Journal of Traditional Chinese Medicine ›› 2026, Vol. 46 ›› Issue (1): 160-171.DOI: 10.19852/j.cnki.jtcm.2026.01.015
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Exploring the mechanism of the Lianshi Jianpi formula (莲实健脾方) in treating impaired glucose tolerance: a network pharmacology, molecular docking, and experimental validation study
JIANG Mingqian1,2, WANG Tong3, HUANG Bowei2, QIU Chen1, LIANG Yanbin4, YE Binhua1(
)
- 1 Department of Endocrinology and Metabolism, People's Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou 350004, China
2 First Clinical Medicine College, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China
3 College of Traditional Chinese Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China
4 Department of Clinical Nutrition, People's Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou 350004, China
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Received:2025-04-19Accepted:2025-10-09Online:2026-02-15Published:2026-01-28 -
Contact:Prof. YE Binhua, Department of Endocrinology and Metabolism, People's Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou 350004, Fujian, China.Ybinhua2022@163.com ;Telephone: +86-13275911822 -
Supported by:Natural Science Foundation of Fujian Province Project: To Investigate the Mechanism of Lianshi Jianpi Formula In Improving Impaired Glucose Tolerance via the Fibroblast Growth Factor 21-Mediated Adenosine 5‘-monophosphate-Activated Protein Kinases Energy Metabolism Pathway(2023J01841);ZHOU Guoying Fujian Province Famous Traditional Chinese Medicine Inheritance Workstation Construction Project(Min Zhong Yi [2023] 56)
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JIANG Mingqian, WANG Tong, HUANG Bowei, QIU Chen, LIANG Yanbin, YE Binhua. Exploring the mechanism of the Lianshi Jianpi formula (莲实健脾方) in treating impaired glucose tolerance: a network pharmacology, molecular docking, and experimental validation study[J]. Journal of Traditional Chinese Medicine, 2026, 46(1): 160-171.
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Figure 1 Herb-compound-target network and GO biological process analysis A: "Herbs-active compounds-hub therapeutic target proteins" network of LSJPF for IGT. Ellipses represent the hub therapeutic targets, V-shaped nodes represent herbs, and diamond-shaped nodes represent active compounds. Edges represent the relationships between herbs, active compounds, and hub therapeutic target proteins; B: GO enrichment analysis of the 12 hub targets: Top 20 biological process terms with the most significant P-values. IGT: impaired glucose tolerance; LSJPF: Lianshi Jianpi formula; GO: gene ontology. SLC6A3: sodium-dependent dopamine transporter; PRKACA: cAMP-dependent protein kinase catalytic subunit alpha; AKT1: RAC-alpha serine/threonine-protein kinase; MMP2: matrix metallopeptidase 2; ALB: albumin; CASP3: caspase-3; CAV1: caveolin-1; PTGS2: prostaglandin-endoperoxide synthase 2; JUN: jun proto-oncogene, AP-1 transcription factor subunit; HSP90AB1: heat shock protein 90 kDa alpha B1; BCL2: B-cell lymphoma 2 family protein; CTNNB1: catenin beta-1.
Figure 1 Herb-compound-target network and GO biological process analysis A: "Herbs-active compounds-hub therapeutic target proteins" network of LSJPF for IGT. Ellipses represent the hub therapeutic targets, V-shaped nodes represent herbs, and diamond-shaped nodes represent active compounds. Edges represent the relationships between herbs, active compounds, and hub therapeutic target proteins; B: GO enrichment analysis of the 12 hub targets: Top 20 biological process terms with the most significant P-values. IGT: impaired glucose tolerance; LSJPF: Lianshi Jianpi formula; GO: gene ontology. SLC6A3: sodium-dependent dopamine transporter; PRKACA: cAMP-dependent protein kinase catalytic subunit alpha; AKT1: RAC-alpha serine/threonine-protein kinase; MMP2: matrix metallopeptidase 2; ALB: albumin; CASP3: caspase-3; CAV1: caveolin-1; PTGS2: prostaglandin-endoperoxide synthase 2; JUN: jun proto-oncogene, AP-1 transcription factor subunit; HSP90AB1: heat shock protein 90 kDa alpha B1; BCL2: B-cell lymphoma 2 family protein; CTNNB1: catenin beta-1.
Figure 2 KEGG pathway enrichment analyses and molecular docking analysis A: sankey-dot plot of KEGG enrichment analysis; B: molecular docking diagrams; B1: AKT1 and beta-sitosterol molecular docking; B2: BCL2 and beta-sitosterol molecular docking; B3: HSP90AB1 and beta-sitosterol molecular docking. SLC6A3: sodium-dependent dopamine transporter; PRKACA: cAMP-dependent protein kinase catalytic subunit alpha; AKT1: RAC-alpha serine/threonine-protein kinase; MMP2: matrix metallopeptidase 2; ALB: albumin; CASP3: caspase-3; CAV1: caveolin-1; PTGS2: prostaglandin-endoperoxide synthase 2; JUN: jun proto-oncogene, AP-1 transcription factor subunit; HSP90AB1: heat shock protein 90 kDa alpha B1; BCL2: B-cell lymphoma 2 family protein; CTNNB1: catenin beta-1; PI3K: phosphatidylinositol-3-kinase.
Figure 2 KEGG pathway enrichment analyses and molecular docking analysis A: sankey-dot plot of KEGG enrichment analysis; B: molecular docking diagrams; B1: AKT1 and beta-sitosterol molecular docking; B2: BCL2 and beta-sitosterol molecular docking; B3: HSP90AB1 and beta-sitosterol molecular docking. SLC6A3: sodium-dependent dopamine transporter; PRKACA: cAMP-dependent protein kinase catalytic subunit alpha; AKT1: RAC-alpha serine/threonine-protein kinase; MMP2: matrix metallopeptidase 2; ALB: albumin; CASP3: caspase-3; CAV1: caveolin-1; PTGS2: prostaglandin-endoperoxide synthase 2; JUN: jun proto-oncogene, AP-1 transcription factor subunit; HSP90AB1: heat shock protein 90 kDa alpha B1; BCL2: B-cell lymphoma 2 family protein; CTNNB1: catenin beta-1; PI3K: phosphatidylinositol-3-kinase.
Figure 3 Effects of LSJPF treatment on body weight, food intake, water intake and glucose metabolism in IGT rats A: effects of LSJPF treatment on body weight, food intake, water intake and glucose metabolism in different time points; A1: body weight; A2: food intake; A3: water intake. A4: FPG; B: OGTT results in each group; B1: curve of OGTT at week 8; B2: AUC of OGTT; C: ITT results in each group; C1: Curve of ITT at week 8; C2: AUC of ITT. Control group: normal SD rats fed with standard diet; IGT group: IGT model rats fed with high-fat diet; LSJPF group: IGT model rats fed with 2/3 of the high-fat diet and 1/3 of the LSJPF. IGT: impaired glucose tolerance; LSJPF: Lianshi Jianpi formula; FPG: fasting plasma glucose; AUC: area under the curve; OGTT: oral glucose tolerance test; ITT: insulin tolerance test. Statistical analyses were measured by using one-way analysis of variance to analyse the differences between the groups. Data were shown as mean ± standard error of the mean (n = 8). aP < 0.05, compared with IGT group; bP < 0.05, compared with Control group.
Figure 3 Effects of LSJPF treatment on body weight, food intake, water intake and glucose metabolism in IGT rats A: effects of LSJPF treatment on body weight, food intake, water intake and glucose metabolism in different time points; A1: body weight; A2: food intake; A3: water intake. A4: FPG; B: OGTT results in each group; B1: curve of OGTT at week 8; B2: AUC of OGTT; C: ITT results in each group; C1: Curve of ITT at week 8; C2: AUC of ITT. Control group: normal SD rats fed with standard diet; IGT group: IGT model rats fed with high-fat diet; LSJPF group: IGT model rats fed with 2/3 of the high-fat diet and 1/3 of the LSJPF. IGT: impaired glucose tolerance; LSJPF: Lianshi Jianpi formula; FPG: fasting plasma glucose; AUC: area under the curve; OGTT: oral glucose tolerance test; ITT: insulin tolerance test. Statistical analyses were measured by using one-way analysis of variance to analyse the differences between the groups. Data were shown as mean ± standard error of the mean (n = 8). aP < 0.05, compared with IGT group; bP < 0.05, compared with Control group.
Table 1 Effects of LSJPF treatment on HbA1c and lipid metabolism in IGT rats ($\bar{x} \pm s$)
| Group | n | HbA1c (%) | Lee’s index | Visceral fat percentage (%) | TG (mmol/L) | HDL-C (mmol/L) | CHOL (mmol/L) | LDL-C (mmol/L) |
|---|---|---|---|---|---|---|---|---|
| Control | 8 | 5.800±0.743 | 294.078±5.751 | 0.273±0.006 | 0.573±0.162 | 0.515±0.092 | 1.965±0.512 | 0.166±0.193 |
| IGT | 8 | 12.171±3.995a | 290.882±13.881 | 0.349±0.275 | 0.946±0.545a | 0.555±0.244 | 3.904±2.003a | 1.570±0.976a |
| LSJPF | 8 | 7.671±3.967b | 301.111±9.263 | 0.319±0.023 | 0.586±0.138b | 0.445±0.065 | 2.213±0.440b | 0.653±0.192b |
Table 1 Effects of LSJPF treatment on HbA1c and lipid metabolism in IGT rats ($\bar{x} \pm s$)
| Group | n | HbA1c (%) | Lee’s index | Visceral fat percentage (%) | TG (mmol/L) | HDL-C (mmol/L) | CHOL (mmol/L) | LDL-C (mmol/L) |
|---|---|---|---|---|---|---|---|---|
| Control | 8 | 5.800±0.743 | 294.078±5.751 | 0.273±0.006 | 0.573±0.162 | 0.515±0.092 | 1.965±0.512 | 0.166±0.193 |
| IGT | 8 | 12.171±3.995a | 290.882±13.881 | 0.349±0.275 | 0.946±0.545a | 0.555±0.244 | 3.904±2.003a | 1.570±0.976a |
| LSJPF | 8 | 7.671±3.967b | 301.111±9.263 | 0.319±0.023 | 0.586±0.138b | 0.445±0.065 | 2.213±0.440b | 0.653±0.192b |
Figure 4 Effects of LSJPF treatment on liver pathology and AMPK/PI3K/AKT pathway in IGT rats A: hematoxylin-eosin staining observes liver tissues. A1: control group; A2: IGT group; A3: LSJPF group; A4: non-alcoholic fatty liver disease activity score; B: oil red O staining observes liver tissues. B1: control group; B2: IGT group; B3: LSJPF group; B4: relative area of lipid droplets. C: protein expression in each group; C1: representative immunoblotting images of p-AMPK, AMPK, p-PI3K, PI3K, p-AKT, AKT and GAPDH; 1: Control group; 2: IGT group; 3: LSJPF group; C2: p-AMPK/AMPK ratio; C3: p- PI3K / PI3K ratio; C4: p-AKT/AKT ration; control group: normal SD rats fed with standard diet; IGT group: IGT model rats fed with high-fat diet; LSJPF group: IGT model rats fed with 2/3 of the high-fat diet and 1/3 of the LSJPF. IGT: impaired glucose tolerance; LSJPF: Lianshi Jianpi formula; p-AMPK: phosphorylated Adenosine 5‘-monophosphate-activated protein kinase; AMPK: Adenosine 5‘-monophosphate-activated protein kinase; p-PI3K: phosphorylated phosphatidylinositol 3-kinase; PI3K: phosphatidylinositol 3-kinase; p-AKT: phosphorylated protein kinase B; AKT: protein kinase B; GAPDH: glyceraldehyde-3-phosphate dehydrogenase. Statistical analyses were measured by using one-way analysis of variance to analyze the differences between the groups. Date were shown as mean ± standard error of the mean (n = 3). aP < 0.05, compared with Control group; bP < 0.05 compared with IGT group.
Figure 4 Effects of LSJPF treatment on liver pathology and AMPK/PI3K/AKT pathway in IGT rats A: hematoxylin-eosin staining observes liver tissues. A1: control group; A2: IGT group; A3: LSJPF group; A4: non-alcoholic fatty liver disease activity score; B: oil red O staining observes liver tissues. B1: control group; B2: IGT group; B3: LSJPF group; B4: relative area of lipid droplets. C: protein expression in each group; C1: representative immunoblotting images of p-AMPK, AMPK, p-PI3K, PI3K, p-AKT, AKT and GAPDH; 1: Control group; 2: IGT group; 3: LSJPF group; C2: p-AMPK/AMPK ratio; C3: p- PI3K / PI3K ratio; C4: p-AKT/AKT ration; control group: normal SD rats fed with standard diet; IGT group: IGT model rats fed with high-fat diet; LSJPF group: IGT model rats fed with 2/3 of the high-fat diet and 1/3 of the LSJPF. IGT: impaired glucose tolerance; LSJPF: Lianshi Jianpi formula; p-AMPK: phosphorylated Adenosine 5‘-monophosphate-activated protein kinase; AMPK: Adenosine 5‘-monophosphate-activated protein kinase; p-PI3K: phosphorylated phosphatidylinositol 3-kinase; PI3K: phosphatidylinositol 3-kinase; p-AKT: phosphorylated protein kinase B; AKT: protein kinase B; GAPDH: glyceraldehyde-3-phosphate dehydrogenase. Statistical analyses were measured by using one-way analysis of variance to analyze the differences between the groups. Date were shown as mean ± standard error of the mean (n = 3). aP < 0.05, compared with Control group; bP < 0.05 compared with IGT group.
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