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方萍,吴增艳,王蓉蓉,马丽,马哲龙.基于PPARγ-LXRα-ABCA1通路研究健脾祛湿方对高脂血症模型 大鼠的影响[J].浙江中西医结合杂志,2026,36(3):
基于PPARγ-LXRα-ABCA1通路研究健脾祛湿方对高脂血症模型 大鼠的影响
Based on the PPARγ-LXRα-ABCA1 pathway, Jianpi Qushi formula were used to study the hyperlipidemia model rat effects
投稿时间:2025-08-19  修订日期:2025-12-03
DOI:
中文关键词:  健脾祛湿方  高脂血症  胆固醇逆转运
英文关键词:Jianpi Qushi formula  hyperlipidemia  Cholesterol reversal
基金项目:杭州市卫生科技计划项目(B20232039)基于胆固醇逆转运的健脾祛湿方调血脂研究
作者单位E-mail
方萍 杭州市临平区中西医结合医院 paradise1208@163.com 
吴增艳 杭州市临平区中西医结合医院  
王蓉蓉 杭州市临平区中西医结合医院  
马丽 杭州市临平区中西医结合医院  
马哲龙* 杭州市临平区中西医结合医院 1074866772@qq.com 
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中文摘要:
      目的:明确健脾祛湿方对高脂饮食诱导的高脂血症模型大鼠血脂水平的改善作用,初步从胆固醇逆转运角度探讨其可能的作用机制。方法:通过连续7周高脂饲料饲喂SD大鼠,建立高脂血症大鼠模型,造模的同时灌胃给予健脾祛湿方三个剂量(1.7、3.4、6.8 g/kg)。实验期间检测大鼠肝功能、血脂及肝脂水平;通过H E染色观察肝脏组织学变化,结合油红O染色评估肝内脂质蓄积程度;qPCR法和IHC法检测肝脏PPARγ-LXRα-ABCA1通路相关分子的mRNA及蛋白表达。结果:与模型组比较,肝细胞空泡化、脂滴面积均明显减少。与正常组比较,模型大鼠血清TC[(3.45±0.31) mmol/L比(1.83±0.16) mmol/L,P<0.01]、LDL-C[(1.38±0.35) mmol/L比(0.30±0.04) mmol/L,P<0.01]、ALT[(60.63±16.09)(U/L)比(37.63±4.75)(U/L),P<0.01]、AST[(286.75±118.66)(U/L)比(115.00±19.94)(U/L),P<0.05]、大鼠肝脏TC[(0.0096±0.0009)(mmol/g)比(0.0051±0.0009)(mmol/g)P<0.01]含量显著升高,血清HDL-c[(0.16±0.04)(mmol/L)比(0.53±0.04)(mmol/L)P<0.01]、大鼠肝脏PPARγ mRNA[(0.43±0.06)比(1.00±0.00),P<0.05]、LXRα mRNA [(0.56±0.05)比(1.01±0.01)P<0.01]与ABCA1 mRNA[(0.23±0.14)比?(1.00±0.00)P<0.01]表达降低。与模型组比较,健脾祛湿方6.8 g/kg组、3.4 g/kg组、1.7 g/kg组大鼠血清TC[(2.36±0.37)mmol/L、(2.17±0.51)mmol/L、(2.34±0.35)mmol/L比(3.45±0.31)mmol/L,P<0.01]、ALT[(34.63±6.46) U/L、(35.88±8.92)U/L、(35.63±6.00)U/L比(60.63±16.09) U/L,P<0.01],健脾祛湿方6.8 g/kg组、3.4 g/kg组大鼠血清LDL-C[(0.81±0.17) mmol/L、(0.82±0.26)mmol/L比(1.38±0.35) mmol/L,P<0.05]、大鼠肝脏TC[(0.0058±0.0015) mmol/g、(0.0071±0.0015)mmol/g比(0.0096±0.0009)mmol/g ,P<0.01],健脾祛湿方6.8 g/kg组AST[(114.25±20.11)(U/L)比(286.75±118.66)(U/L),P<0.05]含量显著降低,健脾祛湿方6.8 g/kg组、3.4 g/kg组、1.7 g/kg组大鼠血清HDL-c[(0.38±0.14) mmol/L、(0.28±0.08)mmol/L、(0.36±0.11)mmol/L比(0.16±0.04)mmol/L,(P<0.05,0.01)]含量增加,健脾祛湿方6.8 g/kg组大鼠肝脏PPARγ [(0.74±0.07)比(0.43±0.06),P<0.05]、LXRα[(0.72±0.07)比(0.56±0.05)P<0.05]mRNA表达增加,健脾祛湿方6.8 g/kg组、3.4 g/kg组大鼠肝脏ABCA1 [(0.98±0.24)、(0.77±0.30)比(0.23±0.14)P<0.01] mRNA表达增加。结论:健脾祛湿方对高脂饮食诱导的高脂血症模型大鼠具有明显的改善作用,其机制可能与抑制肝脏PPARγ-LXRα-ABCA1通路,促进胆固醇逆转运有关。
英文摘要:
      Objective:To clarify the effect of Jianpi Qushi formula on the improvement of blood lipid level in rats with hyperlipidemia induced by high-fat diet, and to explore its possible mechanism from the perspective of cholesterol reversal. Methods:The hyperlipidemia rat model was prepared by SD rats fed with high-fat diet every day for 7 weeks, and three doses (1.7, 3.4, 6.8 g/kg) of the Jianpi Qushi formula were administered by gavage at the same time as the model was administered for 7 weeks. During the experiment, liver function, blood lipids and liver lipid levels were measured. H E staining was used to observe the morphological changes of liver tissue. Oil red O staining method was used to observe liver lipid deposition. qPCR and IHC were used to detect the mRNA and protein expression of PPARγ-LXRα-ABCA1 pathway-related molecules in the liver. Results: Compared with the model group, hepatocyte vacuolation and lipid droplet area were significantly reduced. Compared with the normal group, the model rats showed significantly increased serum TC [(3.45 ± 0.31) mmol/L vs. (1.83 ± 0.16) mmol/L, P < 0.01], LDL-C [(1.38 ± 0.35) mmol/L vs. (0.30 ± 0.04) mmol/L, P < 0.01], ALT [(60.63 ± 16.09) U/L vs. (37.63 ± 4.75) U/L, P < 0.01], AST [(286.75 ± 118.66) U/L vs. (115.00 ± 19.94) U/L, P < 0.05], and liver TC [(0.0096 ± 0.0009) mmol/g vs. (0.0051 ± 0.0009) mmol/g, P < 0.01], while serum HDL-C [(0.16 ± 0.04) mmol/L vs. (0.53 ± 0.04) mmol/L, P < 0.01], liver PPARγ mRNA [(0.43 ± 0.06) vs. (1.00 ± 0.00), P < 0.05], LXRα mRNA [(0.56 ± 0.05) vs. (1.01 ± 0.01), P < 0.01], and ABCA1 mRNA [(0.23 ± 0.14) vs. (1.00 ± 0.00), P < 0.01] expression were significantly decreased.Compared with the model group, the Jianpi Qushi Formula (JPQS) groups at doses of 6.8 g/kg, 3.4 g/kg, and 1.7 g/kg showed significantly reduced serum TC [(2.36 ± 0.37) mmol/L, (2.17 ± 0.51) mmol/L, (2.34 ± 0.35) mmol/L vs. (3.45 ± 0.31) mmol/L, P < 0.01] and ALT [(34.63 ± 6.46) U/L, (35.88 ± 8.92) U/L, (35.63 ± 6.00) U/L vs. (60.63 ± 16.09) U/L, P < 0.01]. The JPQS groups at 6.8 g/kg and 3.4 g/kg also exhibited significantly decreased serum LDL-C [(0.81 ± 0.17) mmol/L, (0.82 ± 0.26) mmol/L vs. (1.38 ± 0.35) mmol/L, P < 0.05] and liver TC [(0.0058 ± 0.0015) mmol/g, (0.0071 ± 0.0015) mmol/g vs. (0.0096 ± 0.0009) mmol/g, P < 0.01]. Additionally, the JPQS 6.8 g/kg group showed significantly reduced AST [(114.25 ± 20.11) U/L vs. (286.75 ± 118.66) U/L, P < 0.05].The JPQS groups at 6.8 g/kg, 3.4 g/kg, and 1.7 g/kg demonstrated increased serum HDL-C [(0.38 ± 0.14) mmol/L, (0.28 ± 0.08) mmol/L, (0.36 ± 0.11) mmol/L vs. (0.16 ± 0.04) mmol/L, (P < 0.05, 0.01)]. Furthermore, the JPQS 6.8 g/kg group exhibited elevated liver PPARγ [(0.74 ± 0.07) vs. (0.43 ± 0.06), P < 0.05] and LXRα [(0.72 ± 0.07) vs. (0.56 ± 0.05), P < 0.05] mRNA expression, while the JPQS 6.8 g/kg and 3.4 g/kg groups showed increased liver ABCA1 mRNA expression [(0.98 ± 0.24), (0.77 ± 0.30) vs. (0.23 ± 0.14), P < 0.01].
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