Article(id=1317115240404332556, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317115107243573307, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2026.04.023, 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=1791954344129, onlineDateStr=2026-10-14, pubDate=1775750400000, pubDateStr=2026-04-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791954344129, onlineIssueDateStr=2026-10-14, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791954344129, creator=13701087609, updateTime=1791954344129, 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=105, endPage=109, ext={EN=ArticleExt(id=1317115240605659149, articleId=1317115240404332556, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Study on Mechanism of Fuyanshu Capsule(妇炎舒胶囊)by Regulating TLR2/MyD88/NF-κB Pathway Through KLF4, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=
Objective

To observe the anti-inflammatory effect of Fuyanshu Capsule(妇炎舒胶囊, FYS)on sequelae of pelvic inflammatory disease(SPID)model rats on Krüppel-like factor 4(KLF4), Toll-like receptor 2(TLR2), nuclear factor-kappa B(NF-κB)and myeloid differentiation factor 88(MyD88).

Methods

Thirty-six rats were randomly divided into blank group, model group, Kangfuyan Capsule(康妇炎胶囊)group(KFY group), FYS high-dose group, FYS medium-dose group, FYS low-dose group. The SPID animal model was established by the method of mixed bacterial liquid injection and mechanical injury. The blank group was treated with distilled water by gavage, and the other groups were given the corresponding drug suspension by gavage for 21 days. HE staining was used to observe the morphology of uterine tissue and score the pathological sections. The mRNA expressions of TLR2, MyD88 and KLF4 were determined by RT-PCR, the expression of NF-κB was observed by immunohistochemistry method, and the relative protein expressions of TLR2, MyD88 and KLF4 in uterine tissues of each group were determined by Western Blot. The correlation between KLF4 and key factors of TLR2/MyD88/NF-κB pathway was analyzed.

Result

Compared with those in the model group, the scores of uterine tissue inflammation in KFY group, FYS medium - and high-dose groups were significantly decreased(P<0.05). KLF4 protein in KFY group and FYS high-dose group was significantly increased(P<0.01). The protein and mRNA of TLR2 in KFY group and FYS high-dose group were significantly decreased(P<0.05). MyD88 protein in KFY group, FYS high-and medium-dose groups was significantly decreased(P<0.05), and MyD88 mRNA in KFY group and FYS high-dose group was significantly decreased(P<0.05). The expressions of NF-κB protein in KFY group, FYS medium - and high-dose groups were significantly decreased(P<0.05). The expression of KLF4 protein was negatively correlated with the expressions of TLR2 protein, MyD88 protein and NF-κB protein(P<0.05).

Conclusion

FYS can inhibit the TLR2/MyD88/NF-κB pathway by up-regulating KLF4 expression.

, authors=Li HUANG, Xiaoli JI, Yan WANG, Xiaolan YIN, Shaobin WEI, authorsList=Li HUANG, Xiaoli JI, Yan WANG, Xiaolan YIN, Shaobin WEI, authorCompany=null, correspAuthors=Shaobin WEI, 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=1317115240836345870, articleId=1317115240404332556, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=从KLF4调控TLR2/MyD88/NF-κB通路探讨妇炎舒胶囊对盆腔炎性疾病后遗症大鼠抗炎作用机制, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=
目的

观察妇炎舒胶囊对盆腔炎性疾病后遗症(Sequelae of pelvic inflammatory disease,SPID)模型大鼠抗炎疗效及对SPID大鼠子宫组织Krüppel样因子4(Krüppel-like factor 4,KLF4)、Toll样受体2(Toll-like receptor 2,TLR2)、髓样分化因子88(Myeloid differentiation factor 88,MyD88)、核转录因子-κB(Nuclear factor-kappa B,NF-κB)的影响。

方法

采用混合菌液注射配合机械损伤法建立大鼠SPID模型,随机数字表法将36只大鼠分为空白组、模型组、康妇炎胶囊组(KFY组)、妇炎舒胶囊高剂量组(FYS高剂量组)、妇炎舒胶囊中剂量组(FYS中剂量组)、妇炎舒胶囊低剂量组(FYS低剂量组)。各组以相应药物混悬液灌胃21 d。病理切片HE染色观察子宫组织形态并评分,RT-PCR法测定TLR2、MyD88、KLF4 mRNA表达,免疫组化法观察NF-κB的表达,Western Blot法测定各组大鼠子宫组织中TLR2、MyD88、KLF4蛋白相对表达含量。分析KLF4与TLR2/MyD88/NF-κB通路关键因子的相关性。

结果

与模型组比较,KFY组、FYS中、高剂量组子宫组织炎症评分显著降低(P<0.05)。KFY组、FYS高剂量组KLF4蛋白显著升高(P<0.01)。KFY组、FYS高剂量组TLR2蛋白和mRNA显著降低(P<0.05)。KFY组、FYS高剂量组MyD88 mRNA显著降低(P<0.05),KFY组、FYS高、中剂量组MyD88蛋白显著降低(P<0.05)。KFY组、FYS中、高剂量组NF-κB蛋白表达显著降低(P<0.05)。KLF4蛋白表达水平与TLR2蛋白、MyD88蛋白、NF-κB蛋白表达均呈显著负相关(P<0.05)。

结论

妇炎舒胶囊可通过上调KLF4表达,抑制TLR2/MyD88/NF-κB通路发挥抗炎作用。

, authors=黄利, 季晓黎, 王妍, 尹小兰, 魏绍斌, authorsList=黄利, 季晓黎, 王妍, 尹小兰, 魏绍斌, authorCompany=null, correspAuthors=魏绍斌, authorNote=

黄利(1991-),女,四川遂宁人,主治医师,博士,研究方向:中医药防治妇科慢性盆腔炎症、痛症的临床与基础。

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魏绍斌(1957-),女,四川成都人,教授、主任医师,博士研究生导师,学士,研究方向:中医药防治妇科慢性盆腔炎症、痛症的临床与基础。E-mail: 。
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黄利(1991-),女,四川遂宁人,主治医师,博士,研究方向:中医药防治妇科慢性盆腔炎症、痛症的临床与基础。

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黄利(1991-),女,四川遂宁人,主治医师,博士,研究方向:中医药防治妇科慢性盆腔炎症、痛症的临床与基础。

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从KLF4调控TLR2/MyD88/NF-κB通路探讨妇炎舒胶囊对盆腔炎性疾病后遗症大鼠抗炎作用机制
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黄利 , 季晓黎 , 王妍 , 尹小兰 , 魏绍斌
中华中医药学刊 | 国家项目点击 2026,44(4): 105-109
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中华中医药学刊 |国家项目点击 2026 , 44 (4) : 105 -109
从KLF4调控TLR2/MyD88/NF-κB通路探讨妇炎舒胶囊对盆腔炎性疾病后遗症大鼠抗炎作用机制
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黄利(1991-),女,四川遂宁人,主治医师,博士,研究方向:中医药防治妇科慢性盆腔炎症、痛症的临床与基础。

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黄利(1991-),女,四川遂宁人,主治医师,博士,研究方向:中医药防治妇科慢性盆腔炎症、痛症的临床与基础。

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黄利, 季晓黎, 王妍, 尹小兰, 魏绍斌
作者信息
  • 成都中医药大学附属医院,四川 成都 610075
通讯作者:
魏绍斌(1957-),女,四川成都人,教授、主任医师,博士研究生导师,学士,研究方向:中医药防治妇科慢性盆腔炎症、痛症的临床与基础。E-mail: 。
作者简介:

黄利(1991-),女,四川遂宁人,主治医师,博士,研究方向:中医药防治妇科慢性盆腔炎症、痛症的临床与基础。

Study on Mechanism of Fuyanshu Capsule(妇炎舒胶囊)by Regulating TLR2/MyD88/NF-κB Pathway Through KLF4
Li HUANG, Xiaoli JI, Yan WANG, Xiaolan YIN, Shaobin WEI
Affiliations
  • Hospital of Chengdu University of Traditional Chineese Medicine, Chengdu 610075, Sichuan, China
出版时间: 2026-04-10 doi: 10.13193/j.issn.1673-7717.2026.04.023
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目的

观察妇炎舒胶囊对盆腔炎性疾病后遗症(Sequelae of pelvic inflammatory disease,SPID)模型大鼠抗炎疗效及对SPID大鼠子宫组织Krüppel样因子4(Krüppel-like factor 4,KLF4)、Toll样受体2(Toll-like receptor 2,TLR2)、髓样分化因子88(Myeloid differentiation factor 88,MyD88)、核转录因子-κB(Nuclear factor-kappa B,NF-κB)的影响。

方法

采用混合菌液注射配合机械损伤法建立大鼠SPID模型,随机数字表法将36只大鼠分为空白组、模型组、康妇炎胶囊组(KFY组)、妇炎舒胶囊高剂量组(FYS高剂量组)、妇炎舒胶囊中剂量组(FYS中剂量组)、妇炎舒胶囊低剂量组(FYS低剂量组)。各组以相应药物混悬液灌胃21 d。病理切片HE染色观察子宫组织形态并评分,RT-PCR法测定TLR2、MyD88、KLF4 mRNA表达,免疫组化法观察NF-κB的表达,Western Blot法测定各组大鼠子宫组织中TLR2、MyD88、KLF4蛋白相对表达含量。分析KLF4与TLR2/MyD88/NF-κB通路关键因子的相关性。

结果

与模型组比较,KFY组、FYS中、高剂量组子宫组织炎症评分显著降低(P<0.05)。KFY组、FYS高剂量组KLF4蛋白显著升高(P<0.01)。KFY组、FYS高剂量组TLR2蛋白和mRNA显著降低(P<0.05)。KFY组、FYS高剂量组MyD88 mRNA显著降低(P<0.05),KFY组、FYS高、中剂量组MyD88蛋白显著降低(P<0.05)。KFY组、FYS中、高剂量组NF-κB蛋白表达显著降低(P<0.05)。KLF4蛋白表达水平与TLR2蛋白、MyD88蛋白、NF-κB蛋白表达均呈显著负相关(P<0.05)。

结论

妇炎舒胶囊可通过上调KLF4表达,抑制TLR2/MyD88/NF-κB通路发挥抗炎作用。

妇炎舒胶囊  /  盆腔炎性疾病后遗症  /  Krüppel样因子4  /  髓样分化因子88  /  核转录因子-κB
Objective

To observe the anti-inflammatory effect of Fuyanshu Capsule(妇炎舒胶囊, FYS)on sequelae of pelvic inflammatory disease(SPID)model rats on Krüppel-like factor 4(KLF4), Toll-like receptor 2(TLR2), nuclear factor-kappa B(NF-κB)and myeloid differentiation factor 88(MyD88).

Methods

Thirty-six rats were randomly divided into blank group, model group, Kangfuyan Capsule(康妇炎胶囊)group(KFY group), FYS high-dose group, FYS medium-dose group, FYS low-dose group. The SPID animal model was established by the method of mixed bacterial liquid injection and mechanical injury. The blank group was treated with distilled water by gavage, and the other groups were given the corresponding drug suspension by gavage for 21 days. HE staining was used to observe the morphology of uterine tissue and score the pathological sections. The mRNA expressions of TLR2, MyD88 and KLF4 were determined by RT-PCR, the expression of NF-κB was observed by immunohistochemistry method, and the relative protein expressions of TLR2, MyD88 and KLF4 in uterine tissues of each group were determined by Western Blot. The correlation between KLF4 and key factors of TLR2/MyD88/NF-κB pathway was analyzed.

Result

Compared with those in the model group, the scores of uterine tissue inflammation in KFY group, FYS medium - and high-dose groups were significantly decreased(P<0.05). KLF4 protein in KFY group and FYS high-dose group was significantly increased(P<0.01). The protein and mRNA of TLR2 in KFY group and FYS high-dose group were significantly decreased(P<0.05). MyD88 protein in KFY group, FYS high-and medium-dose groups was significantly decreased(P<0.05), and MyD88 mRNA in KFY group and FYS high-dose group was significantly decreased(P<0.05). The expressions of NF-κB protein in KFY group, FYS medium - and high-dose groups were significantly decreased(P<0.05). The expression of KLF4 protein was negatively correlated with the expressions of TLR2 protein, MyD88 protein and NF-κB protein(P<0.05).

Conclusion

FYS can inhibit the TLR2/MyD88/NF-κB pathway by up-regulating KLF4 expression.

Fuyanshu Capsule(妇炎舒胶囊)  /  sequelae of pelvic inflammatory disease  /  KLF4  /  MyD88  /  NF-κB
黄利, 季晓黎, 王妍, 尹小兰, 魏绍斌. 从KLF4调控TLR2/MyD88/NF-κB通路探讨妇炎舒胶囊对盆腔炎性疾病后遗症大鼠抗炎作用机制. 中华中医药学刊, 2026 , 44 (4) : 105 -109 . DOI: 10.13193/j.issn.1673-7717.2026.04.023
Li HUANG, Xiaoli JI, Yan WANG, Xiaolan YIN, Shaobin WEI. Study on Mechanism of Fuyanshu Capsule(妇炎舒胶囊)by Regulating TLR2/MyD88/NF-κB Pathway Through KLF4[J]. Chinese Archives of Traditional Chinese Medicine, 2026 , 44 (4) : 105 -109 . DOI: 10.13193/j.issn.1673-7717.2026.04.023
  • 国家自然科学基金面上项目(82174431)
  • 四川省自然科学基金项目(青年科学基金B类2026NSFSC1869)
  • 四川省科技厅科技计划项目(2023NSFC0619)
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doi: 10.13193/j.issn.1673-7717.2026.04.023
  • 首发时间:2026-10-14
  • 出版时间:2026-04-10
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基金
国家自然科学基金面上项目(82174431)
四川省自然科学基金项目(青年科学基金B类2026NSFSC1869)
四川省科技厅科技计划项目(2023NSFC0619)
作者信息
    成都中医药大学附属医院,四川 成都 610075

通讯作者:

魏绍斌(1957-),女,四川成都人,教授、主任医师,博士研究生导师,学士,研究方向:中医药防治妇科慢性盆腔炎症、痛症的临床与基础。E-mail: 。
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红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
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