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.
| 1. |
Stanton AM, Vaduganathan M. Asymptomatic diabetic cardiomyopathy: an underrecognized entity in type 2 diabetes. Curr Diab Rep 2021; 21: 41.
DOI |
| 2. |
Uryash A, Mijares A, Flores V, Adams JA, Lopez JR. Effects of naringin on cardiomyocytes from a rodent model of type 2 diabetes. Front Pharmacol 2021; 12: 719268.
DOI URL |
| 3. |
Xu Q, Tan X, Xian W, et al. Changes of necroptosis in irbesartan medicated cardioprotection in diabetic rats. Diabetes Metab Syndr Obes 2021; 14: 3851-63.
DOI URL |
| 4. |
Baguet JP, Barone-Rochette G, Tamisier R, Levy P, Pépin JL. Mechanisms of cardiac dysfunction in obstructive sleep apnea. Nat Rev Cardiol 2012; 9: 679-88.
DOI |
| 5. |
Ye L, Chen X, Wang M, et al. Curcumin analogue C 66 attenuates obesity-induced myocardial injury by inhibiting JNK-mediated inflammation. Biomed Pharmacother 2021; 143: 112121.
DOI URL |
| 6. |
Ciftci TU, Kokturk O, Bukan N, Bilgihan A. The relationship between serum cytokine levels with obesity and obstructive sleep apnea syndrome. Cytokine 2004; 28: 87-91.
DOI PMID |
| 7. |
Mehra R, Benjamin EJ, Shahar E, et al. Association of nocturnal arrhythmias with sleep-disordered breathing: the sleep heart health study. Am J Respir Crit Care Med 2006; 173: 910-6.
DOI URL |
| 8. |
Wang ZH, Zhu D, Xie S, et al. Inhibition of rho-kinase attenuates left ventricular remodeling caused by chronic intermittent hypoxia in rats via suppressing myocardial inflammation and apoptosis. J Cardiovasc Pharmacol 2017; 70: 102-9.
DOI URL |
| 9. | Badran M, Abuyassin B. Uncoupling of vascular nitric oxide synthase caused by intermittent hypoxia. Oxid Med Cell Longev 2016; 2016: 2354870. |
| 10. |
Takahashi N, Yoshida H, Kimura H, et al. Chronic hypoxia exacerbates diabetic glomerulosclerosis through mesangiolysis and podocyte injury in db/db mice. Nephrol Dial Transplant 2020; 35: 1678-88.
DOI URL |
| 11. |
Zhang JH, Yang HZ, Su H, et al. Berberine and Ginsenoside Rb1 ameliorate depression-like behavior in diabetic rats. Am J Chin Med 2021; 49: 1195-213.
DOI URL |
| 12. |
Wang M, Zhang Z. Interventional clinical trials on diabetic peripheral neuropathy: aretrospective analysis. J Pain Res 2021; 14: 2651-64.
DOI URL |
| 13. |
Luong Huynh D, Nguyen NH, Nguyen CT. Pharmacological properties of ginsenosides in inflammation-derived cancers. Mol Cell Biochem 2021; 476: 3329-40.
DOI |
| 14. | Hashimoto R, Yu J, Koizumi H, Ouchi Y, Okabe T. Ginsenoside Rb1 prevents MPP(+)-induced apoptosis in PC12 cells by stimulating estrogen receptors with consequent activation of ERK1/2, Akt and inhibition of SAPK/JNK, p38 MAPK. Evid Based Complement Alternat Med 2012; 2012: 693717. |
| 15. |
Wang J, Qiao L, Li S, Yang G. Protective effect of ginsenoside Rb1 against lung injury induced by intestinal ischemia-reperfusion in rats. Molecules 2013; 18: 1214-26.
DOI PMID |
| 16. |
Huang XP, Qiu YY, Wang B, et al. Effects of Astragaloside Ⅳ combined with the active components of Panax notoginseng on oxidative stress injury and nuclear factor-erythroid 2-related factor 2/heme oxygenase-1 signaling pathway after cerebral ischemia-reperfusion in mice. Pharmacogn Mag 2014; 10: 402-9.
DOI URL |
| 17. |
Cheng Y, Shen LH, Zhang JT. Anti-amnestic and anti-aging effects of ginsenoside Rg1 and Rb1 and its mechanism of action. Acta Pharmacol Sin 2005; 26: 143-9.
DOI PMID |
| 18. |
Mo C, Wang L, Zhang J, et al. The crosstalk between Nrf2 and AMPK signal pathways is important for the anti-inflammatory effect of berberine in LPS-stimulated macrophages and endotoxin-shocked mice. Antioxid Redox Signal 2014; 20: 574-88.
DOI URL |
| 19. |
Liu XM, Peyton KJ, Shebib AR, Wang H, Korthuis RJ, Durante W. Activation of AMPK stimulates heme oxygenase-1 gene expression and human endothelial cell survival. Am J Physiol Heart Circ Physiol 2011; 300: H84-93.
DOI URL |
| 20. |
Kong HL, Wang JP, Li ZQ, Zhao SM, Dong J, Zhang WW. Anti-hypoxic effect of ginsenoside Rbl on neonatal rat cardiomyocytes is mediated through the specific activation of glucose transporter-4 ex vivo. Acta Pharmacol Sin 2009; 30: 396-403.
DOI |
| 21. |
Zhao Y, Yang S, Guo Q, Guo Y, Zheng Y, Ji E. Shashen-Maidong decoction improved chronic intermittent hypoxia-induced cognitive impairment through regulating glutamatergic signaling pathway. J Ethnopharmacol 2021; 274: 114040.
DOI URL |
| 22. |
Sun ZM, Guan P, Luo LF, et al. Resveratrol protects against CIH-induced myocardial injury by targeting Nrf2 and blocking NLRP 3 inflammasome activation. Life Sci 2020; 245: 117362.
DOI URL |
| 23. |
Xie Z, Loi Truong T, Zhang P, Xu F, Xu X, Li P. Danqi prescription ameliorates insulin resistance through overall corrective regulation of glucose and fat metabolism. J Ethnopharmacol 2015; 172: 70-9.
DOI URL |
| 24. | Yang R, Jiang X, He X, Liang D, Sun S, Zhou G. Ginsenoside Rb1 improves cognitive impairment induced by insulin resistance through Cdk5/p35-NMDAR-IDE pathway. Biomed Res Int 2020; 3905719. |
| 25. | Burke SJ, Batdorf HM, Burk DH, et al. db/db Mice exhibit features of human type 2 diabetes that are not present in weight-matched C57BL/6J mice fed a western diet. J Diabetes Res 2017; 2017: 8503754. |
| 26. |
Chen C, You LJ, Huang Q, et al. Modulation of gut microbiota by mulberry fruit polysaccharide treatment of obese diabetic db/db mice. Food Funct 2018; 9: 3732-42.
DOI PMID |
| 27. |
Zhou S, Yin X, Jin J, et al. Intermittent hypoxia-induced cardiomyopathy and its prevention by Nrf2 and metallothionein. Free Radic Biol Med 2017; 112: 224-39.
DOI URL |
| 28. |
Fang ZY, Prins JB, Marwick TH. Diabetic cardiomyopathy: evidence, mechanisms, and therapeutic implications. Endocr Rev 2004; 25: 543-67.
DOI PMID |
| 29. |
Bugger H, Abel ED. Molecular mechanisms of diabetic cardiomyopathy. Diabetologia 2014; 57: 660-71.
DOI PMID |
| 30. |
Jia G, DeMarco VG, Sowers JR. Insulin resistance and hyperinsulinaemia in diabetic cardiomyopathy. Nat Rev Endocrinol 2016; 12: 144-53.
DOI PMID |
| 31. |
Guan P, Sun ZM, Wang N, et al. Resveratrol prevents chronic intermittent hypoxia-induced cardiac hypertrophy by targeting the PI3K/AKT/mTOR pathway. Life Sci 2019; 233: 116748.
DOI URL |
| 32. |
Jia G, Whaley-Connell A, Sowers JR. Diabetic cardiomyopathy: a hyperglycaemia- and insulin-resistance-induced heart disease. Diabetologia 2018; 61: 21-8.
DOI PMID |
| 33. |
Wu P, Chen J, Chen J, et al. Trimethylamine N-oxide promotes apoE(-/-) mice atherosclerosis by inducing vascular endothelial cell pyroptosis via the SDHB/ROS pathway. J Cell Physiol 2020; 235: 6582-91.
DOI URL |
| 34. |
Weihong C, Bin C, Jianfeng Y. Transmembrane protein 126B protects against high fat diet (HFD)-induced renal injury by suppressing dyslipidemia via inhibition of ROS. Biochem Biophys Res Commun 2019; 509: 40-7.
DOI URL |
| 35. |
Wu Y, Xia ZY, Dou J, et al. Protective effect of ginsenoside Rb1 against myocardial ischemia/reperfusion injury in streptozotocin-induced diabetic rats. Mol Biol Rep 2011; 38: 4327-35.
DOI PMID |
| 36. |
Kosuru R, Kandula V, Rai U, Prakash S, Xia Z, Singh S. Pterostilbene decreases cardiac oxidative stress and inflammation via activation of AMPK/Nrf2/HO-1 pathway in fructose-fed diabetic rats. Cardiovasc Drugs Ther 2018; 32: 147-63.
DOI PMID |
| 37. |
Ko JR, Seo DY, Park SH, et al. Aerobic exercise training decreases cereblon and increases AMPK signaling in the skeletal muscle of STZ-induced diabetic rats. Biochem Biophys Res Commun 2018; 501: 448-53.
DOI URL |
| 38. |
Sun X, Song M, Wang H, et al. TRB3 gene silencing activates AMPK in adipose tissue with beneficial metabolic effects in obese and diabetic rats. Biochem Biophys Res Commun 2017; 488: 22-8.
DOI URL |
| 39. |
Shih AY, Johnson DA, Wong G, et al. Coordinate regulation of glutathione biosynthesis and release by Nrf2-expressing glia potently protects neurons from oxidative stress. J Neurosci 2003; 23: 3394-406.
PMID |
| 40. | Tkachev VO, Menshchikova EB, Zenkov NK. Mechanism of the Nrf2/Keap1/ARE signaling system. Biochemistry (Mosc) 2011; 76: 407-22. |
| 41. | Cosso L, Maineri EP, Traverso N, et al. Induction of heme oxygenase 1 in liver of spontaneously diabetic rats. Free Radic Res 2001; 34: 189-91. |
| 42. |
Kong HL, Li ZQ, Zhao YJ, et al. Ginsenoside Rb1 protects cardiomyocytes against CoCl2-induced apoptosis in neonatal rats by inhibiting mitochondria permeability transition pore opening. Acta Pharmacol Sin 2010; 31: 687-95.
DOI |
| 43. |
Yu HT, Zhen J, Pang B, Gu JN, Wu SS. Ginsenoside Rg1 ameliorates oxidative stress and myocardial apoptosis in streptozotocin-induced diabetic rats. J Zhejiang Univ Sci B 2015; 16: 344-54.
DOI URL |
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