血必净注射液通过上调磷脂转运蛋白调控巨噬细胞JNK/c-JUN通路改善脓毒症相关急性呼吸窘迫综合征

doi:10.12122/j.issn.1673-4254.2026.09.04

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (9): 2035-2045.doi: 10.12122/j.issn.1673-4254.2026.09.04

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血必净注射液通过上调磷脂转运蛋白调控巨噬细胞JNK/c-JUN通路改善脓毒症相关急性呼吸窘迫综合征

徐璐¹(), 潘缘瑾¹, 汪雨辰², 陈振宇¹, 蒋伟², 於江泉¹^,²(), 郑瑞强¹^,²()

^1.徐州医科大学扬州临床学院重症医学科，江苏扬州 225001
^2.扬州大学附属苏北人民医院重症医学科，江苏扬州 225001

收稿日期:2026-02-04 出版日期:2026-09-20 发布日期:2026-09-30
通讯作者: 於江泉,郑瑞强 E-mail:sxmuxl@163.com;yujiangquan2021@163.com;zhengruiqiang2021@163.com
作者简介:徐璐，在读硕士研究生，E-mail: sxmuxl@163.com
基金资助:
国家临床重点专科建设项目（176[2022]）;国家中西医结合旗舰科室建设项目（60[2023]）;江苏省中医药科技发展计划重点项目(ZD202427);江苏省医学重点学科培育单位(JSDW20221);江苏省前沿技术研发计划(BF2025639);扬州市卫生健康委科研重点项目(2023-1-02);江苏省苏北人民医院管理课题(YYGL202306);扬州市社会发展项目(YZ2023105)

Xuebijing Injection ameliorates sepsis-associated acute respiratory distress syndrome in mice by upregulating phospholipid transfer protein to regulate macrophage JNK/c-JUN pathway

Lu XU¹(), Yuanjin PAN¹, Yuchen WANG², Zhenyu CHEN¹, Wei JIANG², Jiangquan YU¹^,²(), Ruiqiang ZHENG¹^,²()

^1.Department of Critical Care Medicine, Yangzhou Clinical College of Xuzhou Medical University, Yangzhou 225001, China
^2.Department of Critical Care Medicine, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou 225001, China

Received:2026-02-04 Online:2026-09-20 Published:2026-09-30
Contact: Jiangquan YU, Ruiqiang ZHENG E-mail:sxmuxl@163.com;yujiangquan2021@163.com;zhengruiqiang2021@163.com
Supported by:
National Key Clinical Specialty Construction Project (176[2022]);National Flagship Department of Integrated Chinese and Western Medicine Construction Project (60(2023)

摘要/Abstract

摘要：

目的探讨血必净对脂多糖（LPS）诱导的脓毒症相关急性呼吸窘迫综合征（ARDS）小鼠模型的保护作用及其分子机制。方法体内实验：C57BL/6J小鼠随机分为对照组、LPS模型组、LPS+低剂量血必净注射液组（LPS+LXBJ）和LPS+高剂量血必净注射液组（LPS+HXBJ）（n=15）。检测生存率、肺组织病理（HE染色、肺损伤评分、湿/干质量比）、炎症因子［肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）］水平、磷脂转运蛋白（PLTP）表达（转录组测序、实时荧光定量PCR、Western blotting、酶联免疫吸附试验、免疫荧光）。体外实验：RAW264.7巨噬细胞给予LPS与不同浓度血必净处理，检测细胞活力、形态、炎症因子及PLTP表达，并利用过表达PLTP验证其功能。信号通路：检测JNK/c-JUN和NF-κB通路蛋白表达。结果与LPS组相比，血必净治疗（尤其是高剂量组）提高脓毒症ARDS小鼠的4 d生存率（P<0.05），降低肺组织病理学损伤评分（P<0.001）和湿/干质量比（P<0.001）。血必净降低了血清及肺泡灌洗液中TNF-α、IL-6和IL-1β的水平：在血清中，低剂量血必净即可降低上述指标（P<0.05），高剂量血必净作用更为显著；在肺泡灌洗液中，低、高剂量血必净均可降低IL-1β水平（P<0.05），高剂量血必净降低TNF-α、IL-6（P<0.05）水平，而低剂量血必净的作用未达到统计学意义（P>0.05）。转录组测序及实验验证显示，LPS下调肺组织PLTP表达（P<0.001），而血必净干预可逆转该趋势（P<0.05）。体外实验显示，血必净呈剂量依赖性地抑制LPS诱导的RAW264.7细胞炎症因子释放（P<0.05），并上调PLTP表达。机制研究显示，血必净通过上调PLTP，抑制了JNK/c-JUN和NF-κB信号通路的磷酸化激活（P<0.05），而过表达PLTP则增强其效果（P<0.05）。结论血必净通过上调PLTP表达，抑制JNK/c-JUN和NF-κB信号通路，减轻脓毒症相关ARDS的炎症反应与组织损伤，提示PLTP可能为其作用的关键靶点。

关键词: 血必净注射液, 脓毒症, 急性呼吸窘迫综合征, 磷脂转运蛋白, 巨噬细胞, JNK/c-JUN通路, NF-κB通路

Abstract:

Objective To investigate the ameliorative effect of Xuebijing Injection in a mouse model of sepsis-associated acute respiratory distress syndrome (ARDS) and its molecular mechanisms. Methods In a C57BL/6J mouse model of sepsis-associated ARDS induced by lipopolysaccharide (LPS), the ameliorative effect of pretreatment with Xuebijing injection at low and high doses prior to modeling were evaluated by analyzing survival rates, lung histopathology, levels of inflammatory cytokines, and expressions of phospholipid transfer protein (PLTP) using transcriptomics, qPCR, Western blotting, ELISA, and immunofluorescence staining. In the cell experiment, RAW264.7 macrophages treated with LPS and different concentrations of Xuebijing were examined for changes in cell viability, morphology, inflammatory cytokine levels, and PLTP expression. PLTP overexpression experiment was carried out to verify the function of PLTP, and the changes in expressions of JNK/c-JUN and NF-κB pathway proteins were detected. Results Xuebijing pretreatment, especially at the high dose, significantly increased the 4-day survival rate, reduced lung histopathological injury score, and decreased lung wet/dry weight ratio in mice with sepsis-associated ARDS. High-dose Xuebijing more effectively lowered serum levels of TNF-α, IL-6, and IL-1β than the low dose, while at both doses, Xuebijing significantly decreased IL-1β levels in the bronchoalveolar lavage fluid (BALF); Xuebijing at the high dose, but not the low dose, significantly reduced BALF levels of TNF‑α and IL-6. LPS significantly downregulated PLTP expression in mouse lung tissue, a trend effectively ameliorated by Xuebijing pretreatment. In cultured RAW264.7 cells, Xuebijing dose-dependently inhibited LPS-induced inflammatory cytokine release and upregulated PLTP expression, resulting also in suppressed phosphorylation and activation of the JNK/c-JUN and NF-κB signaling pathways, and this effect was significantly enhanced by PLTP overexpression. Conclusion Xuebijing alleviates sepsis-associated ARDS by upregulating PLTP and inhibiting JNK/c-JUN and NF-κB signaling pathways, suggesting the potential of PLTP as a therapeutic target for this condition.

Key words: Xuebijing injection, sepsis, acute respiratory distress syndrome, phospholipid transfer protein, macrophages, JNK/c-JUN pathway, NF-κB pathway

徐璐, 潘缘瑾, 汪雨辰, 陈振宇, 蒋伟, 於江泉, 郑瑞强. 血必净注射液通过上调磷脂转运蛋白调控巨噬细胞JNK/c-JUN通路改善脓毒症相关急性呼吸窘迫综合征[J]. 南方医科大学学报, 2026, 46(9): 2035-2045.

Lu XU, Yuanjin PAN, Yuchen WANG, Zhenyu CHEN, Wei JIANG, Jiangquan YU, Ruiqiang ZHENG. Xuebijing Injection ameliorates sepsis-associated acute respiratory distress syndrome in mice by upregulating phospholipid transfer protein to regulate macrophage JNK/c-JUN pathway[J]. Journal of Southern Medical University, 2026, 46(9): 2035-2045.

图/表 8

表1 siRNA序列

Tab.1 siRNA sequences

siRNA	Sequence (5'-3')
siPLTP-sense	GGUUUCAAAUCUACUCAAATTT
siPLTP-antisense	UUUGAGUAGAUUUGAAACCTT
siNC-sense	UUCUCCGAACGUGUCACGUTT
siNC-antisense	ACGUGACACGUUCGGAGAATT

表2 qPCR引物序列

Tab.2 qPCR primer sequences

Primer	Sequence (5'-3')
PLTP(mouse)-F	TTCCTCCTCAACCAGCAGATCT
PLTP(mouse)-R	CAGGAGGGAGTTGAGCAACAC
GAPDH(mouse)-F	TGACGTGCCGCCTGGAGAAA
GAPDH(mouse)-R	AGTGTAGCCCAAGATGCCCTTCAG

图1 血必净对脓毒症相关ARDS小鼠的保护作用

Fig.1 Protective effect of Xuebijing against sepsis-associated ARDS in mice. A: Schematic diagram of the experimental procedure. B: Four-day survival curves of the mice in each group (n=15). C: HE staining of mouse lung tissues. D: Lung injury scores (n=6). E: Lung wet/dry weight (W/D) ratio (n=10). ###P<0.001 vs Control group; ***P<0.001 vs LPS group.

图2 血必净改善脓毒症相关ARDS小鼠的炎症反应

Fig.2 Xuebijing ameliorates inflammatory response in mice with sepsis-associated ARDS. A: Expressions of TNF-α and IL-6 in CD31+ endothelial cells detected by immunofluorescence co-localization (Scale bar=50 μm). B: Expression of TNF‑α and IL-6 in F4/80+ macrophages detected by immunofluorescence co-localization (Scale bar=50 μm). C-H: Results of ELISA for measuring concentrations of TNF-α, IL-6, and IL-1β in serum (C-E) and bronchoalveolar lavage fluid (BALF) (F-H) of the mice (n=6). ###P<0.001 vs Control group; *P<0.05, **P<0.01, ***P<0.001 vs LPS group.

图3 血必净上调脓毒症相关ARDS小鼠的PLTP表达

Fig.3 Xuebijing upregulates PLTP expression in sepsis-associated ARDS mice. A: Transcriptomic sequencing analysis showing downregulation of PLTP by LPS and upregulation by Xuebijing. B: Heatmap of PLTP expression in different groups. C: Venn diagram of differentially expressed genes between LPS and XBJ groups (n=3). D: qRT-PCR analysis of PLTP mRNA levels in mouse lung tissue. E, F: Western blotting for detecting PLTP protein expression in mouse lung tissue. G: ELISA measurement of serum PLTP levels. H: Immunofluorescence co-localization analysis of PLTP (green) with CD31+ endothelial cells (orange) in mouse lung tissue (Scale bar=50 μm). I: Immunofluorescence co-localization analysis of PLTP (red) with F4/80+ macrophages (green) in mouse lung tissue (Scale bar=50 μm). #P<0.05, ##P<0.01, ###P<0.001 vs Control group; *P<0.05, ***P<0.001 vs LPS group.

图4 血必净增强RAW264.7细胞活力并抑制LPS诱导的炎症因子释放

Fig.4 Xuebijing enhances viability and suppresses LPS-induced inflammatory cytokine release in RAW264.7 cells. A: Effect of Xuebijing at different dilutions on RAW264.7 cell viability measured by CCK-8 assay (n=3). B: Morphological changes of RAW264.7 cells induced by LPS and pretreatment with different concentrations of Xuebijing observed under optical microscope (Scale bar=100 μm). C-E: ELISA measurement of TNF-α (C), IL-6 (D), and IL-1β (E) levels in the supernatant of RAW264.7 cells pretreated with different concentrations of Xuebijing and stimulated with LPS (n=3). ###P<0.001 vs Control group; **P<0.01,***P<0.001 vs LPS group.

图5 血必净通过调节PLTP介导的JNK/c-JUN和NF-κB通路激活发挥作用

Fig.5 Xuebijing regulates PLTP-mediated activation of JNK/c-JUN and NF-κB pathways. A: qPCR analysis of the effects of LPS and Xuebijing on PLTP mRNA expression in RAW264.7 cells (n=3). B, C: Western blotting for detecting PLTP protein expression in response to LPS stimulation (n=3). D, E: Western blotting for detecting PLTP protein expression following treatment with different concentrations of Xuebijing (n=4). F: KEGG enrichment analysis of differentially expressed genes between PLTP knockdown (siPLTP)+LPS group and control (siNC)+LPS group. G-K: Western blotting for analyzing the effects of LPS and Xuebijing treatment on the expressions of p-JNK, JNK, p-c-JUN, c-JUN, p-NF-κB p65, and NF-κB p65 proteins in RAW264.7 cells (n=3). #P<0.05, ##P<0.01 vs Control group; *P<0.05, **P<0. 01 vs LPS group.

图6 PLTP过表达增强血必净对炎症通路及因子产生的抑制作用

Fig.6 PLTP overexpression enhances the inhibitory effect of Xuebijing on inflammatory pathways and cytokine production. A-C: Validation of PLTP overexpression efficiency in RAW264.7 cells by qPCR (A) and Western blotting (B, C) (n=3; ##P<0.01,###P<0.001 vs Flag-Vector group). D-H: Western blotting for analyzing the effects of PLTP overexpression and Xuebijing treatment on LPS-induced expressions of p-JNK, JNK, p-c-JUN, c-JUN, p-NF-κB p65, and NF-κB p65 proteins (n=3). I-K: Results of ELISA for measurement of the levels of IL-6 (I), IL-1β (J), and TNF‑α (K) in the supernatant of LPS-stimulated RAW264.7 cells with PLTP overexpression and XBJ treatment (n=3). #P<0.05, ##P<0.01, ###P<0.001 vs Flag-Vector+LPS group; *P<0.05, **P<0.01, ***P<0.001 vs Flag-PLTP+LPS group.

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血必净注射液通过上调磷脂转运蛋白调控巨噬细胞JNK/c-JUN通路改善脓毒症相关急性呼吸窘迫综合征

Xuebijing Injection ameliorates sepsis-associated acute respiratory distress syndrome in mice by upregulating phospholipid transfer protein to regulate macrophage JNK/c-JUN pathway

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