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引用本文:杨洞洞,张青,蒋镥.小青龙汤通过调节细胞外组蛋白HATs/HDACs平衡减轻脓毒症所致急性呼吸窘迫综合症[J].中国现代应用药学,2025,42(3):75-82.
Yang Dongdong,Zhang Qing,Jiang Lu.Xiao-Qing-Long-Tang Attenuates Sepsis-induced Acute Respiratory Distress Syndrome via Regulating Extracellular Histone Acetyltransferases/Histone Deacetylases Balance[J].Chin J Mod Appl Pharm(中国现代应用药学),2025,42(3):75-82.
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小青龙汤通过调节细胞外组蛋白HATs/HDACs平衡减轻脓毒症所致急性呼吸窘迫综合症
杨洞洞, 张青, 蒋镥
浙江中医药大学附属第一医院
摘要:
目的:小青龙汤在急性呼吸窘迫综合征(ARDS)的临床和动物研究中疗效显著。在这里,我们探索了小青龙汤在治疗脓毒症诱导的ARDS小鼠中的具体作用机制。方法:通过盲肠结扎和穿孔(CLP)在BALB/c小鼠中诱导脓毒症。用小青龙汤处理后,分别用适当的试剂盒检测组蛋白乙酰转移酶(HAT)和组蛋白去乙酰化酶(HDAC)活性。Western blot用于分析小鼠肺组织中乙酰组蛋白H3、凋亡相关蛋白、HDAC2、HDAC7和HDAC8的表达。使用酶联免疫吸附试验(ELISA)检测脓毒症相关细胞因子的浓度。实时定量PCR(qRT-PCR)确定了小鼠血液中脓毒症相关细胞因子的水平、小鼠肺组织中HDAC的表达和凋亡相关蛋白的表达。肺组织切片用苏木精和伊红染色以观察病理状况。结果:小青龙汤减轻了ARDS小鼠中HAT活性和乙酰组蛋白H3含量的下降,提高了HDAC活性,抑制及脓毒症相关细胞因子浓度的上升,缓解了肺损伤和肺细胞凋亡。小青龙汤对乙酰组蛋白H3表达的促进作用及其对肺损伤和肺细胞凋亡的缓解作用被HDAC2过表达所逆转。结论:小青龙汤通过调节细胞外HATs/HDACs平衡减轻脓毒症诱导的ARDS。
关键词:  小青龙汤  急性呼吸窘迫综合征  组蛋白乙酰转移酶  组蛋白去乙酰化酶
DOI:10.13748/j.cnki.issn1007-7693.20223380
分类号:R284.1;R917.101
基金项目:1.National Natural Science Foundation of China (NSFC):82104763 2.Zhejiang Provincial Natural Science Foundation of China (LY18H270010). 3.Zhejiang TCM Science and Technology Plan(2020ZB070) 4.General Scientific Research Project of Zhejiang Education Department(Y202045269) 5.Zhejiang TCM Science and Technology Plan(2021ZB103)
Xiao-Qing-Long-Tang Attenuates Sepsis-induced Acute Respiratory Distress Syndrome via Regulating Extracellular Histone Acetyltransferases/Histone Deacetylases Balance
Yang Dongdong, Zhang Qing, Jiang Lu
The First Afliated Hospital of Zhejiang Chinese Medical University
Abstract:
Background: Xiao-Qing-Long-Tang (XQLT) is of obvious curative effect in the clinical and animal studies of acute respiratory distress syndrome (ARDS). Here, we explored the specific action mechanism of XQLT in the treatment of mice suffering from sepsis-induced ARDS.Methods: Sepsis was induced by cecal ligation and puncture (CLP) in BALB/c mice. After treatment with XQLT, histone acetyltransferase (HAT) and histone deacetylase (HDAC) activities were detected by appropriate kits respectively. Western blot was used to analyze Acetyl Histone H3, apoptosis-related proteins, HDAC2, HDAC7 and HDAC8 expression in lung tissue of mice. The concentrations of sepsis-related cellular factors were examined using Enzyme-linked immune sorbent assay (ELISA). Quantitative real-time PCR (qRT-PCR) identified sepsis-related cellular factor levels in the mouse blood, HDAC expression and apoptosis-related protein expression in mouse lung tissue. Lung tissue sections were stained with hematoxylin and eosin for the observation of pathological condition.Results: XQLT attenuated decline in HAT activity and Acetyl Histone H3 content, facilitated HDAC activity, suppressed concentration of sepsis-related cellular factors, alleviated lung injury and lung cell apoptosis in CLP mice. The promotion of XQLT on Acetyl Histone H3 expression and its mitigative effect on the lung injury as well as lung cell apoptosis were overturned by HDAC2 overexpression.Conclusions: XQLT attenuated sepsis-induced ARDS via regulating extracellular HATs/HDACs balance.
Key words:  XQLT  sepsis-induced ARDS  HAT  HDAC
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