Article(id=1291404569322450962, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404554201985968, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.06.009, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1731859200000, receivedDateStr=2024-11-18, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824442462, onlineDateStr=2026-08-04, pubDate=1743091200000, pubDateStr=2025-03-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824442462, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824442462, creator=13701087609, updateTime=1785824442462, updator=13701087609, issue=Issue{id=1291404554201985968, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='6', pageStart='751', pageEnd='900', issueExtLink='null', onlineDate='null', pubDate='1743091200000', pubDateStr='2025-03-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824438858, creator='13701087609', updateTime=1785897146949, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291709514101846462, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404554201985968, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291709514101846463, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404554201985968, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=794, endPage=799, ext={EN=ArticleExt(id=1291404569704132627, articleId=1291404569322450962, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Aloe-emodin regulates p53 signal pathway to inhibit epithelial mesenchymal transformation in pathological scar fibroblasts, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective

To explore the effects of aloe-emodin on the proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) of pathological scar fibroblasts, as well as its regulatory mechanisms.

Methods

Proliferative scar fibroblasts (HSFb) were randomly divided into the following groups: HSFb control group (normal culture), HSFb low-dose group (25.00 μg·mL-1 aloe-emodin), HSFb medium-dose group (50.00 μg·mL-1 aloe-emodin), HSFb high-dose group (100.00 μg·mL-1 aloe-emodin), and HSFb-PFT-α group (100.00 μg·mL-1 aloe-emodin + 20.00 μmol·L-1 p53-specific inhibitor PFT-α). Keloid fibroblast (KFb) cells were randomly divided into the following groups: KFb control group (normal culture), KFb low-dose group (25.00 μg·mL-1 aloe-emodin), KFb medium-dose group (50.00 μg·mL-1 aloe-emodin), KFb high-dose group (100.00 μg·mL-1 aloe-emodin), and KFb-PFT-α group (100.00 μg·mL-1 aloe-emodin + 20.00 μmol·L-1 p53-specific inhibitor PFT-α). Cell viability was assessed using the cell counting kit-8 (CCK-8) assay, Western blotting was performed to detect the expression of p53 and EMT-related proteins, apoptosis was measured using the TUNEL assay.

Results

The cell survival rates of the KFb control group, KFb low-dose group, KFb medium-dose group, and KFb high-dose group were (100.00±5.17)%, (84.13±8.34)%, (73.81±7.62)% and (54.59±3.47)%, respectively; the cell survival rates of the HSFb control group, HSFb low-dose group, HSFb medium-dose group, and HSFb high-dose group were (100.00±6.77)%, (83.50±6.08)%, (71.43±2.70)% and (61.80±4.79)%, respectively. The relative expression levels of p53 protein in the KFb control group, KFb low-dose group, KFb high-dose group, and KFb-PFT-α group were 0.31±0.04, 0.52±0.04, 0.76±0.06 and 0.38±0.05, respectively; the relative expression levels of E-cadherin protein were 0.35±0.04, 0.58±0.08, 0.76±0.13 and 0.41±0.06, respectively; the apoptosis rates were (4.82±0.59)%, (11.72±1.68)%, (20.36±1.93)% and (12.46±1.28)%, respectively; the relative expression levels of p53 protein in the HSFb control group, HSFb low-dose group, HSFb high-dose group, and HSFb-PFT-α group were 0.37±0.03, 0.48±0.05, 0.65±0.07 and 0.46±0.04, respectively; the relative expression levels of E-cadherin protein were 0.26±0.03, 0.46±0.05, 0.63±0.08 and 0.34±0.05, respectively; the apoptosis rates were (4.89±0.28)%, (13.98±0.83)%, (21.51±1.08)% and (12.95±1.10)%, respectively. The differences between the KFb low- and high-dose groups and the KFb control group, the KFb-PFT-α group and the KFb high-dose group, the HSFb low- and high-dose groups and the HSFb control group, and the HSFb-PFT-α group and the HSFb high-dose group were statistically significant (P<0.05, P<0.01, P<0.001).

Conclusion

Aloe-emodin may inhibit the proliferation of pathological fibroblasts, EMT, and induce apoptosis by regulating the p53-related signaling pathway.

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目的

探究芦荟大黄素对病理性瘢痕成纤维细胞增殖、凋亡及上皮间质转化(EMT)的影响及调控机制。

方法

将增生性瘢痕成纤维细胞(HSFb)随机分为HSFb对照组(正常培养)、HSFb低剂量组(25.00 μg·mL-1芦荟大黄素)、HSFb中剂量组(50.00 μg·mL-1芦荟大黄素)、HSFb高剂量组(100.00 μg·mL-1芦荟大黄素)、HSFb-PFT-α组(100.00 μg·mL-1芦荟大黄素+20.00 μmol·L-1 p53特异性抑制药PFT-α)。将人原代瘢痕疙瘩成纤维细胞(KFb)随机分为KFb对照组(正常培养)、KFb低剂量组(25.00 μg·mL-1芦荟大黄素)、KFb中剂量组(50.00 μg·mL-1芦荟大黄素)、KFb高剂量组(100.00 μg·mL-1芦荟大黄素)、KFb-PFT-α组(100.00 μg·mL-1芦荟大黄素+20.00 μmol·L-1 p53特异性抑制药PFT-α)。用细胞计数试剂盒-8(CCK-8)实验检测细胞存活率,用蛋白质印迹法检测p53及EMT相关蛋白的表达,原位末端标记法(Tunel)实验检测细胞凋亡。

结果

KFb对照组、KFb低剂量组、KFb中剂量组、KFb高剂量组的细胞存活率分别为(100.00±5.17)%、(84.13±8.34)%、(73.81±7.62)%和(54.59±3.47)%;HSFb对照组、HSFb低剂量组、HSFb中剂量组、HSFb高剂量组的细胞存活率分别为(100.00±6.77)%、(83.50±6.08)%、(71.43±2.70)%和(61.80±4.79)%;KFb对照组、KFb低剂量组、KFb高剂量、KFb-PFT-α组的调节蛋白53(p53)蛋白相对表达水平分别为0.31±0.04、0.52±0.04、0.76±0.06和0.38±0.05,上皮细胞钙黏蛋白(E-cadherin)蛋白相对表达水平分别为0.35±0.04、0.58±0.08、0.76±0.13和0.41±0.06,凋亡率分别为(4.82±0.59)%、(11.72±1.68)%、(20.36±1.93)%和(12.46±1.28)%;HSFb对照组、HSFb低剂量组、HSFb高剂量组、HSFb-PFT-α组的p53蛋白相对表达水平分别为0.37±0.03、0.48±0.05、0.65±0.07和0.46±0.04,E-cadherin蛋白相对表达水平分别为0.26±0.03、0.46±0.05、0.63±0.08和0.34±0.05,凋亡率分别为(4.89±0.28)%、(13.98±0.83)%、(21.51±1.08)%和(12.95±1.10)%。KFb低、高剂量组的上述指标与KFb对照组比较,KFb-PFT-α组的上述指标与KFb高剂量组比较,HSFb低、高剂量组的上述指标与HSFb对照组比较,HSFb-PFT-α组的上述指标与HSFb高剂量组比较,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

芦荟大黄素可能通过调控p53相关信号抑制病理性成纤维细胞增殖、EMT并诱导凋亡。

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杨毅斌(1983-),男,主管技师,主要从事病理技术方面工作和研究

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杨毅斌 MP: 13696976586 E-mail:
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芦荟大黄素调控p53信号通路抑制病理性瘢痕成纤维细胞的上皮间质转化的研究
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杨毅斌 , 黄宗涌 , 黄燚彬 , 黄爱本
中国临床药理学杂志 | 临床与基础桥接研究 2025,41(6): 794-799
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中国临床药理学杂志 |临床与基础桥接研究 2025 , 41 (6) : 794 -799
芦荟大黄素调控p53信号通路抑制病理性瘢痕成纤维细胞的上皮间质转化的研究
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杨毅斌 , 黄宗涌, 黄燚彬, 黄爱本
作者信息
  • 厦门大学 附属妇女儿童医院、厦门市妇幼保健院 病理科,福建 厦门 361003
通讯作者:
杨毅斌 MP: 13696976586 E-mail:
作者简介:

杨毅斌(1983-),男,主管技师,主要从事病理技术方面工作和研究

Aloe-emodin regulates p53 signal pathway to inhibit epithelial mesenchymal transformation in pathological scar fibroblasts
Yi-bin YANG , Zong-yong HUANG, Yi-bin HUANG, Ai-ben HUANG
Affiliations
  • Department of Pathology, Women and Children’s Hospital Affiliated to Xiamen University, Xiamen Maternal and Child Health Hospital, Xiamen 361003, Fujian Province, China
出版时间: 2025-03-28 doi: 10.13699/j.cnki.1001-6821.2025.06.009
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目的

探究芦荟大黄素对病理性瘢痕成纤维细胞增殖、凋亡及上皮间质转化(EMT)的影响及调控机制。

方法

将增生性瘢痕成纤维细胞(HSFb)随机分为HSFb对照组(正常培养)、HSFb低剂量组(25.00 μg·mL-1芦荟大黄素)、HSFb中剂量组(50.00 μg·mL-1芦荟大黄素)、HSFb高剂量组(100.00 μg·mL-1芦荟大黄素)、HSFb-PFT-α组(100.00 μg·mL-1芦荟大黄素+20.00 μmol·L-1 p53特异性抑制药PFT-α)。将人原代瘢痕疙瘩成纤维细胞(KFb)随机分为KFb对照组(正常培养)、KFb低剂量组(25.00 μg·mL-1芦荟大黄素)、KFb中剂量组(50.00 μg·mL-1芦荟大黄素)、KFb高剂量组(100.00 μg·mL-1芦荟大黄素)、KFb-PFT-α组(100.00 μg·mL-1芦荟大黄素+20.00 μmol·L-1 p53特异性抑制药PFT-α)。用细胞计数试剂盒-8(CCK-8)实验检测细胞存活率,用蛋白质印迹法检测p53及EMT相关蛋白的表达,原位末端标记法(Tunel)实验检测细胞凋亡。

结果

KFb对照组、KFb低剂量组、KFb中剂量组、KFb高剂量组的细胞存活率分别为(100.00±5.17)%、(84.13±8.34)%、(73.81±7.62)%和(54.59±3.47)%;HSFb对照组、HSFb低剂量组、HSFb中剂量组、HSFb高剂量组的细胞存活率分别为(100.00±6.77)%、(83.50±6.08)%、(71.43±2.70)%和(61.80±4.79)%;KFb对照组、KFb低剂量组、KFb高剂量、KFb-PFT-α组的调节蛋白53(p53)蛋白相对表达水平分别为0.31±0.04、0.52±0.04、0.76±0.06和0.38±0.05,上皮细胞钙黏蛋白(E-cadherin)蛋白相对表达水平分别为0.35±0.04、0.58±0.08、0.76±0.13和0.41±0.06,凋亡率分别为(4.82±0.59)%、(11.72±1.68)%、(20.36±1.93)%和(12.46±1.28)%;HSFb对照组、HSFb低剂量组、HSFb高剂量组、HSFb-PFT-α组的p53蛋白相对表达水平分别为0.37±0.03、0.48±0.05、0.65±0.07和0.46±0.04,E-cadherin蛋白相对表达水平分别为0.26±0.03、0.46±0.05、0.63±0.08和0.34±0.05,凋亡率分别为(4.89±0.28)%、(13.98±0.83)%、(21.51±1.08)%和(12.95±1.10)%。KFb低、高剂量组的上述指标与KFb对照组比较,KFb-PFT-α组的上述指标与KFb高剂量组比较,HSFb低、高剂量组的上述指标与HSFb对照组比较,HSFb-PFT-α组的上述指标与HSFb高剂量组比较,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

芦荟大黄素可能通过调控p53相关信号抑制病理性成纤维细胞增殖、EMT并诱导凋亡。

芦荟大黄素  /  病理性瘢痕  /  成纤维细胞  /  上皮间质转化  /  p53信号通路
Objective

To explore the effects of aloe-emodin on the proliferation, apoptosis, and epithelial-mesenchymal transition (EMT) of pathological scar fibroblasts, as well as its regulatory mechanisms.

Methods

Proliferative scar fibroblasts (HSFb) were randomly divided into the following groups: HSFb control group (normal culture), HSFb low-dose group (25.00 μg·mL-1 aloe-emodin), HSFb medium-dose group (50.00 μg·mL-1 aloe-emodin), HSFb high-dose group (100.00 μg·mL-1 aloe-emodin), and HSFb-PFT-α group (100.00 μg·mL-1 aloe-emodin + 20.00 μmol·L-1 p53-specific inhibitor PFT-α). Keloid fibroblast (KFb) cells were randomly divided into the following groups: KFb control group (normal culture), KFb low-dose group (25.00 μg·mL-1 aloe-emodin), KFb medium-dose group (50.00 μg·mL-1 aloe-emodin), KFb high-dose group (100.00 μg·mL-1 aloe-emodin), and KFb-PFT-α group (100.00 μg·mL-1 aloe-emodin + 20.00 μmol·L-1 p53-specific inhibitor PFT-α). Cell viability was assessed using the cell counting kit-8 (CCK-8) assay, Western blotting was performed to detect the expression of p53 and EMT-related proteins, apoptosis was measured using the TUNEL assay.

Results

The cell survival rates of the KFb control group, KFb low-dose group, KFb medium-dose group, and KFb high-dose group were (100.00±5.17)%, (84.13±8.34)%, (73.81±7.62)% and (54.59±3.47)%, respectively; the cell survival rates of the HSFb control group, HSFb low-dose group, HSFb medium-dose group, and HSFb high-dose group were (100.00±6.77)%, (83.50±6.08)%, (71.43±2.70)% and (61.80±4.79)%, respectively. The relative expression levels of p53 protein in the KFb control group, KFb low-dose group, KFb high-dose group, and KFb-PFT-α group were 0.31±0.04, 0.52±0.04, 0.76±0.06 and 0.38±0.05, respectively; the relative expression levels of E-cadherin protein were 0.35±0.04, 0.58±0.08, 0.76±0.13 and 0.41±0.06, respectively; the apoptosis rates were (4.82±0.59)%, (11.72±1.68)%, (20.36±1.93)% and (12.46±1.28)%, respectively; the relative expression levels of p53 protein in the HSFb control group, HSFb low-dose group, HSFb high-dose group, and HSFb-PFT-α group were 0.37±0.03, 0.48±0.05, 0.65±0.07 and 0.46±0.04, respectively; the relative expression levels of E-cadherin protein were 0.26±0.03, 0.46±0.05, 0.63±0.08 and 0.34±0.05, respectively; the apoptosis rates were (4.89±0.28)%, (13.98±0.83)%, (21.51±1.08)% and (12.95±1.10)%, respectively. The differences between the KFb low- and high-dose groups and the KFb control group, the KFb-PFT-α group and the KFb high-dose group, the HSFb low- and high-dose groups and the HSFb control group, and the HSFb-PFT-α group and the HSFb high-dose group were statistically significant (P<0.05, P<0.01, P<0.001).

Conclusion

Aloe-emodin may inhibit the proliferation of pathological fibroblasts, EMT, and induce apoptosis by regulating the p53-related signaling pathway.

aloe-emodin  /  pathological scar  /  fibroblast  /  epithelial mesenchymal transformation  /  p53 signal pathway
杨毅斌, 黄宗涌, 黄燚彬, 黄爱本. 芦荟大黄素调控p53信号通路抑制病理性瘢痕成纤维细胞的上皮间质转化的研究. 中国临床药理学杂志, 2025 , 41 (6) : 794 -799 . DOI: 10.13699/j.cnki.1001-6821.2025.06.009
Yi-bin YANG, Zong-yong HUANG, Yi-bin HUANG, Ai-ben HUANG. Aloe-emodin regulates p53 signal pathway to inhibit epithelial mesenchymal transformation in pathological scar fibroblasts[J]. Chinese Journal of Clinical Pharmacology, 2025 , 41 (6) : 794 -799 . DOI: 10.13699/j.cnki.1001-6821.2025.06.009

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doi: 10.13699/j.cnki.1001-6821.2025.06.009
  • 接收时间:2024-11-18
  • 首发时间:2026-08-04
  • 出版时间:2025-03-28
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  • 收稿日期:2024-11-18
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    厦门大学 附属妇女儿童医院、厦门市妇幼保健院 病理科,福建 厦门 361003

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