Article(id=1292135499196551402, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135444850955150, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.09.016, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1756224000000, receivedDateStr=2025-08-27, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785998709724, onlineDateStr=2026-08-06, pubDate=1778947200000, pubDateStr=2026-05-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785998709724, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785998709724, creator=13701087609, updateTime=1785998709724, updator=13701087609, issue=Issue{id=1292135444850955150, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='9', pageStart='1201', pageEnd='1350', issueExtLink='null', onlineDate='null', pubDate='1778947200000', pubDateStr='2026-05-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785998696767, creator='13701087609', updateTime=1786014392260, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201276780081469, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135444850955150, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201276784275774, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135444850955150, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1301, endPage=1307, ext={EN=ArticleExt(id=1292135499402072299, articleId=1292135499196551402, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of osthol on melanocyte loss in vitiligo mice by regulating the Wnt/β-catenin signaling pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To discuss the effects of osthol (Ost) on melanocyte loss in vitiligo mice by regulating the Wnt/β-catenin signaling pathway.
Methods A mouse model of vitiligo was established by applying hydroquinone cream. The successfully modeled mice were divided into model group (only modeling), low-dose experimental group (15 mg·kg-1 Ost), high-dose experimental group (45 mg·kg-1 Ost), positive control group (50.4 mg·mL-1 vitiligo capsules) and inhibitor group (45 mg·kg-1 Ost + 10 mg·kg-1 XAV939). The control group was given an equal volume of normal saline. Each group consisted of 10 mice. After the intervention, the degree of skin depigmentation in the treatment area was scored; orbital blood was collected, and the levels of malondialdehyde (MDA), α-melanocyte-stimulating hormone (α-MSH), tyrosinase (TYR) and tumor necrosis factor-α (TNF-α) in the serum were detected by enzyme-linked immunosorbent assay (ELISA); skin lesion tissues were collected, and the number of melanin-containing hair follicles and melanocytes in the basal layer were evaluated by hematoxylin-eosin (HE) and Masson staining; the positive expression levels of tyrosinase-related protein (TRP) 1 and TRP2 in the skin lesion tissues was detected by immunohistochemistry; the mRNA expression levels of tyrosinase (TYR) and microphthalmia-associated transcription factor (MITF) mRNA in the skin lesion tissues were detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction (qRT-PCR); the protein expression levels of β-catenin and phosphorylated glycogen synthase kinase-3β (p-GSK-3β)/GSK-3β in the skin lesion tissues were detected by Western blotting.
Results The depigmentation scores of control group, model group, low-dose experimental group, high-dose experimental group, positive control group and inhibitor group were (0±0), (4.11±0.52), (2.41±0.28), (0.77±0.09), (0.55±0.07) and (2.55±0.28) score, respectively; the levels of α-MSH were (26.53±2.84), (7.56±0.84), (12.62±1.36), (22.91±2.44), (23.51±2.48) and (13.05±1.38) μg·L-1, respectively; the levels of MDA were (2.05±0.24), (7.94±0.85), (4.31±0.49), (2.27±0.25), (2.19±0.24) and (4.28±0.45) nmol·mg prot-1, respectively; the levels of TNF-α were (38.52±4.02), (105.65±10.94), (68.84±7.05), (42.84±4.45), (41.85±4.37) and (70.05±7.21) ng·mL-1, respectively; the levels of TYR were (105.62±11.14), (45.22±4.67), (65.41±6.77), (98.62±9.98), (97.65±9.89) and (66.08±6.81) μg·L-1, respectively; the numbers of melanocytes in the basal layer were (148.62±15.08), (52.11±5.34), (68.84±6.91), (108.64±11.14), (112.08±11.44) and (70.54±7.21) cells, respectively; the numbers of melanin-containing hair follicles were (98.64±9.98), (41.52±4.31), (62.05±6.37), (95.62±9.74), (96.05±9.78) and (61.08±6.29) cells, respectively; the positive expression levels of TRP1 were 17.05±1.94, 4.62±0.77, 8.05±0.85, 14.98±1.58, 15.22±1.64 and 8.11±0.88, respectively; the positive expressions levels of TRP2 were 14.32±1.55, 3.05±0.33, 5.74±0.66, 10.42±1.15, 11.05±1.17 and 6.05±0.62, respectively; the relative expression levels of TYR mRNA were 1.09±0.12, 0.19±0.02, 0.49±0.05, 0.79±0.08, 0.88±0.09 and 0.55±0.07, respectively; the relative expression levels of MITF mRNA were 0.98±0.11, 0.24±0.03, 0.44±0.05, 0.81±0.09, 0.85±0.10 and 0.51±0.06, respectively; the relative expression levels of β-catenin were 1.25±0.13, 0.34±0.05, 0.68±0.08, 1.07±0.11, 1.11±0.12 and 0.71±0.09, respectively; the relative expression levels of p-GSK-3β/GSK-3β were 0.85±0.09, 0.22±0.03, 0.44±0.06, 0.71±0.08, 0.79±0.09 and 0.42±0.05, respectively. There were statistically significant differences between model group and control group, between low, high dose experimental group and model group, and between inhibitor group and high-dose experimental group (all P<0.05).
Conclusion Ost reduces melanocyte loss in vitiligo mice by activating the Wnt/β-catenin signaling pathway.
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目的 探讨蛇床子素(Ost)调节Wnt/β-连环蛋白(Wnt/β-catenin)信号通路对白癜风小鼠黑素细胞丢失的作用。
方法 通过涂抹氢醌乳膏建立白癜风小鼠模型,将建模成功的小鼠分为模型组(仅建模)、低剂量实验组(15 mg·kg-1 Ost)、高剂量实验组(45 mg·kg-1 Ost)、阳性对照组(50.4 mg·mL-1白癜风胶囊)和抑制剂组(45 mg·kg-1 Ost+ 10 mg·kg-1XAV939),对照组给等体积生理盐水,每组10只。干预结束后,对治疗区域皮肤脱色程度进行评分;收集眼眶血液,用酶联免疫吸附试验法检测血清中丙二醛(MDA)、α-黑色素细胞刺激素(α-MSH)、酪氨酸酶(TYR)和肿瘤坏死因子α(TNF-α)水平;收集皮损组织,用苏木精伊红(HE)及马松染色法评估黑色素毛囊数和基底层黑素细胞数;用免疫组化法检测皮损组织中酪氨酸酶相关蛋白(TRP)1和TRP2阳性表达水平;用实时荧光定量逆转录聚合酶链反应(qRT-PCR)法检测皮损组织中的酪氨酸酶(TYR)和小眼症相关转录调节因子(MITF)mRNA表达水平;用蛋白质印迹法检测β-catenin和磷酸化糖原合成酶激酶-3β(p-GSK-3β)/GSK-3β蛋白表达。
结果 对照组、模型组、低剂量实验组、高剂量实验组、阳性对照组和抑制剂组的脱色评分分别为(0±0)、(4.11±0.52)、(2.41±0.28)、(0.77±0.09)、(0.55±0.07)和(2.55±0.28)分;ɑ-MSH水平分别为(26.53±2.84)、(7.56±0.84)、(12.62±1.36)、(22.91±2.44)、(23.51±2.48)和(13.05±1.38)μg·L-1;MDA水平分别为(2.05±0.24)、(7.94±0.85)、(4.31±0.49)、(2.27±0.25)、(2.19±0.24)和(4.28±0.45)nmol·mg prot-1;TNF-α水平分别为(38.52±4.02)、(105.65±10.94)、(68.84±7.05)、(42.84±4.45)、(41.85±4.37)和(70.05±7.21)ng·mL-1;TYR水平分别为(105.62±11.14)、(45.22±4.67)、(65.41±6.77)、(98.62±9.98)、(97.65±9.89)和(66.08±6.81)μg·L-1;基底层黑素细胞数量分别为(148.62±15.08)、(52.11±5.34)、(68.84±6.91)、(108.64±11.14)、(112.08±11.44)和(70.54±7.21)个;黑色素毛囊数分别为(98.64±9.98)、(41.52±4.31)、(62.05±6.37)、(95.62±9.74)、(96.05±9.78)和(61.08±6.29)个;TRP1阳性表达水平分别为17.05±1.94、4.62±0.77、8.05±0.85、14.98±1.58、15.22±1.64和8.11±0.88;TRP2阳性表达水平分别为14.32±1.55、3.05±0.33、5.74±0.66、10.42±1.15、11.05±1.17和6.05±0.62;TYR mRNA相对表达水平分别为1.09±0.12、0.19±0.02、0.49±0.05、0.79±0.08、0.88±0.09和0.55±0.07;MITF mRNA相对表达水平分别为0.98±0.11、0.24±0.03、0.44±0.05、0.81±0.09、0.85±0.10和0.51±0.06;β-catenin相对表达水平分别为1.25±0.13、0.34±0.05、0.68±0.08、1.07±0.11、1.11±0.12和0.71±0.09;p-GSK-3β/GSK-3β相对表达水平分别为0.85±0.09、0.22±0.03、0.44±0.06、0.71±0.08、0.79±0.09和0.42±0.05,模型组和对照组比较,低、高剂量实验组和模型组比较,抑制剂组与高剂量实验组比较,上述指标在统计学上差异均有统计学意义(均P<0.05)。
结论 Ost通过激活Wnt/β-catenin信号通路减少白癜风小鼠黑素细胞丢失。
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许丛丛(1990-),女,主治医师,主要从事皮肤相关研究工作
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