Effect of <italic style="font-style: italic">Jianpi Huazhuo Tiaozhi Granule</italic>（健脾化浊调脂颗粒）on Perivascular Adipose Tissue Browning and PI3K/AKT Pathway in the Aorta of Atherosclerosis Model Mice

WANG Zhuhua; WANG Yanfang; ZHONG Mingshu; CHEN Shupeng; YUAN Yishun; HUANG Shan; LIU Yanwei; LIU Zhongyong

doi:10.13288/j.11-2166/r.2026.11.012

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Effect of Jianpi Huazhuo Tiaozhi Granule（健脾化浊调脂颗粒）on Perivascular Adipose Tissue Browning and PI3K/AKT Pathway in the Aorta of Atherosclerosis Model Mice

更新时间：2026-05-29

- Effect of Jianpi Huazhuo Tiaozhi Granule（健脾化浊调脂颗粒）on Perivascular Adipose Tissue Browning and PI3K/AKT Pathway in the Aorta of Atherosclerosis Model Mice
- Journal of Traditional Chinese Medicine Vol. 67, Issue 11, Pages: 1200-1210(2026)
- 作者机构：
  
  1.江西中医药大学，江西省南昌市新建区梅岭大道1688号，330004
  2.江西省瑞金市中医院
  3.江西中医药大学附属医院
- 作者简介：
- 基金信息：
- DOI：10.13288/j.11-2166/r.2026.11.012
  CLC：
- Received：22 November 2025，
  
  Revised：2026-03-24，
  
  Accepted：14 January 2026，
  
  Published：02 June 2026
- 稿件说明：
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王珠华,王艳芳,钟鸣书等.健脾化浊调脂颗粒对动脉粥样硬化模型小鼠主动脉血管周围脂肪组织褐变和PI3K/AKT通路的影响[J].中医杂志,2026,67(11):1200-1210.

WANG Zhuhua,WANG Yanfang,ZHONG Mingshu,et al.Effect of Jianpi Huazhuo Tiaozhi Granule（健脾化浊调脂颗粒）on Perivascular Adipose Tissue Browning and PI3K/AKT Pathway in the Aorta of Atherosclerosis Model Mice[J].Journal of Traditional Chinese Medicine,2026,67(11):1200-1210.
王珠华,王艳芳,钟鸣书等.健脾化浊调脂颗粒对动脉粥样硬化模型小鼠主动脉血管周围脂肪组织褐变和PI3K/AKT通路的影响[J].中医杂志,2026,67(11):1200-1210. DOI： 10.13288/j.11-2166/r.2026.11.012.

WANG Zhuhua,WANG Yanfang,ZHONG Mingshu,et al.Effect of Jianpi Huazhuo Tiaozhi Granule（健脾化浊调脂颗粒）on Perivascular Adipose Tissue Browning and PI3K/AKT Pathway in the Aorta of Atherosclerosis Model Mice[J].Journal of Traditional Chinese Medicine,2026,67(11):1200-1210. DOI： 10.13288/j.11-2166/r.2026.11.012.

摘要

目的

基于磷脂酰肌醇3-激酶/蛋白激酶B（PI3K/AKT）信号通路调控血管周围脂肪组织（PVAT）褐变探讨健脾化浊调脂颗粒治疗动脉粥样硬化（AS）的可能作用机制。

方法

15只SPF级雄性C57BL/6J小鼠设为对照组，76只ApoE

-/-

小鼠先予高脂饲料饲养16周建立AS小鼠模型，造模成功后随机分为模型组16只，褐变组及健脾化浊调脂低、中、高剂量组各15只。褐变组以1 mg/（kg·d）的β3肾上腺素受体激动剂CL 316243腹腔注射，每日1次；健脾化浊调脂低、中、高剂量组分别以4.3、8.6、17.2 g/（kg·d）健脾化浊调脂颗粒灌胃，对照组、模型组以生理盐水10 ml/（kg·d）灌胃，均每日1次。各组均连续干预4周后，取主动脉进行大体油红O染色法检测斑块占比，HE染色法检测横切面斑块面积，Masson染色法检测脉斑块中胶原纤维占比，透射电镜观察脂肪细胞内线粒体和脂滴数量及形态变化；检测血清甘油三酯（TG）、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）水平，PVAT及主动脉中肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）水平，PVAT中的脂联素、瘦素蛋白水平及PI3K、磷酸化磷脂酰肌醇3-激酶（p-PI3K）、AKT、磷酸化蛋白激酶B（p-AKT）、解偶联蛋白1（UCP1）、过氧化物酶体增殖物激活受体γ辅激活因子-1α（PGC-1α）、PR结构域锌指蛋白16（PRDM16）蛋白水平，PVAT中

UCP1、PGC

1α、PRDM16

mRNA表达。

结果

与对照组比较，模型组小鼠血清TG、TC、LDL-C水平升高，HDL-C水平降低，PVAT与主动脉中TNF-α、IL-6升高，脂联素平均荧光强度降低，瘦素平均荧光强度升高，p-PI3K/PI3K、p-AKT/AKT值和UCP1、PGC-1α、PRDM16蛋白水平及mRNA表达降低（

＜0.01）。病理结果显示，对照组小鼠主动脉无明显斑块形成；模型组小鼠主动脉均可见多发性斑块，斑块内可见大量泡沫细胞、胆固醇结晶和炎症细胞聚集，可见少量蓝色胶原纤维。与模型组比较，褐变组及健脾化浊调脂高剂量组可显著改善上述指标及主动脉病理变化（

＜0.05或

＜0.01）。健脾化浊调脂各剂量组在降低LDL-C、大体油红O染色斑块占比，升高脂联素平均荧光强度、p-AKT/AKT值、PGC-1α蛋白水平、

UCP1

及

PRDM16

mRNA表达方面呈剂量依赖性（

＜0.05）。健脾化浊调脂高剂量组与褐变组在改善主动脉病理方面疗效相当。

结论

健脾化浊调脂颗粒可能通过激活PI3K/AKT通路促进AS模型小鼠PVAT褐变，改善PVAT内分泌功能，抑制主动脉炎症，从而减轻AS斑块形成。

Abstract

Objective

To explore the possible mechanism of

Jianpi Huazhuo Tiaozhi Granule

（健脾化浊调脂颗粒， JHTG） in treating atherosclerosis （AS） based on the regulation of perivascular adipose tissue （PVAT） browning via the phosphoinositide 3-kinase/protein kinase B （PI3K/AKT） signaling pathway.

Methods

Fifteen SPF male C57BL/6J mice served as control group， while 76 ApoE

-/-

mice were first fed a high-fat diet for 16 weeks to establish AS model. After successful modeling， they were rand

omly divided into model group （n=16）， as well as the browning group， the low-， medium- and high-dose JHTG group， with 15 mice in each group. The browning group was intraperitoneally injected with β3-adrenergic receptor agonist CL 316243 at 1 mg/（kg·d） once daily. The low-， medium- and high-dose JHTG groups were treated with 4.3 g/（kg·d）， 8.6 g/（kg·d）， and 17.2 g/（kg·d） of JHTG by gavage， respectively， while the control group and the model group were given normal saline at 10 ml/（kg·d） by intragastric administration， once daily. All groups received continuous intervention for 4 weeks. The aorta was collected to assess the plaque ratio by gross oil red O staining. HE staining was used to measure the plaque area in cross-sections. Masson staining was employed to detect the proportion of collagen fibers in plaque. Transmission electron microscopy was used to observe the quantity and morphological changes of mitochondria and lipid droplets in adipocytes. The levels of serum triglycerides （TG）， total cholesterol （TC）， high-density lipoprotein cholesterol （HDL-C）， and low-density lipoprotein cholesterol （LDL-C） were detected， as well as tumor necrosis factor α （TNF-α） and interleukin 6 （IL-6） levels in the PVAT and aorta. The protein levels of adiponectin and leptin in PVAT， and protein expression levels of phosphoinositide 3-kinase （PI3K）， phosphorylated phosphoinositide 3-kinase （p-PI3K）， protein kinase B （AKT）， phosphorylated protein kinase B （p-AKT）， uncoupling protein 1 （UCP1）， peroxisome proliferator-activated receptor γ coactivator 1α （PGC-1α）， and PR domain containing 16 （PRDM16） were measured. The mRNA expression levels of

UCP1

，

PGC

1α

and

PRDM16

in PVAT were detected.

Results

Compared to the control group， the model group showed increased serum TG， TC， and LDL-C levels and decreased HDL-C level， elevated TNF-α and IL-6 levels in PVAT and aorta， decreased average fluorescence intensity of adiponectin， increased av

erage fluorescence intensity of leptin， reduced p-PI3K/PI3K and p-AKT/AKT values as well as protein levels and mRNA expression levels of

UCP1

，

PGC

1α

and

PRDM16

（

＜0.01）. The pathological results showed that no significant plaque formation was observed in the aortas of mice in the control group. In the model group， multiple plaques were observed in the aortas， with large numbers of foam cells， cholesterol crystals， and inflammatory cell aggregation in the plaques. Compared to the model group， the browning group and the high-dose JHTG group significantly improved the above indicators and aortic pathological changes （

＜0.05 or

＜0.01）. Three JHTG groups showed a dose-dependent effect in reducing LDL-C level and plaque ratio by gross oil red O staining， elevating the average fluorescence intensity of adiponectin， the p-AKT/AKT value， the protein level of PGC-1α， and the mRNA expression levels of

UCP1

and

PRDM16

（

＜0.05）. The high-dose JHTG group and the browning group showed similar efficacy in improving the pathology of the aorta.

Conclusion

JHTG

may promote PVAT browning in AS model mice through the PI3K/AKT pathway， improve the endocrine function of PVAT， inhibit aortic inflammation， and thereby ameliorate the formation of AS plaques.

关键词

Keywords

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Effect of Jianpi Huazhuo Tiaozhi Granule（健脾化浊调脂颗粒）on Perivascular Adipose Tissue Browning and PI3K/AKT Pathway in the Aorta of Atherosclerosis Model Mice

DOI：10.13288/j.11-2166/r.2026.11.012

摘要

Abstract

关键词

Keywords

references