Qige decoction (芪葛汤) ameliorates hyperlipidemia in rats by modulating the intestinal microbiota and liver metabolism

doi:10.19852/j.cnki.jtcm.2026.05.009

Journal of Traditional Chinese Medicine ›› 2026, Vol. 46 ›› Issue (5): 1149-1159.DOI: 10.19852/j.cnki.jtcm.2026.05.009

• Original Articles • Previous Articles Next Articles

Qige decoction (芪葛汤) ameliorates hyperlipidemia in rats by modulating the intestinal microbiota and liver metabolism

ZHOU Zunming¹^,², TAN Meiao²^,³, YU Xiaoqing⁴, KE Xuehong⁴(), HUANG Keer²()

¹ Department of Acupuncture and Moxibustion, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen 510008, China
² Department of Gastroenterology, the First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China
³ Lingnan Medical Research Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China
⁴ Laboratory Center, the First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China

Received:2025-07-04 Accepted:2026-01-11 Online:2026-10-15 Published:2026-10-09
Contact: HUANG Keer, Department of Gastroenterology, the First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China. hke1234567@163.com; KE Xuehong, Laboratory Center, the First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China, 2804613799@qq.com
Supported by:
National Natural Science Foundation of China Project: Mechanism of the Huangqi-Gegen Herb Pair with Added Chenpi in Ameliorating Non-alcoholic Fatty Liver Disease via Activation of the Sirtuin 6-Peroxisome proliferator-activated Receptor α Signaling Pathway(82074099);Guangdong Basic and Applied Basic Research Project: Foundation Mechanisms of Qige Decoction in Ameliorating Non-alcoholic Fatty Liver Disease via Peroxisome Proliferator-activated Receptor α Signaling Pathway: A Study on Its Dual-Regulatory Effect on Glucose and Lipid Metabolism(2023A1515011126);Research Special Project of Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Mechanism of Thread-Embedding Therapy in Preventing and Treating Non-alcoholic Fatty Liver Disease via the Gut Microbiota/Choline/Trimethylamine/Trimethylamine N-oxide Metabolic Pathway(GZYSY2024012);Guangzhou Science and Technology Qige decoction granule Development Project(202102010476)

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Abstract

Abstract:

OBJECTIVE: To evaluate the effects of Qige decoction (芪葛汤, QG), Huangqi-Gegen decoction (黄芪葛根汤, HG), and Chenpi decoction (陈皮汤, CP) on hyperlipidemic (HLP) rats, and further explore the potential protective mechanisms involved.

METHODS: A high-fat, high-cholesterol diet (HFHCD) was used to induce HLP model rats. For 20 d of HFHCD feeding, the rats received a daily oral administration of atorvastatin calcium (ATO, 5 mg·kg^-1·d^-1), QG (5 g·kg^-1·d^-1), HG (4.5 g·kg^-1·d^-1), or CP (0.5 g·kg^-1·d^-1). Serum biochemical indices, histopathological evaluations, fecal microbiota 16S rRNA sequencing, liver lipidomics, and Western blot (WB) analyses were used to investigate the influences of QG, HG, and CP on HLP model rats.

RESULTS: QG supplementation significantly improved dyslipidemia and pathological changes in HLP rats. 16S rRNA sequencing and lipidomics analysis revealed that HLP rats exhibited severe gut microbiota dysfunction and liver lipid metabolite disorders, which were partially reversed by QG supplementation. Specifically, QG supplementation restored the abundance of gut microbiota and increased the abundance of several beneficial bacteria (e.g. Intestinimonas, Ruminoco-ccaceae_UCG-005, Flavobacterium, Turicibacter, and Phocea) while decreasing the abundances of harmful ones (e.g. Collinsella, Allisonella, [Eubacterium]_hallii_ group, Staphylococcus, and Escherichia-Shigella). Regarding liver lipid metabolites, QG supplementation reduced the levels of 37 triglyceride metabolites, whose biological functions were primarily associated with cholesterol metabolism. WB results showed that QG downregulated the expression of Niemann-Pick C1-Like 1 protein in the small intestine and upregulated the expression of adenosine triphosphat-binding cassette G5/8 (ABCG5/8) proteins in the liver and small intestine, thereby regulating cholesterol metabolism. Interestingly, the intervention effects of QG were superior to those of HG and CP in HLP rats.

CONCLUSIONS: These findings indicate that the ameliorative effects of QG on HLP may be associated with the correction of gut microbiota dysbiosis, the modulation of lipid metabolites, and the regulation of cholesterol metabolism.

Key words: Hyperlipidemia, Qige decoction, intestinal microbiota, lipidomics, cholesterol metabolism

ZHOU Zunming, TAN Meiao, YU Xiaoqing, KE Xuehong, HUANG Keer. Qige decoction (芪葛汤) ameliorates hyperlipidemia in rats by modulating the intestinal microbiota and liver metabolism[J]. Journal of Traditional Chinese Medicine, 2026, 46(5): 1149-1159.

Figures/Tables 7

Table 1 Effect of QG on serum lipid profile in HLP rats (mmol/L, $\bar{x}±s$)

Group	n	TC	TG	HDL-C	LDL-C
CON	9	1.13±0.11^a	0.63±0.12^a	0.85±0.16^a	0.83±0.12^a
MOD	9	2.64±0.43	1.37±0.22	0.58±0.15	1.37±0.28
ATO	9	1.83±0.51^a	0.75±0.22^a	0.58±0.13	0.90±0.30^a
QG	9	1.868±0.25^a	0.89±0.21^a	0.61±0.14	1.01±0.17^a
HG	9	2.26±0.33^b	1.22±0.19^c	0.64±0.24	1.23±0.36
CP	9	2.23±0.35^b	1.22±0.21^c	0.65±0.20	1.19±0.19

Figure 1 Effect of QG on liver pathology in HLP rats A: liver HE staining at magnification × 200. Black arrows indicate the steatosis of hepatocytes; B: liver oil red O staining at magnification × 400; C: the proportion of liver fat area from oil red O staining Red area indicate the steatosis of hepatocytes; A1, B1: normal control group; A2, B2: model group; A3, B3: atorvastatin group; A4, B4: QG group; A5, B5: HG group; A6, B6: CP group. CON: normal control (fed by normal chow diet); MOD: model group (fed by HFHCD); ATO: atorvastatin group (5 mg/kg atorvastatin+HFHCD); QG: QG group (5 g/kg QG + HFHCD); HG: HG group (4.5 g/kg HG + HFHCD); CP: CP group (0.5 g/kg CP + HFHCD). HLP: hyperlipidemic; CON: control; MOD: model; ATO: atorvastatin; QG: Qige decoction; HG: Huangqi-Gegen decoction; CP: Chenpi decoction; HFHCD: high-fat high-cholesterol diet; ANOVA: analysis of variance. Variables conformed to normal distributions but with different variances, Welch's ANOVA was used to evaluate the statistical significance of the lipid area. All data are expressed as the mean ± standard deviation (n = 6). aP < 0.01, compared to the MOD group; bP < 0.01, compared to the QG group.

Figure 2 Effect of QG on gut microbiota community in HLP rats A: rarefaction curve; B: C vs M group ( F = 5.5535, R2 = 0.35706, P = 0.005, unweighted_unifrac PcoA plot); C: M vs QG group (F = 1.4852, R2 = 0.12931, P = 0.003, unweighted_unifrac PcoA plot); D: M vs HG group (F = 1.9699, R2 = 0.16457, P = 0.075, euclidean_nolabel PcoA plot); E: M vs CP group (F = 1.1746, R2 = 0.10511, P = 0.278, weighted_unifrac PcoA plot); F: M vs HG vs CP group (F = 1.6581, R2 = 0.18105, P = 0.001, unweighted_unifrac PcoA plot); C: normal control (fed by normal chow diet); M: model group (fed by HFHCD); QGL: QG group (5 g/kg QG + HFHCD); HG: HG group (4.5 g/kg HG + HFHCD); CP: CP group (0.5 g/kg CP + HFHCD). HLP: hyperlipidemic; C: control; M: model; QG: Qige decoction; HG: Huangqi-Gegen decoction; CP: Chenpi decoction; HFHCD: high-fat high-cholesterol diet. Variables did not conform to the normal distributions and variance homogeneity, Kruskal-Wallis was used to evaluate the statistical significance of Chao1, PD, and Shannon index. All data are expressed as the mean ± standard deviation (n = 6).

Table 2 Effect of QG on relative abundances of microbes at the phylum levels and the F/B ratio in HLP rats ($\bar{x}±s$)

Bacterium and F/B ratio	CON (n = 6)	MOD (n = 6)	QG (n = 6)	HG (n = 6)	CP (n = 6)
Firmicutes	0.3980±0.1134	0.3122±0.0851	0.2868±0.0956	0.2858±0.0852	0.3775±0.0809
Bacteroidetes	0.5255±0.1327	0.5314±0.0878	0.5844±0.1029	0.5861±0.0985	0.5101±0.0683
Actinobacteria	0.0108±0.0007^a	0.0495±0.0183	0.0296±0.0057^a	0.0384±0.0111	0.0484±0.0132^c
Gemmatimonadetes	0.0019±0.0002^b	0.0025±0.0005	0.0019±0.0002^b	0.0014±0.0003^a	0.0010±0.0002^a
F/B ratio	0.8463±0.4340	0.6270±0.2913	0.5280±0.2548	0.5223±0.2483	0.7686±0.2645

Table 3 Effect of QG on relative abundances of microbes at the genus levels in HLP rats (%,$\bar{x}±s$)

Bacterium	CON (n = 6)	MOD (n = 6)	QG (n = 6)	HG (n = 6)	CP (n = 6)
Collinsella	0.0356±0.0273^a	3.7961±1.7565	1.5633±0.4499^c	2.9817±1.0998^d	3.9656±1.4132^f
Ruminococcaceae_UCG-005	1.4229±1.2446^b	0.1089±0.0546	0.2856±0.1867^b	0.2719±0.2306	0.3326±0.2971
Turicibacter	0.2347±0.1542^b	0.0509±0.0902	0.2229±0.1962^b	0.1195±0.1223	0.0456±0.0794^d
Escherichia-Shigella	0.0943±0.0123^b	0.1347±0.0383	0.0754±0.0143^c	0.0747±0.0339^b	0.0576±0.0147^c
Intestinimonas	0.4558±0.2121^c	0.0826±0.0574	0.2052±0.1202^c	0.0765±0.0495^c	0.1233±0.0768^c
Allisonella	0.0009±0.0011^a	0.1477±0.0536	0.0769±0.0528^b	0.0918±0.0257^b	0.1254±0.0747
[Eubacterium]_hallii_group	0.0019±0.0023^b	0.2395±0.2461	0.0543±0.0303^c	0.1399±0.1337	0.2160±0.1104^f
Phocea	0.0010±0.0020^a	0.0667±0.0295	0.1187±0.0237^c	0.1061±0.0382	0.0875±0.0486
Flavobacterium	0.0036±0.0014^b	0.0019±0.0015	0.0173±0.0045^a	0.0025±0.0011^e	0.0016±0.0006^e
Staphylococcus	0.0000±0.0000^a	0.0049±0.0031	0.0010±0.0012^c	0.0039±0.0019^d	0.0067±0.0068

Figure 3 Scores plots of PCOA, OPLS-permutation, and related pathway between CON, MOD, and QG groups (n = 6) A: scores plots of PCA between CON, MOD, and QG groups; B: scores plots of PCOA between CON and MOD groups; C: scores plots of PCOA between MOD and QG groups; D: scores plots of OPLS-permutation between CON and MOD groups; E: scores plots of OPLS-Permutation between MOD and QG groups; F: summary of pathway analysis of liver samples. CON: normal control (fed by normal chow diet); MOD: model group (fed by HFHCD); QG: QG group (5 g/kg QG + HFHCD); CON: control; MOD: model; QG: Qige decoction; HG: Huangqi-Gegen decoction; CP: Chenpi decoction; HFHCD: high-fat high-cholesterol diet; PCOA: principal coordinate analysis‌; OPLS: orthogonal partial least squares; PCA: principal component analysis.

Figure 4 Effect of QG on the expression of NPC1L1, ABCG5, and ABCG8 proteins in HLP rats A: representative Western blot image of liver ABCG5, and ABCG8 proteins; B and C: relative expression level of liver ABCG5 (B) and ABCG8 (C); D: representative Western blot image of small intestine NPC1L1, ABCG5, and ABCG8 proteins; E-G: relative expression level of small intestine ABCG5 (E), ABCG8 (F), and NPC1L1 (G). CON: normal control (fed by normal chow diet); MOD: model group (fed by HFHCD); ATO: atorvastatin group (5 mg/kg atorvastatin+HFHCD); QG: QG group (5 g/kg QG + HFHCD); HG: HG group (4.5 g/kg HG + HFHCD); CP: CP group (0.5 g/kg CP + HFHCD). HLP: hyperlipidemic; CON: control; MOD: model; ATO: atorvastatin; QG: Qige decoction; HG: Huangqi-Gegen decoction; CP: Chenpi decoction; TG: triglycerides; TC: total cholesterol; LDL-C: low-density lipoprotein cholesterol; HDL-C: high-density lipoprotein cholesterol; HFHCD: high-fat high-cholesterol diet. NPC1L1: Niemann-Pick C1-like 1; ABCG5: ATP-binding cassette G5; ABCG8: ATP-binding cassette G8. Variables did not conform to the normal distributions and variance homogeneity, Kruskal-Wallis was used to evaluate the statistical significance of NPC1L1, ABCG5, and ABCG8 proteins. All data are expressed as the mean±standard deviation (n = 3); aP < 0.05 and bP < 0.01, compared to the MOD group; cP < 0.05, compared to the QG group.

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