Article(id=1321426318575649682, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1321426285826519296, articleNumber=null, orderNo=null, doi=10.20251/j.cnki.1003-3734.2026.16.011, 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=1753286400000, acceptedDateStr=2025-07-24, onlineDate=1792982185261, onlineDateStr=2026-10-26, pubDate=1788019200000, pubDateStr=2026-08-30, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1792982185261, onlineIssueDateStr=2026-10-26, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1792982185261, creator=13701087609, updateTime=1792982185261, updator=13701087609, issue=Issue{id=1321426285826519296, tenantId=1146029695717560320, journalId=1235980733773295621, year='2026', volume='35', issue='16', pageStart='1681', pageEnd='1792', issueExtLink='null', onlineDate='null', pubDate='1788019200000', pubDateStr='2026-08-30', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1792982177454, creator='13701087609', updateTime=1792982881356, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1321429238297776921, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1321426285826519296, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1321429238297776922, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1321426285826519296, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1763, endPage=1769, ext={EN=ArticleExt(id=1321426318772781971, articleId=1321426318575649682, tenantId=1146029695717560320, journalId=1235980733773295621, language=EN, title=Antipyretic mechanism of Binafuxi Granules on dry yeast-induced fever rat model, columnId=null, journalTitle=Chinese Journal of New Drugs, columnName=null, runingTitle=null, highlight=null, articleAbstract=
Objective: To evaluate the antipyretic effect of Binafuxi Granules on dry yeast-induced fever model in rats and further explore its antipyretic mechanism, in order to provide a theoretical basis for the clinical application of Binafuxi Granules.
Methods: The rat fever model induced by dry yeast was established, and the antipyretic mechanism of Binafuxi Granules on fungal fever rats was investigated by rat anal temperature measurement, ELISA detection, qPCR detection, and Western blot detection.
Results: The dry yeast-induced fever model experiment showed that compared with the model group, the rectal temperature of rats in each administration group of Binafuxi Granules decreased significantly in a continuous period of time (P<0.01). Compared with the model group, the contents of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) in serum and the contents of prostaglandin E2 (PGE2) and cyclic adenosine monophosphate (cAMP) in hypothalamus were significantly decreased in each administration group (P<0.01). The mRNA expression levels of Toll-like receptor 4 (TLR4), cyclooxygenase-2 (COX2), nuclear factor κB p65 (NF-κB p65) and other immune and inflammatory response-related genes in the hypothalamus of rats were significantly inhibited (P<0.05). The expression levels of immune and inflammatory response-related proteins TLR4 and p-NF-κBP65 in the hypothalamus of model rats were significantly down-regulated (P<0.05).
Conclusion: Binafuxi Granules may inhibit the production of heat-causing inflammatory factors by regulating TLR4/NF-кB signaling pathway and exert antipyretic effect.
, authors=ALITUNGULI Aihemaiti
1, ELIZIERE Shawuti
2, SHAMISINUR Abulimiti
3, Fu-xiang LUO
4, Jian-mei LI
4, Ming YAN
4, Li GAO
4, *, authorsList=ALITUNGULI Aihemaiti, ELIZIERE Shawuti, SHAMISINUR Abulimiti, Fu-xiang LUO, Jian-mei LI, Ming YAN, Li GAO, authorCompany=null, correspAuthors=Li GAO, 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=1321426319037023124, articleId=1321426318575649682, tenantId=1146029695717560320, journalId=1235980733773295621, language=CN, title=比那甫西颗粒对干酵母致热大鼠模型的解热作用机制研究, columnId=1236330556003242277, journalTitle=中国新药杂志, columnName=实验研究, runingTitle=null, highlight=null, articleAbstract=
目的: 本研究评估比那甫西颗粒对干酵母诱导大鼠发热模型的解热效果,并深入探讨其解热作用机制,以期为比那甫西颗粒的临床应用提供理论依据。
方法: 建立干酵母诱导大鼠发热模型,通过大鼠肛温测量、ELISA检测、qPCR检测和Western blot检测等方法考察比那甫西颗粒对真菌性发热大鼠解热的作用机制。
结果: 干酵母诱导的发热模型实验结果显示,与模型组相比,比那甫西颗粒各给药组大鼠连续时间段内肛温均显著下降(P<0.01);与模型组相比,比那甫西颗粒各给药组明显降低大鼠血清中致热炎性因子白细胞介素-1β(interleukin-1β, IL-1β)、白细胞介素-6(interleukin-6, IL-6)、肿瘤坏死因子-α(tumor necrosis factor-α, TNF-α)和干扰素-γ(inerferon-γ, IFN-γ)的含量以及下丘脑组织中前列腺素E2(prostaglandin E2, PGE2)和环磷酸腺苷(cyclic adenosine monophosphat, cAMP)的含量(P<0.01),明显抑制大鼠下丘脑中Toll样受体4(Toll-like receptor4, TLR4)、环氧合酶-2(cyclooxygenase 2, COX2)、核因子κB p65(nuclear factor-κB p65, NF-κB p65)等免疫和炎症反应相关基因的mRNA表达水平(P<0.05),显著下调模型大鼠下丘脑中免疫和炎症反应相关蛋白TLR4、p-NF-κB p65的表达水平(P<0.05)。
结论: 比那甫西颗粒可能通过调控TLR4/NF-κB信号通路,抑制致热炎性因子的产生,发挥解热作用。
, authors=阿丽屯古丽·艾合买提
1, 伊丽孜热·沙吾提
2, 沙米西奴尔·阿不力米提
3, 罗福祥
4, 李建梅
4, 闫明
4, 高莉
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