) and (15.52±2.16) mg·g-1, respectively. The malondialdehyde levels in Model group, MGF group and MGF+miR-195-3p mimics group were (9.63±1.22), (7.79±0.91) and (9.11±1.16) mmol·g-1, respectively, super oxide dismutase was (110.42±14.57), (251.36±36.26) and (181.45±20.95) U·g-1, and Nrf2 mRNA was 1.00±0.12, 1.97±0.20, 1.29±0.15, respectively. The mRNA of HO-1 was 1.00±0.14, 2.84±0.35 and 1.81±0.29, respectively. Comparison of Model group with NC group, MGF group with Model group and MGF+miR-195-3p mimics group with MGF group showed statistically significant differences in the above indexes (all P<0.05).

Conclusion

Mangiferin can reduce liver injury and regulate glucose and lipid metabolism in obese rats, and its mechanism may be related to the down-regulation of miR-195-3p expression and activation of Nrf2/HO-1 signaling pathway.

mangiferin  /  oxidative stress  /  high fat and sugar  /  obesity  /  liver injury  /  nuclear factor erythroidderived 2-like 2
韩凤超, 唐坤龙, 代艳楠, 高夏青. 基于氧化应激信号通路探究芒果苷通过调节miR-195-3p减轻高脂高糖饮食诱导肥胖大鼠肝损伤的研究. 中国临床药理学杂志, 2025 , 41 (22) : 3221 -3227 . DOI: 10.13699/j.cnki.1001-6821.2025.22.011
Feng-chao HAN, Kun-long TANG, Yan-nan DAI, Xia-qing GAO. Research of mangiferin alleviating liver injury induced by high-fat and high-sugar diet in obese rats by regulating miR-195-3p based on oxidative stress signaling pathway[J]. Chinese Journal of Clinical Pharmacology, 2025 , 41 (22) : 3221 -3227 . DOI: 10.13699/j.cnki.1001-6821.2025.22.011
  • 2025年度河北省医学科学研究课题计划项目基金资助项目(20250221)
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doi: 10.13699/j.cnki.1001-6821.2025.22.011
  • 接收时间:2025-05-20
  • 首发时间:2026-08-05
  • 出版时间:2025-11-28
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  • 收稿日期:2025-05-20
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2025年度河北省医学科学研究课题计划项目基金资助项目(20250221)
作者信息
    唐山工人医院 心内四科,河北 唐山 063000

通讯作者:

高夏青,副主任医师 MP: 15132551417 E-mail:
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
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