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引用本文:李海龙,彭苏玉,钦润泽,王霞,唐若楠,李美芽,蒋福升.畲药异叶茴芹茎杆挥发油对LPS/D-GalN诱导的小鼠急性肝损伤保护作用研究[J].中国现代应用药学,2025,42(6):102-111.
Li Hailong,Peng Suyu,Qin Runze,Wang Xia,Tang Ruonan,Li Meiya,Jiang Fusheng.Investigation on the Protective Effect of the Essential Oil from the Stem of Pimpinella diversifolia on LPS/D-GalN-Induced Acute Liver Injury in Mice[J].Chin J Mod Appl Pharm(中国现代应用药学),2025,42(6):102-111.
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畲药异叶茴芹茎杆挥发油对LPS/D-GalN诱导的小鼠急性肝损伤保护作用研究
李海龙1, 彭苏玉2, 钦润泽2, 王霞2, 唐若楠2, 李美芽2, 蒋福升2
1.浙江广厦建设职业技术大学;2.浙江中医药大学
摘要:
目的 探究异叶茴芹茎杆挥发油(PDSEO)对LPS/D-GalN诱导小鼠急性肝损伤保护作用及其分子机理。 方法 同时蒸馏萃取法制备PDSEO,并采用气质联用色谱法(GC/MS)鉴定化学成分;以LPS/D-GalN为诱导剂制备急性肝损伤模型,检测血清ALT、AST和ALP水平,通过流式多因子检测(CBA)法分析血清中炎症因子水平; HE染色分析肝组织病变情况,肝组织匀浆检测MDA水平,荧光定量PCR分析肝组织炎症因子和抗氧化酶相关基因表达水平,TUNEL法分析肝细胞凋亡情况,综合评价PDSEO保肝活性和机制。结果 共鉴定PDSEO中46个成分,其中萜类化合物33种。PDSEO低(50 mg?kg-1)、高(100 mg?kg-1)剂量组均可显著降低LPS/D-GalN诱导的血清ALT、AST和ALP肝损伤指标;也可有效降低肝组织炎症基因IL-6、TNF-α和MCP-1表达以及血清中炎症因子水平;PDSEO低、高剂量组处理后肝组织中SOD1、SOD2、CAT和Gpx4等抗氧化相关基因表达上调,同时肝组织中SOD、CAT酶活力和GSH水平显著升高,而脂质过氧化产物MDA显著下降;HE和TUNEL凋亡染色进一步证实,PDSEO低、高剂量组均可有效抑制肝细胞凋亡,减轻肝组织损伤。结论 异叶茴芹茎杆富含挥发油,其可通过抑制肝组织过度炎症反应,提高抗氧化系统水平降低肝组织过度氧化应激,减少肝细胞凋亡,有效缓解LPS/D-GalN诱导的小鼠急性肝损伤,在预防肝组织损伤药物开发方面表现出潜在开发利用价值。
关键词:  异叶茴芹  肝损伤  挥发油  炎症因子  氧化应激  凋亡
DOI:
分类号:
基金项目:浙江省自然科学基金项目(LY23H280004)
Investigation on the Protective Effect of the Essential Oil from the Stem of Pimpinella diversifolia on LPS/D-GalN-Induced Acute Liver Injury in Mice
Li Hailong1, Peng Suyu2, Qin Runze2, Wang Xia2, Tang Ruonan2, Li Meiya2, Jiang Fusheng2
1.Zhejiang Guangsha Vocational and Technical University of Construction;2.Zhejiang Chinese Medical University
Abstract:
OBJECTIVE To explore the protective effect of the Pimpinella diversifolia stem essential oil (PDSEO) on LPS/D-GalN induced acute liver injury in mice and its possible molecular mechanism. METHODS PDSEO was prepared through the simultaneous distillation and extraction method and identified by GC/MS. The acute liver injury model was established using LPS/D-GalN as the inducer. The serum levels of ALT, AST, and ALP were determined, and the serum levels of inflammatory factors were analyzed by cytometric bead array assay (CBA). Liver tissue slices were stained with HE and TUNEL for the analysis of liver tissue lesions and hepatic cell apoptosis. Liver tissue homogenates were examined for MDA levels, and quantitative fluorescent PCR was employed to analyze the expression levels of inflammatory factors and antioxidase-related genes in liver tissue, thereby comprehensively evaluating the hepatoprotective activity and mechanism of PDSEO. RESULTS A total of 46 components of PDSEO were identified, among which 33 were terpenoids. Both low (50 mg/kg) and high (100 mg/kg) doses of PDSEO could conspicuously reduce the elevation of serum ALT, AST and ALP liver injury indices induced by LPS/D-GalN. It could also efficaciously decrease the expression of inflammatory genes IL-6, TNF-α and MCP-1 in liver tissue as well as the level of serum inflammatory factors. After the treatment with low and high doses of PDSEO, the expression of anti-oxidation-related genes such as SOD1, SOD2, CAT and Gpx4 in liver tissue was up-regulated. Meanwhile, the activities of SOD and CAT enzymes and the GSH levels in liver tissue were significantly augmented, while the lipid peroxidation product MDA was significantly diminished. HE and TUNEL apoptotic staining of liver tissue sections further confirmed that both the low and high dose PDSEO groups could effectively alleviate hepatocyte apoptosis and liver tissue injury. CONCLUSION The stems of Pimpinella diversifolia abound in essential oil, which is capable of suppressing excessive inflammation of liver tissue, enhancing the level of the antioxidant system, alleviating the emergency response of excessive oxidation of liver tissue, decrease liver cell apoptosis, effectively mitigating LPS/D-GalN-induced acute liver injury in mice, and demonstrating potential development and utilization value in the development of drugs for preventing liver tissue injury.
Key words:  Pimpinella diversifolia DC.  acute liver injury  essential oil  inflammatory factor  oxidative stress  apoptosis
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