Journal of Traditional Chinese Medicine ›› 2026, Vol. 46 ›› Issue (5): 1072-1081.DOI: 10.19852/j.cnki.jtcm.2026.05.002
• Original Articles • Previous Articles Next Articles
Hongqu (Ultivarietas Oryzae Sativae et Monasci) attenuates non-alcoholic fatty liver disease progression by inhibiting lipogenesis and promoting fatty acid oxidation through regulating the adenosine 5'-monophosphate-activated protein kinase/sterol regulatory element-binding protein 1c signaling pathway
YAO Xingqin, WANG Haixia, WU Min, ZHANG Haibin, ZHANG Yili, WU Yuanfen, YANG Xiaojia(
), JIANG Meng()
Department of Pharmacy ,Hangzhou Hospital of Traditional Chinese Medicine Hangzhou 310007, China
-
Received:2025-05-13Accepted:2025-11-19Online:2026-10-15Published:2026-10-09 -
Contact:JIANG Meng, Department of Pharmacy, Hangzhou Hospital of Traditional Chinese Medicine, Hangzhou 310007, China. anna_sewell@163.com,Telephone: + 86-13989880942; YANG Xiaojia, Department of Pharmacy, Hangzhou Hospital of Traditional Chinese Medicine, Hangzhou 310007, China. yang86272388@163.com,Telephone: + 86-13989880942 -
Supported by:Zhejiang Province Traditional Chinese Medicine Science and Technology Project under Grant: Investigation of the Mechanism of Hongqu (Ultivarietas Oryzae Sativae et Monasci) in regulating Lipid Metabolic Disorders to Treat Nonalcoholic Fatty Liver Disease via the Adenosine 5'-Monophosphate-activated Protein Kinase/Sterol Regulatory Element-Binding Protein 1c Pathway(2024ZL657)
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YAO Xingqin, WANG Haixia, WU Min, ZHANG Haibin, ZHANG Yili, WU Yuanfen, YANG Xiaojia, JIANG Meng. Hongqu (Ultivarietas Oryzae Sativae et Monasci) attenuates non-alcoholic fatty liver disease progression by inhibiting lipogenesis and promoting fatty acid oxidation through regulating the adenosine 5'-monophosphate-activated protein kinase/sterol regulatory element-binding protein 1c signaling pathway[J]. Journal of Traditional Chinese Medicine, 2026, 46(5): 1072-1081.
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Figure 1 RYR treatment ameliorated pathological damage and lipid accumulation in NAFLD mice A: observation of liver histomorphology, n = 6; B: assessment of liver weight, n = 6; C: detection of liver index, n = 6; D: representative photomicrographs of HE staining in liver tissues of mice, n = 3; E: representative photomicrographs of oil red O staining in mouse liver tissues, n = 3; F: lipid deposition in mouse liver tissues was assessed using oil red O staining, n = 3; D1-D5, E1-E5: × 200, scale bar: 100 μm; D6-D10, E6-E10: × 400, scale bar: 50 μm; A1, D1, D6, E1, E6: sham group; A2, D2, D7, E2, E7: NAFLD group; A3, D3, D8, E3, E8: NAFLD + RYR-L group; A4, D4, D9, E4, E9: NAFLD + RYR-H group; A5, D5, D10, E5, E10: NAFLD + Silymarin group. Sham group: mice were fed with control diet for 12 weeks and 0.2 mL of 0.5% CMC-Na was gavaged once daily; NAFLD group: mice were fed with HFD (60% fat, 20% carbohydrate, 20% protein) for 12 weeks and 0.2 mL of 0.5% CMC-Na was gavaged once daily; NAFLD + RYR-L group: mice were fed with HFD for 12 weeks and low dose of RYR (150 mg/kg, which was dissolved in 0.2 mL of 0.5% CMC-Na) was gavaged once daily; NAFLD + RYR-H group: mice were fed with HFD for 12 weeks and high dose of RYR (300 mg/kg) was gavaged once daily; NAFLD + Silymarin group: mice were fed with HFD for 12 weeks and silymarin (200 mg/kg, which was dissolved in 0.2 mL of 0.5% CMC-Na) was gavaged once daily. RYR: red yeast rice; NAFLD: non-alcoholic fatty liver disease; HFD: high-fat diet; HE: hematoxylin and eosin. Results were presented as the mean ± standard deviation. Statistical analyses were measured by using one-way analysis of variance. aP < 0.01 vs Sham group; bP < 0.05 and cP < 0.01 vs NAFLD group.
Figure 1 RYR treatment ameliorated pathological damage and lipid accumulation in NAFLD mice A: observation of liver histomorphology, n = 6; B: assessment of liver weight, n = 6; C: detection of liver index, n = 6; D: representative photomicrographs of HE staining in liver tissues of mice, n = 3; E: representative photomicrographs of oil red O staining in mouse liver tissues, n = 3; F: lipid deposition in mouse liver tissues was assessed using oil red O staining, n = 3; D1-D5, E1-E5: × 200, scale bar: 100 μm; D6-D10, E6-E10: × 400, scale bar: 50 μm; A1, D1, D6, E1, E6: sham group; A2, D2, D7, E2, E7: NAFLD group; A3, D3, D8, E3, E8: NAFLD + RYR-L group; A4, D4, D9, E4, E9: NAFLD + RYR-H group; A5, D5, D10, E5, E10: NAFLD + Silymarin group. Sham group: mice were fed with control diet for 12 weeks and 0.2 mL of 0.5% CMC-Na was gavaged once daily; NAFLD group: mice were fed with HFD (60% fat, 20% carbohydrate, 20% protein) for 12 weeks and 0.2 mL of 0.5% CMC-Na was gavaged once daily; NAFLD + RYR-L group: mice were fed with HFD for 12 weeks and low dose of RYR (150 mg/kg, which was dissolved in 0.2 mL of 0.5% CMC-Na) was gavaged once daily; NAFLD + RYR-H group: mice were fed with HFD for 12 weeks and high dose of RYR (300 mg/kg) was gavaged once daily; NAFLD + Silymarin group: mice were fed with HFD for 12 weeks and silymarin (200 mg/kg, which was dissolved in 0.2 mL of 0.5% CMC-Na) was gavaged once daily. RYR: red yeast rice; NAFLD: non-alcoholic fatty liver disease; HFD: high-fat diet; HE: hematoxylin and eosin. Results were presented as the mean ± standard deviation. Statistical analyses were measured by using one-way analysis of variance. aP < 0.01 vs Sham group; bP < 0.05 and cP < 0.01 vs NAFLD group.
Figure 2 RYR treatment alleviated lipid metabolism disorder by modulating the AMPK/SREBP-1c pathway in NAFLD mice A: representative Western blot of p-AMPK/AMPK, SREBP-1c, p-ACC/ACC, and FAS protein expression; B: changes in p-AMPK/AMPK expression; C: changes in SREBP-1c expression; D: changes in p-ACC/ACC expression; E: changes in FAS expression. Sham group: mice were fed with control diet for 12 weeks and 0.2 mL of 0.5% CMC-Na was gavaged once daily; NAFLD group: mice were fed with HFD (60% fat, 20% carbohydrate, 20% protein) for 12 weeks and 0.2 mL of 0.5% CMC-Na was gavaged once daily; NAFLD + RYR-L group: mice were fed with HFD for 12 weeks and low dose of RYR (150 mg/kg, which was dissolved in 0.2 mL of 0.5% CMC-Na) was gavaged once daily; NAFLD + RYR-H group: mice were fed with HFD for 12 weeks and high dose of RYR (300 mg/kg) was gavaged once daily; NAFLD + Silymarin group: mice were fed with HFD for 12 weeks and silymarin (200 mg/kg, which was dissolved in 0.2 mL of 0.5% CMC-Na) was gavaged once daily. RYR: red yeast rice; NAFLD: non-alcoholic fatty liver disease; HFD: high-fat diet; AMPK: adenosine 5'-monophosphate-activated protein kinase; SREBP-1c: sterol regulatory element-binding protein 1c; FAS: fatty acid synthase; ACC: acetyl-CoA carboxylase. Results were presented as the mean ± standard deviation (n = 3). Statistical analyses were measured by using one-way analysis of variance. aP < 0.01 vs Sham group; bP < 0.05 and cP < 0.01 vs NAFLD group.
Figure 2 RYR treatment alleviated lipid metabolism disorder by modulating the AMPK/SREBP-1c pathway in NAFLD mice A: representative Western blot of p-AMPK/AMPK, SREBP-1c, p-ACC/ACC, and FAS protein expression; B: changes in p-AMPK/AMPK expression; C: changes in SREBP-1c expression; D: changes in p-ACC/ACC expression; E: changes in FAS expression. Sham group: mice were fed with control diet for 12 weeks and 0.2 mL of 0.5% CMC-Na was gavaged once daily; NAFLD group: mice were fed with HFD (60% fat, 20% carbohydrate, 20% protein) for 12 weeks and 0.2 mL of 0.5% CMC-Na was gavaged once daily; NAFLD + RYR-L group: mice were fed with HFD for 12 weeks and low dose of RYR (150 mg/kg, which was dissolved in 0.2 mL of 0.5% CMC-Na) was gavaged once daily; NAFLD + RYR-H group: mice were fed with HFD for 12 weeks and high dose of RYR (300 mg/kg) was gavaged once daily; NAFLD + Silymarin group: mice were fed with HFD for 12 weeks and silymarin (200 mg/kg, which was dissolved in 0.2 mL of 0.5% CMC-Na) was gavaged once daily. RYR: red yeast rice; NAFLD: non-alcoholic fatty liver disease; HFD: high-fat diet; AMPK: adenosine 5'-monophosphate-activated protein kinase; SREBP-1c: sterol regulatory element-binding protein 1c; FAS: fatty acid synthase; ACC: acetyl-CoA carboxylase. Results were presented as the mean ± standard deviation (n = 3). Statistical analyses were measured by using one-way analysis of variance. aP < 0.01 vs Sham group; bP < 0.05 and cP < 0.01 vs NAFLD group.
Figure 3 RYR treatment inhibited lipid accumulation and apoptosis in THLE-2 cells A: determination of TC content, n = 6; B: determination of TG content, n = 6; C: representative photomicrographs of oil red O staining in THLE-2 cells, n = 3; D: lipid deposition in THLE-2 cells was assessed using oil red O staining, n = 3; E: detection of apoptosis was performed by flow cytometry assay, n = 3; F: changes of apoptosis rates, n = 3; C1-C4: magnification × 200, scale bar: 100 μm; C5-C7: magnification × 400, scale bar: 50 μm; C1, C5, E1: Control group; C2, C6, E2: OA group; C3, C7, E3: OA+RYR group; C4, C8, E4: OA + RYR + Compound C group. Control group: basal medium; OA group: THLE-2 cells were treated with 0.2 mM OA for 24 h; OA+RYR group: THLE-2 cells were treated with 0.2 mM OA for 24 h and subsequent 674 µg/mL of RYR for 24 h; OA + RYR + Compound C group: THLE-2 cells were cultured with 1 mM of Compound C for 0.5 h, 0.2 mM OA for 24 h and subsequent 674 µg/mL of RYR for 24 h. RYR: red yeast rice; THLE-2: normal human liver epithelial cell line; OA: oleic acid; TC: total cholesterol; TG: triglyceride. Results were presented as the mean ± standard deviation. Statistical analyses were measured by using one-way analysis of variance. aP < 0.01 vs Control group; bP < 0.01 vs OA group; cP < 0.01 vs OA+RYR group; dP < 0.05 vs OA group.
Figure 3 RYR treatment inhibited lipid accumulation and apoptosis in THLE-2 cells A: determination of TC content, n = 6; B: determination of TG content, n = 6; C: representative photomicrographs of oil red O staining in THLE-2 cells, n = 3; D: lipid deposition in THLE-2 cells was assessed using oil red O staining, n = 3; E: detection of apoptosis was performed by flow cytometry assay, n = 3; F: changes of apoptosis rates, n = 3; C1-C4: magnification × 200, scale bar: 100 μm; C5-C7: magnification × 400, scale bar: 50 μm; C1, C5, E1: Control group; C2, C6, E2: OA group; C3, C7, E3: OA+RYR group; C4, C8, E4: OA + RYR + Compound C group. Control group: basal medium; OA group: THLE-2 cells were treated with 0.2 mM OA for 24 h; OA+RYR group: THLE-2 cells were treated with 0.2 mM OA for 24 h and subsequent 674 µg/mL of RYR for 24 h; OA + RYR + Compound C group: THLE-2 cells were cultured with 1 mM of Compound C for 0.5 h, 0.2 mM OA for 24 h and subsequent 674 µg/mL of RYR for 24 h. RYR: red yeast rice; THLE-2: normal human liver epithelial cell line; OA: oleic acid; TC: total cholesterol; TG: triglyceride. Results were presented as the mean ± standard deviation. Statistical analyses were measured by using one-way analysis of variance. aP < 0.01 vs Control group; bP < 0.01 vs OA group; cP < 0.01 vs OA+RYR group; dP < 0.05 vs OA group.
Figure 4 RYR treatment ameliorated lipid metabolism disorder by modulating the AMPK/SREBP-1c pathway in OA-treated THLE-2 cells A: assessment of FAS expression using qRT-PCR assay; B: assessment of CPT-1 mRNA expression using qRT-PCR assay; C: determination of p-AMPK/AMPK, SREBP-1c, and p-ACC/ACC protein expression in THLE-2 cells was conducted by Western blot assay; C1: representative Western blot of p-AMPK/AMPK, SREBP-1c, and p-ACC/ACC protein expression; C2: changes in p-AMPK/AMPK expression; C3: changes in SREBP-1c expression; C4: changes in p-ACC/ACC expression. Control group: basal medium; OA group: THLE-2 cells were treated with 0.2 mM OA for 24 h; OA+RYR group: THLE-2 cells were treated with 0.2 mM OA for 24 h and subsequent 674 µg/mL of RYR for 24 h; OA + RYR + Compound C group: THLE-2 cells were cultured with 1 mM of Compound C for 0.5 h, 0.2 mM OA for 24 h and subsequent 674 µg/mL of RYR for 24 h. RYR: red yeast rice; OA: oleic acid; AMPK: adenosine 5'-monophosphate-activated protein kinase; SREBP-1c: sterol regulatory element-binding protein 1c; THLE-2: normal human liver epithelial cell line; FAS: fatty acid synthase; qRT-PCR: quantitative real-time polymerase chain reaction; CPT-1: carnitine palmitoyl transferase 1; ACC: acetyl-CoA carboxylase. Results were presented as the mean ± standard deviation (n = 3). Statistical analyses were measured by using one-way analysis of variance. aP < 0.01 vs Control group; bP < 0.01 vs OA group; cP < 0.01 vs OA + RYR group.
Figure 4 RYR treatment ameliorated lipid metabolism disorder by modulating the AMPK/SREBP-1c pathway in OA-treated THLE-2 cells A: assessment of FAS expression using qRT-PCR assay; B: assessment of CPT-1 mRNA expression using qRT-PCR assay; C: determination of p-AMPK/AMPK, SREBP-1c, and p-ACC/ACC protein expression in THLE-2 cells was conducted by Western blot assay; C1: representative Western blot of p-AMPK/AMPK, SREBP-1c, and p-ACC/ACC protein expression; C2: changes in p-AMPK/AMPK expression; C3: changes in SREBP-1c expression; C4: changes in p-ACC/ACC expression. Control group: basal medium; OA group: THLE-2 cells were treated with 0.2 mM OA for 24 h; OA+RYR group: THLE-2 cells were treated with 0.2 mM OA for 24 h and subsequent 674 µg/mL of RYR for 24 h; OA + RYR + Compound C group: THLE-2 cells were cultured with 1 mM of Compound C for 0.5 h, 0.2 mM OA for 24 h and subsequent 674 µg/mL of RYR for 24 h. RYR: red yeast rice; OA: oleic acid; AMPK: adenosine 5'-monophosphate-activated protein kinase; SREBP-1c: sterol regulatory element-binding protein 1c; THLE-2: normal human liver epithelial cell line; FAS: fatty acid synthase; qRT-PCR: quantitative real-time polymerase chain reaction; CPT-1: carnitine palmitoyl transferase 1; ACC: acetyl-CoA carboxylase. Results were presented as the mean ± standard deviation (n = 3). Statistical analyses were measured by using one-way analysis of variance. aP < 0.01 vs Control group; bP < 0.01 vs OA group; cP < 0.01 vs OA + RYR group.
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