Journal of Traditional Chinese Medicine ›› 2023, Vol. 43 ›› Issue (5): 906-914.DOI: 10.19852/j.cnki.jtcm.20221206.004
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Ginsenoside Rb1 alleviates chronic intermittent hypoxia-induced diabetic cardiomyopathy in db/db mice by regulating the adenosine monophosphate-activated protein kinase/Nrf2/heme oxygenase-1 signaling pathway
LIU Bingbing1, LI Jieru1,2, SI Jianchao1, CHEN Qi1, YANG Shengchang1,2(
), JI Ensheng1,2()
- 1 Department of Physiology, Hebei University of Chinese Medicine, Shijiazhuang 050200, China
2 Hebei Technology Innovation Center of TCM Combined Hydrogen Medicine, Shijiazhuang 050200, China
-
Received:2022-04-07Accepted:2022-08-08Online:2023-10-15Published:2022-12-06 -
Contact:YANG Shengchang, Department of Physiology, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.yscdekaoyan@163.com ; Prof. JI Ensheng, Department of Physiology, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.jesphy@126.com.Telephone : +86-311-89926098 -
Supported by:Natural Science Foundation of Hebei Province: the Central Regulatory Mechanism of Tanshinone IIA on Angiotensin Ⅱ Induced Sympathetic Excitation in Intermittent Hypoxia(H2019423136);Fundamental Research Funds for the Provisional Universities of Hebei University of Chinese Medicine: a Study on the Protective Mechanism of Hydrogen on Chronic Intermittent Hypoxia-induced Microglia Inflammatory Response(YTZ2019001);a Study on the Molecular Mechanism of Improving Effect Danggui Buxue Decoction on Vascular Endothelial Cell Senescence in Chronic Intermittent Hypoxia through Nrf2/HO-1 Signaling Pathway(YXTD2021005);Graduate Innovation Fund of Hebei University of Chinese Medicine: the Effect of Jinlida Granules on the Myocardial Improvement of Chronic Intermittent Hypoxia Aggravated Diabetic Cardiomyopathy in db/db Mice(XCXZZBS2022013)
Cite this article
LIU Bingbing, LI Jieru, SI Jianchao, CHEN Qi, YANG Shengchang, JI Ensheng. Ginsenoside Rb1 alleviates chronic intermittent hypoxia-induced diabetic cardiomyopathy in db/db mice by regulating the adenosine monophosphate-activated protein kinase/Nrf2/heme oxygenase-1 signaling pathway[J]. Journal of Traditional Chinese Medicine, 2023, 43(5): 906-914.
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Figure 1 Effect of Rb1 treatment on lipid metabolism and glucose metabolism in model mice A-C: levels of TC, TG, and HDL-C; D: insulin resistance index; E: AUC analyses for OGTT; F: AUC analyses for IPITT. the db/m group and the model group were given distilled water by gavage; the Rb1 low-dose group was given Rb1 20 mg·kg-1·d-1 by gavage; the Rb1 high-dose group was given Rb1 40 mg·kg-1·d-1 by gavage; the GLP-1 group was given liraglutide 0.1 mg·kg-1·d-1 by intraperitoneal injection. TC: total cholesterol; TG: triglyceride; HDL-C: high-density lipoprotein cholesterol; OGTT: oral glucose tolerance test; IPITT: intraperitoneal insulin tolerance test; HOMA-IR: homeostasis model assessment for insulin resistance; AUC: area under the curve; Rb1: ginsenoside Rb1; GLP-1: glucagon-like peptide-1. n = 5. Data are presented as mean ± standard error of mean. aP < 0.01, compared with the db/m group; bP < 0.05, cP < 0.01 compared with the model group.
Figure 1 Effect of Rb1 treatment on lipid metabolism and glucose metabolism in model mice A-C: levels of TC, TG, and HDL-C; D: insulin resistance index; E: AUC analyses for OGTT; F: AUC analyses for IPITT. the db/m group and the model group were given distilled water by gavage; the Rb1 low-dose group was given Rb1 20 mg·kg-1·d-1 by gavage; the Rb1 high-dose group was given Rb1 40 mg·kg-1·d-1 by gavage; the GLP-1 group was given liraglutide 0.1 mg·kg-1·d-1 by intraperitoneal injection. TC: total cholesterol; TG: triglyceride; HDL-C: high-density lipoprotein cholesterol; OGTT: oral glucose tolerance test; IPITT: intraperitoneal insulin tolerance test; HOMA-IR: homeostasis model assessment for insulin resistance; AUC: area under the curve; Rb1: ginsenoside Rb1; GLP-1: glucagon-like peptide-1. n = 5. Data are presented as mean ± standard error of mean. aP < 0.01, compared with the db/m group; bP < 0.05, cP < 0.01 compared with the model group.
Figure 2 Effect of Rb1 treatment on cardiac histopathology in model mice A-B: the cardiac tissue with HE staining and Masson staining (×200, scale bars =100 μm); C-D: expression of collagen I and collagen III protein in cardiac tissue was detected by immunohistochemistry (×400, scale bars = 50 μm); A1, B1, C1, D1: cardiac tissue of the db/m group; A2, B2, C2, D2: cardiac tissue of the model group; A3, B3, C3, D3: cardiac tissue of the Rb1 low-dose group; A4, B4, C4, D4: cardiac tissue of the Rb1 high-dose group; A5, B5, C5, D5: cardiac tissue of the GLP-1 group. E: fibrosis area of cardiac tissues; F-G: protein expression level of collagen I and collagen III was determined. the db/m group and the model group were given distilled water by gavage; the Rb1 low-dose group was given Rb1 20 mg·kg-1·d-1 by gavage; the Rb1 high-dose group was given Rb1 40 mg·kg-1·d-1 by gavage; the GLP-1 group was given liraglutide 0.1 mg·kg-1·d-1 by intraperitoneal injection. HE: hematoxylin-eosin; Collagen I: collagen type I; Collagen III: collagen type III; Rb1: ginsenoside Rb1; GLP-1: glucagon-like peptide-1. n = 3. Data are presented as means ± standard error of mean. aP < 0.01, compared with the db/m group; bP < 0.05, cP < 0.01 compared with the model group.
Figure 2 Effect of Rb1 treatment on cardiac histopathology in model mice A-B: the cardiac tissue with HE staining and Masson staining (×200, scale bars =100 μm); C-D: expression of collagen I and collagen III protein in cardiac tissue was detected by immunohistochemistry (×400, scale bars = 50 μm); A1, B1, C1, D1: cardiac tissue of the db/m group; A2, B2, C2, D2: cardiac tissue of the model group; A3, B3, C3, D3: cardiac tissue of the Rb1 low-dose group; A4, B4, C4, D4: cardiac tissue of the Rb1 high-dose group; A5, B5, C5, D5: cardiac tissue of the GLP-1 group. E: fibrosis area of cardiac tissues; F-G: protein expression level of collagen I and collagen III was determined. the db/m group and the model group were given distilled water by gavage; the Rb1 low-dose group was given Rb1 20 mg·kg-1·d-1 by gavage; the Rb1 high-dose group was given Rb1 40 mg·kg-1·d-1 by gavage; the GLP-1 group was given liraglutide 0.1 mg·kg-1·d-1 by intraperitoneal injection. HE: hematoxylin-eosin; Collagen I: collagen type I; Collagen III: collagen type III; Rb1: ginsenoside Rb1; GLP-1: glucagon-like peptide-1. n = 3. Data are presented as means ± standard error of mean. aP < 0.01, compared with the db/m group; bP < 0.05, cP < 0.01 compared with the model group.
Figure 3 Effect of Rb1 treatment on cardiac function in model mice A: representative M-mode echocardiography images; A1: M-mode image of the db/m group; A2: M-mode image of the model group; A3: M-mode image of the Rb1 low-dose group; A4: M-mode image of the Rb1 high-dose group; A5: M-mode image of the GLP-1 group; B: representative Doppler echocardiography images; the E and A waves are labeled; B1: Doppler image of the db/m group; B2: Doppler image of the model group; B3: Doppler image of the Rb1 low-dose group; B4: Doppler image of the Rb1 high-dose group; B5: Doppler image of the GLP-1 group; C-G: measurement of LVEF, LVFS, LVDd, LVDs, and CO. n = 3. H: ratio of MV E/A. n = 3. I-K: the levels of cTnI, CK-MB, and LDH. the db/m group and the model group were given distilled water by gavage; the Rb1 low-dose group was given Rb1 20 mg·kg-1·d-1 by gavage; the Rb1 high-dose group was given Rb1 40 mg·kg-1·d-1 by gavage; the GLP-1 group was given liraglutide 0.1 mg·kg-1·d-1 by intraperitoneal injection. Rb1: ginsenoside Rb1; GLP-1: glucagon-like peptide-1; LVEF: the left ventricular ejection fraction; LVFS: the left ventricular fraction shortening; LVDd: the left ventricular diastolic diameter; LVDs: the left ventricular systolic diameter; CO: cardiac output; MV E/A: the velocity ratio of the E peak to the A peak in the cardiac mitral valve; cTnI: cardiac troponin I; CK-MB: creatine kinase MB; LDH: lactate dehydrogenase; M-mode: motion mode. n = 5. Data are presented as mean ± standard error of mean. aP < 0.01, compared with the db/m group; bP < 0.05, cP < 0.01 compared with the model group.
Figure 3 Effect of Rb1 treatment on cardiac function in model mice A: representative M-mode echocardiography images; A1: M-mode image of the db/m group; A2: M-mode image of the model group; A3: M-mode image of the Rb1 low-dose group; A4: M-mode image of the Rb1 high-dose group; A5: M-mode image of the GLP-1 group; B: representative Doppler echocardiography images; the E and A waves are labeled; B1: Doppler image of the db/m group; B2: Doppler image of the model group; B3: Doppler image of the Rb1 low-dose group; B4: Doppler image of the Rb1 high-dose group; B5: Doppler image of the GLP-1 group; C-G: measurement of LVEF, LVFS, LVDd, LVDs, and CO. n = 3. H: ratio of MV E/A. n = 3. I-K: the levels of cTnI, CK-MB, and LDH. the db/m group and the model group were given distilled water by gavage; the Rb1 low-dose group was given Rb1 20 mg·kg-1·d-1 by gavage; the Rb1 high-dose group was given Rb1 40 mg·kg-1·d-1 by gavage; the GLP-1 group was given liraglutide 0.1 mg·kg-1·d-1 by intraperitoneal injection. Rb1: ginsenoside Rb1; GLP-1: glucagon-like peptide-1; LVEF: the left ventricular ejection fraction; LVFS: the left ventricular fraction shortening; LVDd: the left ventricular diastolic diameter; LVDs: the left ventricular systolic diameter; CO: cardiac output; MV E/A: the velocity ratio of the E peak to the A peak in the cardiac mitral valve; cTnI: cardiac troponin I; CK-MB: creatine kinase MB; LDH: lactate dehydrogenase; M-mode: motion mode. n = 5. Data are presented as mean ± standard error of mean. aP < 0.01, compared with the db/m group; bP < 0.05, cP < 0.01 compared with the model group.
Figure 4 Effect of Rb1 treatment on the AMPK/Nrf2/HO-1 signaling pathway in model mice A: representative blot images of AMPK, Nrf2, and HO-1 expression; 1: blot image of the db/m group; 2: blot image of the model group; 3: blot image of the Rb1 low-dose group; 4: blot image of the Rb1 high-dose group; 5: blot image of the GLP-1 group. B-D: quantitative analysis of AMPK, Nrf2, and HO-1 expression; E: translocation of nuclear-Nrf2 was detected by immunofluorescence (×200, scale bars = 100 μm); E1: nuclear-Nrf2 expression of the db/m group; E2: nuclear-Nrf2 expression of the model group; E3: nuclear-Nrf2 expression of the Rb1 low-dose group; E4: nuclear-Nrf2 expression of the Rb1 high-dose group; E5: nuclear-Nrf2 expression of the GLP-1 group. the db/m group and the model group were given distilled water by gavage; the Rb1 low-dose group was given Rb1 20 mg·kg-1·d-1 by gavage; the Rb1 high-dose group was given Rb1 40 mg·kg-1·d-1 by gavage; the GLP-1 group was given liraglutide 0.1 mg·kg-1·d-1 by intraperitoneal injection. Rb1: ginsenoside Rb1; GLP-1: glucagon-like peptide-1; AMPK: adenosine monophosphate-activated protein kinase; P-AMPK: phosphorylated adenosine monophosphate-activated protein kinase; Nrf2: nuclear factor erythroid2-related factor2; HO-1: heme oxygenase-1. n = 3. Data are presented as mean ± standard error of mean. aP < 0.01, compared with the db/m group; bP < 0.01, cP < 0.05 compared with the model group.
Figure 4 Effect of Rb1 treatment on the AMPK/Nrf2/HO-1 signaling pathway in model mice A: representative blot images of AMPK, Nrf2, and HO-1 expression; 1: blot image of the db/m group; 2: blot image of the model group; 3: blot image of the Rb1 low-dose group; 4: blot image of the Rb1 high-dose group; 5: blot image of the GLP-1 group. B-D: quantitative analysis of AMPK, Nrf2, and HO-1 expression; E: translocation of nuclear-Nrf2 was detected by immunofluorescence (×200, scale bars = 100 μm); E1: nuclear-Nrf2 expression of the db/m group; E2: nuclear-Nrf2 expression of the model group; E3: nuclear-Nrf2 expression of the Rb1 low-dose group; E4: nuclear-Nrf2 expression of the Rb1 high-dose group; E5: nuclear-Nrf2 expression of the GLP-1 group. the db/m group and the model group were given distilled water by gavage; the Rb1 low-dose group was given Rb1 20 mg·kg-1·d-1 by gavage; the Rb1 high-dose group was given Rb1 40 mg·kg-1·d-1 by gavage; the GLP-1 group was given liraglutide 0.1 mg·kg-1·d-1 by intraperitoneal injection. Rb1: ginsenoside Rb1; GLP-1: glucagon-like peptide-1; AMPK: adenosine monophosphate-activated protein kinase; P-AMPK: phosphorylated adenosine monophosphate-activated protein kinase; Nrf2: nuclear factor erythroid2-related factor2; HO-1: heme oxygenase-1. n = 3. Data are presented as mean ± standard error of mean. aP < 0.01, compared with the db/m group; bP < 0.01, cP < 0.05 compared with the model group.
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