Research progress on pharmacological mechanism of traditional Chinese medicine targeting type 2 diabetes related pathways

doi:10.12092/j.issn.1009-2501.2026.04.009

Abstract

Abstract:

Type 2 diabetes mellitus (T2DM) is a common chronic metabolic disease characterized by hyperglycemia. Traditional Chinese medicine has the characteristics of overall regulation, syndrome differentiation and treatment, multi-target and multi-mechanism regulation, and has great potential in the treatment of T2DM. Recent studies have shown that, effective components and compound of traditional Chinese medicine regulate AMP-activated protein kinase (AMPK), nuclear transcription factor-κB (NF-κB), transforming growth factor-β (TGF-β), mitogen-activated protein kinases (MAPK), Phosphoinositol 3-kinase (PI3K) / protein kinase B (Akt), nuclear factor-erythroid 2 related factor 2 (Nrf2), wingless type MMTV integration site family (Wnt) / β-catenin, and other signaling pathways. It can inhibit the apoptosis of islet β cells, promote the proliferation of islet β cells, improve islet function, reduce oxidative stress and inflammatory response, inhibit liver gluconeogenesis, and improve insulin resistance (IR), thus playing a role in the treatment of T2DM. This paper summarizes and analyzes the research progress of the effective components of traditional Chinese medicine and compound intervention in T2DM and the mechanism of related pathways, in order to provide a new direction and reference for the treatment of T2DM.

Key words: type 2 diabetes mellitus, effective components and compound of traditional Chinese medicine, signal pathway, mechanism, research progress

CLC Number:

R285.5
R966

Ying ZHOU, Juntong LIU, Qingfeng WANG, Yufeng YANG, Yan SHI. Research progress on pharmacological mechanism of traditional Chinese medicine targeting type 2 diabetes related pathways[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2026, 31(4): 500-508.

Figures/Tables 3

References 61

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中药有效成分	调控通路	分子靶点	作用机制	文献
薯蓣皂苷元	AMPK	AMPK↑，mTOR↓	减少胰岛β细胞凋亡，改善胰岛功能	[12]
五味子乙素	AMPK	AMPK-LKB1↑	改善氧化应激与炎症反应	[13]
青钱柳三萜酸	AMPK	AMPK↑	抑制肝脏糖异生	[14]
绞股蓝总皂苷	NF-κB	NF-κB↓	降低炎症反应	[22]
桑叶总黄酮	NF-κB	TLR4/MyD88/NF-κB↓	降低炎症反应	[23]
茯苓多糖	MAPK	MAPK↓	改善氧化应激	[38]
金丝桃苷	MAPK	MAPK↓	改善氧化应激及细胞凋亡	[39]
根皮苷	PI3K/AKt	IRS-1/PI3K/Akt↑	促进肝脏糖原合成，抑制肝脏糖异生	[44]
鸡内金多糖	Nrf2	Nrf2↑	抑制氧化应激，促进胰岛β细胞增殖，抑制凋亡	[51]
木犀草素	Wnt/β-catenin	Wnt/β-catenin↑	减轻胰岛素抵抗	[59]

中药有效成分	调控通路	分子靶点	作用机制	文献
薯蓣皂苷元	AMPK	AMPK↑，mTOR↓	减少胰岛β细胞凋亡，改善胰岛功能	[12]
五味子乙素	AMPK	AMPK-LKB1↑	改善氧化应激与炎症反应	[13]
青钱柳三萜酸	AMPK	AMPK↑	抑制肝脏糖异生	[14]
绞股蓝总皂苷	NF-κB	NF-κB↓	降低炎症反应	[22]
桑叶总黄酮	NF-κB	TLR4/MyD88/NF-κB↓	降低炎症反应	[23]
茯苓多糖	MAPK	MAPK↓	改善氧化应激	[38]
金丝桃苷	MAPK	MAPK↓	改善氧化应激及细胞凋亡	[39]
根皮苷	PI3K/AKt	IRS-1/PI3K/Akt↑	促进肝脏糖原合成，抑制肝脏糖异生	[44]
鸡内金多糖	Nrf2	Nrf2↑	抑制氧化应激，促进胰岛β细胞增殖，抑制凋亡	[51]
木犀草素	Wnt/β-catenin	Wnt/β-catenin↑	减轻胰岛素抵抗	[59]

中药复方	相关通路	分子靶点	作用机制	文献
天黄方	AMPK	AMPK/MICU1↑	调控脂肪细胞线粒体功能	[15]
葛根芩连汤	NF-κB	TLR4/IKKβ/NF-κB↓	抑制炎症反应	[24]
抵当芪桂汤	TGF-β	TGF-β1↓	避免胰岛组织纤维化，保护胰岛β细胞功能	[31]
新降糖颗粒	TGF-β	TGF-β1↓	抑制糖异生、促进糖原合成，抑制氧化应激	[32]
消渴平复方	TGF-β	TGF-β/Smad↓	抑制纤维化	[33]
健脾清化方	MAPK	p38MAPK↓	改善胰岛素抵抗	[40]
肾气丸加减方	PI3K/AKt	PI3K/Akt/GSK-3β↑	保护胰岛β细胞线粒体嵴结构，减少氧化应激，保护胰岛β细胞功能	[45]
玉屏风散	PI3K/AKt	IRS/PI3K/Akt↑	缓解胰岛素抵抗	[46]
补青颗粒	Nrf2	Keap1-Nrf2↑	减轻氧化应激	[52]
参七糖络丸	Nrf2	Nrf2/HO-1/NQO1↑	改善骨骼肌氧化应激，缓解胰岛素抵抗	[53]
六味地黄丸	Wnt/β-catenin	Wnt/β-catenin↑	缓解胰岛素抵抗	[60]
藏药三果汤	Wnt/β-catenin	Wnt/β-catenin↑	抑制胰岛β细胞凋亡，促进β细胞增殖	[61]

中药复方	相关通路	分子靶点	作用机制	文献
天黄方	AMPK	AMPK/MICU1↑	调控脂肪细胞线粒体功能	[15]
葛根芩连汤	NF-κB	TLR4/IKKβ/NF-κB↓	抑制炎症反应	[24]
抵当芪桂汤	TGF-β	TGF-β1↓	避免胰岛组织纤维化，保护胰岛β细胞功能	[31]
新降糖颗粒	TGF-β	TGF-β1↓	抑制糖异生、促进糖原合成，抑制氧化应激	[32]
消渴平复方	TGF-β	TGF-β/Smad↓	抑制纤维化	[33]
健脾清化方	MAPK	p38MAPK↓	改善胰岛素抵抗	[40]
肾气丸加减方	PI3K/AKt	PI3K/Akt/GSK-3β↑	保护胰岛β细胞线粒体嵴结构，减少氧化应激，保护胰岛β细胞功能	[45]
玉屏风散	PI3K/AKt	IRS/PI3K/Akt↑	缓解胰岛素抵抗	[46]
补青颗粒	Nrf2	Keap1-Nrf2↑	减轻氧化应激	[52]
参七糖络丸	Nrf2	Nrf2/HO-1/NQO1↑	改善骨骼肌氧化应激，缓解胰岛素抵抗	[53]
六味地黄丸	Wnt/β-catenin	Wnt/β-catenin↑	缓解胰岛素抵抗	[60]
藏药三果汤	Wnt/β-catenin	Wnt/β-catenin↑	抑制胰岛β细胞凋亡，促进β细胞增殖	[61]

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