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Article(id=1291404928673633276, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404807152067353, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.08.004, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1728835200000, receivedDateStr=2024-10-14, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824528138, onlineDateStr=2026-08-04, pubDate=1745769600000, pubDateStr=2025-04-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824528138, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824528138, creator=13701087609, updateTime=1785824528138, updator=13701087609, issue=Issue{id=1291404807152067353, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='8', pageStart='1051', pageEnd='1200', issueExtLink='null', onlineDate='null', pubDate='1745769600000', pubDateStr='2025-04-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824499166, creator='13701087609', updateTime=1785824499166, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=1067, endPage=1071, ext={EN=ArticleExt(id=1291404928870765565, articleId=1291404928673633276, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of Tilianin liposomes downregulating ROS/NLRP3 pathway to improve macrophage pyroptosis, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective

To explore the mechanism of regulating reactive oxygen species (ROS)/Nod-like receptor family pyrin domain-contain-ning protein 3 (NLRP3) by Tilianin liposomes improved macrophage pyroptosis.

Methods

Macrophage pyroptosis model using lipopolysaccharide (LPS) combined with adenosine triphosphate (ATP) was established. They were divided into control group, model group, and experimental group (RAW 264.7 macrophages). The experimental group was treated with 5 μg·mL-1 Tilianin liposomes for 12 hours, while the control group and model group were cultured normally in complete culture medium without medication for 12 hours. Microplate method was used to detect the release of lactate dehydrogenase (LDH). Enzyme linked immunosorbent assay was used to detect the contents of interleukin (IL)-1β and IL-18. Detection of ROS content in cells was done by flow cytometry. Western blotting was used to detect the relative expression levels of NLRP3.

Results

The LDH release levels in the experimental, control and model groups were (568.54±68.04), (556.05±83.31) and (984.41±138.82) U·L-1; the IL-1β contents were (8.99±2.17), (5.51±0.49) and (38.78±3.33) pg·mL-1; the IL-18 contents were (35.95±5.24), (20.95±2.36) and (64.14±9.73) pg·mL-1; the ROS release levels were 4.00±0.48, 0.68±0.50 and 9.58±0.42; the relative expression levels of NLRP3 protein were 2.44±0.46, 1.00±0.10 and 4.76±0.61, respectively. The above indicators in the experimental and control groups were compared with those in the model group, and there were statistically significant differences (all P<0.01).

Conclusion

Tilianin liposomes can reduce endogenous ROS production and improve LPS/ATP induced RAW 264.7 macrophage pyroptosis, which may be related to the regulation of ROS/NLRP3 inflammasome signaling pathway.

, authors=Hui-ling YANG1a, Min SUN1b, Zhong-shan HE2, Meng-ran GUO2, Yao-yao LUO2, Ru-yue LIU1b, Xu-li RUAN1b, Xiang-rong SONG2, Wen-jiang CAO1b, Xin-chun WANG1b, Zhong WANG1a, authorsList=Hui-ling YANG, Min SUN, Zhong-shan HE, Meng-ran GUO, Yao-yao LUO, Ru-yue LIU, Xu-li RUAN, Xiang-rong SONG, Wen-jiang CAO, Xin-chun WANG, Zhong WANG, authorCompany=null, correspAuthors=Zhong WANG, 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=1291404929386664958, articleId=1291404928673633276, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=田蓟苷脂质体下调ROS/NLRP3途径改善巨噬细胞焦亡的研究, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的

探究田蓟苷脂质体调控活性氧（ROS）/Nod样受体热蛋白结构域相关蛋白3（NLRP3）改善巨噬细胞焦亡的作用机制。

方法

用脂多糖（LPS）联合腺苷三磷酸（ATP）建立巨噬细胞焦亡模型。将小鼠RAW 264.7巨噬细胞分为对照组、模型组和实验组。模型组和实验组在造模后，实验组在含5 μg·mL-1田蓟苷脂质体的完全培养基中培养12 h，对照组和模型组均在不含药的完全培养基中正常培养12 h。用微板法检测乳酸脱氢酶（LDH）的释放情况，用酶联免疫吸附试验法检测白细胞介素（IL）-1β和IL-18含量，用流式细胞术检测细胞中ROS含量，用蛋白质印迹法检测NLRP3的表达水平。

结果

实验组、对照组和模型组的LDH释放量分别为（568.54±68.04）、（556.05±83.31）和（984.41±138.82）U·L-1，IL-1β含量分别为（8.99±2.17）、（5.51±0.49）和（38.78±3.33）pg·mL-1，IL-18含量分别为（35.95±5.24）、（20.95±2.36）和（64.14±9.73）pg·mL-1，ROS释放量分别为4.00±0.48、0.68±0.50和9.58±0.42，NLRP3蛋白相对表达水平分别为2.44±0.46、1.00±0.10和4.76±0.61。实验组和对照组的上述指标与模型组比较，在统计学上差异均有统计学意义（均P<0.01）。

结论

田蓟苷脂质体可以降低内源性ROS的产生，改善LPS/ATP诱导的RAW 264.7巨噬细胞焦亡，其机制可能与调控ROS/NLRP3炎症小体信号通路有关。

, authors=杨慧玲1a, 孙敏1b, 何中山2, 国梦然2, 罗尧尧2, 刘茹月1b, 阮徐莉1b, 宋相容2, 曹文疆1b, 王新春1b, 王忠1a, authorsList=杨慧玲, 孙敏, 何中山, 国梦然, 罗尧尧, 刘茹月, 阮徐莉, 宋相容, 曹文疆, 王新春, 王忠, authorCompany=null, correspAuthors=王忠, authorNote=

杨慧玲（1996-），女，硕士研究生，主要从事心血管方向的相关研究

, correspAuthorsNote=
王忠，主任医师，博士生导师 Tel: （0993）2855827 E-mail:
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杨慧玲（1996-），女，硕士研究生，主要从事心血管方向的相关研究

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田蓟苷脂质体下调ROS/NLRP3途径改善巨噬细胞焦亡的研究
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杨慧玲 1a , 孙敏 1b , 何中山 2 , 国梦然 2 , 罗尧尧 2 , 刘茹月 1b , 阮徐莉 1b , 宋相容 2 , 曹文疆 1b , 王新春 1b , 王忠 1a
中国临床药理学杂志 | 临床与基础桥接研究 2025,41(8): 1067-1071
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中国临床药理学杂志 |临床与基础桥接研究 2025 , 41 (8) : 1067 -1071
田蓟苷脂质体下调ROS/NLRP3途径改善巨噬细胞焦亡的研究
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杨慧玲1a, 孙敏1b, 何中山2, 国梦然2, 罗尧尧2, 刘茹月1b, 阮徐莉1b, 宋相容2, 曹文疆1b, 王新春1b, 王忠1a
作者信息
  • 1a.石河子大学 第一附属医院，心内科，新疆维吾尔自治区 石河子 832008
  • 1b.石河子大学 第一附属医院，药剂科，新疆维吾尔自治区 石河子 832008
  • 2.四川大学 华西医院 重症医学科，四川 成都 610041
通讯作者:
王忠，主任医师，博士生导师 Tel: （0993）2855827 E-mail:
作者简介:

杨慧玲（1996-），女，硕士研究生，主要从事心血管方向的相关研究

Research of Tilianin liposomes downregulating ROS/NLRP3 pathway to improve macrophage pyroptosis
Hui-ling YANG1a, Min SUN1b, Zhong-shan HE2, Meng-ran GUO2, Yao-yao LUO2, Ru-yue LIU1b, Xu-li RUAN1b, Xiang-rong SONG2, Wen-jiang CAO1b, Xin-chun WANG1b, Zhong WANG1a
Affiliations
  • 1a.Department of Cardiology, The First Affiliated Hospital of Shihezi University, Shihezi 832008, Xinjiang Uygur Autonomous Region, China
  • 1b.Department of Pharmacy, The First Affiliated Hospital of Shihezi University, Shihezi 832008, Xinjiang Uygur Autonomous Region, China
  • 2.Department of Critical Care Medicine, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China
出版时间: 2025-04-28 doi: 10.13699/j.cnki.1001-6821.2025.08.004
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摘要
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目的

探究田蓟苷脂质体调控活性氧（ROS）/Nod样受体热蛋白结构域相关蛋白3（NLRP3）改善巨噬细胞焦亡的作用机制。

方法

用脂多糖（LPS）联合腺苷三磷酸（ATP）建立巨噬细胞焦亡模型。将小鼠RAW 264.7巨噬细胞分为对照组、模型组和实验组。模型组和实验组在造模后，实验组在含5 μg·mL-1田蓟苷脂质体的完全培养基中培养12 h，对照组和模型组均在不含药的完全培养基中正常培养12 h。用微板法检测乳酸脱氢酶（LDH）的释放情况，用酶联免疫吸附试验法检测白细胞介素（IL）-1β和IL-18含量，用流式细胞术检测细胞中ROS含量，用蛋白质印迹法检测NLRP3的表达水平。

结果

实验组、对照组和模型组的LDH释放量分别为（568.54±68.04）、（556.05±83.31）和（984.41±138.82）U·L-1，IL-1β含量分别为（8.99±2.17）、（5.51±0.49）和（38.78±3.33）pg·mL-1，IL-18含量分别为（35.95±5.24）、（20.95±2.36）和（64.14±9.73）pg·mL-1，ROS释放量分别为4.00±0.48、0.68±0.50和9.58±0.42，NLRP3蛋白相对表达水平分别为2.44±0.46、1.00±0.10和4.76±0.61。实验组和对照组的上述指标与模型组比较，在统计学上差异均有统计学意义（均P<0.01）。

结论

田蓟苷脂质体可以降低内源性ROS的产生，改善LPS/ATP诱导的RAW 264.7巨噬细胞焦亡，其机制可能与调控ROS/NLRP3炎症小体信号通路有关。

田蓟苷脂质体  /  Nod样受体热蛋白结构域相关蛋白3  /  细胞焦亡  /  活性氧
Objective

To explore the mechanism of regulating reactive oxygen species (ROS)/Nod-like receptor family pyrin domain-contain-ning protein 3 (NLRP3) by Tilianin liposomes improved macrophage pyroptosis.

Methods

Macrophage pyroptosis model using lipopolysaccharide (LPS) combined with adenosine triphosphate (ATP) was established. They were divided into control group, model group, and experimental group (RAW 264.7 macrophages). The experimental group was treated with 5 μg·mL-1 Tilianin liposomes for 12 hours, while the control group and model group were cultured normally in complete culture medium without medication for 12 hours. Microplate method was used to detect the release of lactate dehydrogenase (LDH). Enzyme linked immunosorbent assay was used to detect the contents of interleukin (IL)-1β and IL-18. Detection of ROS content in cells was done by flow cytometry. Western blotting was used to detect the relative expression levels of NLRP3.

Results

The LDH release levels in the experimental, control and model groups were (568.54±68.04), (556.05±83.31) and (984.41±138.82) U·L-1; the IL-1β contents were (8.99±2.17), (5.51±0.49) and (38.78±3.33) pg·mL-1; the IL-18 contents were (35.95±5.24), (20.95±2.36) and (64.14±9.73) pg·mL-1; the ROS release levels were 4.00±0.48, 0.68±0.50 and 9.58±0.42; the relative expression levels of NLRP3 protein were 2.44±0.46, 1.00±0.10 and 4.76±0.61, respectively. The above indicators in the experimental and control groups were compared with those in the model group, and there were statistically significant differences (all P<0.01).

Conclusion

Tilianin liposomes can reduce endogenous ROS production and improve LPS/ATP induced RAW 264.7 macrophage pyroptosis, which may be related to the regulation of ROS/NLRP3 inflammasome signaling pathway.

Tilianin liposomes  /  Nod-like receptor family pyrin domain-contain-ning protein 3  /  cell pyroptosis  /  reactive oxygen species
杨慧玲, 孙敏, 何中山, 国梦然, 罗尧尧, 刘茹月, 阮徐莉, 宋相容, 曹文疆, 王新春, 王忠. 田蓟苷脂质体下调ROS/NLRP3途径改善巨噬细胞焦亡的研究. 中国临床药理学杂志, 2025 , 41 (8) : 1067 -1071 . DOI: 10.13699/j.cnki.1001-6821.2025.08.004
Hui-ling YANG, Min SUN, Zhong-shan HE, Meng-ran GUO, Yao-yao LUO, Ru-yue LIU, Xu-li RUAN, Xiang-rong SONG, Wen-jiang CAO, Xin-chun WANG, Zhong WANG. Research of Tilianin liposomes downregulating ROS/NLRP3 pathway to improve macrophage pyroptosis[J]. Chinese Journal of Clinical Pharmacology, 2025 , 41 (8) : 1067 -1071 . DOI: 10.13699/j.cnki.1001-6821.2025.08.004
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  • 国家自然科学基金资助项目(81960766)
  • 兵团科技计划项目重点领域科技攻关计划基金资助项目(2022AB020)
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doi: 10.13699/j.cnki.1001-6821.2025.08.004
  • 接收时间：2024-10-14
  • 首发时间：2026-08-04
  • 出版时间：2025-04-28
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  • 收稿日期：2024-10-14
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国家自然科学基金资助项目(81960766)
兵团科技计划项目重点领域科技攻关计划基金资助项目(2022AB020)
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    1a.石河子大学 第一附属医院，心内科，新疆维吾尔自治区 石河子 832008
    1b.石河子大学 第一附属医院，药剂科，新疆维吾尔自治区 石河子 832008
    2.四川大学 华西医院 重症医学科，四川 成都 610041

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2种不同金属材料的力学参数
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Family		 属数
Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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