Oleanolic acid protects against diabetic cardiomyopathy via modulation of the nuclear factor erythroid 2 and insulin signaling pathways

Li, Wei‐Fang; Wang, Peng; Li, Hua; Li, Tianyi; Ming, Feng; Chen, Sufang

doi:10.3892/etm.2017.4527

Cited by 13 publications

(7 citation statements)

References 25 publications

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“…The marked activation of Nrf2 by OA could explain, at least in part, the OA hepatoprotection against various toxic stimuli listed in Table . OA activation of Nrf2 also offers the protection in other organs and diseases …”

Section: Mechanisms For Paradoxical Hepatoprotective and Hepatotoxic mentioning

confidence: 99%

“…OA activation of Nrf2 also offers the protection in other organs and diseases. 75 In addition to Nrf2 activation, other mechanisms also offer OAinduced hepatoprotection, such as a decrease in CYP2E1 (eg CCl 4 , 27 acetaminophen 23 ), decrease in Oatp1b2 (eg phalloidin 34 ), modulation of the immune response and inflammation (eg d-Gal/LPS 28 ). These mechanisms play an integrated role in programming the liver against toxic stimuli.…”

Section: Nrf2/are Pathway In Oa Hepatoprotection and Hepatotoxicitymentioning

confidence: 99%

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Oleanolic acid reprograms the liver to protect against hepatotoxicants, but is hepatotoxic at high doses

Liu

Lü

et al. 2018

Liver International

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Oleanolic acid (OA) is a triterpenoid that exists widely in fruits, vegetables and medicinal herbs. OA is included in some dietary supplements and is used as a complementary and alternative medicine (CAM) in China, India, Asia, the USA and European countries. OA is effective in protecting against various hepatotoxicants, and one of the protective mechanisms is reprogramming the liver to activate the nuclear factor erythroid 2-related factor 2 (Nrf2). OA derivatives, such as CDDO-Im and CDDO-Me, are even more potent Nrf2 activators. OA has recently been shown to also activate the Takeda G-protein-coupled receptor (TGR5). However, whereas a low dose of OA is hepatoprotective, higher doses and long-term use of OA can produce liver injury, characterized by cholestasis. This paradoxical hepatotoxic effect occurs not only for OA, but also for other OA-type triterpenoids. Dose and length of time of OA exposure differentiate the ability of OA to produce hepatoprotection vs hepatotoxicity. Hepatotoxicity produced by herbs is increasingly recognized and is of global concern. Given the appealing nature of OA in dietary supplements and its use as an alternative medicine around the world, as well as the development of OA derivatives (CDDO-Im and CDDO-Me) as therapeutics, it is important to understand not only that they program the liver to protect against hepatotoxic chemicals, but also how they produce hepatotoxicity.

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Section: Mechanisms For Paradoxical Hepatoprotective and Hepatotoxic mentioning

confidence: 99%

Section: Nrf2/are Pathway In Oa Hepatoprotection and Hepatotoxicitymentioning

confidence: 99%

Oleanolic acid reprograms the liver to protect against hepatotoxicants, but is hepatotoxic at high doses

Liu

Lü

et al. 2018

Liver International

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“…In 2014, an estimated 387 million individuals worldwide were diagnosed with DM and the prevalence is expected to rise to 592 million by 2035 (1). In addition, patients with DM have a high mortality rate that is often caused by diabetic cardiomyopathy (DCM) (2,3).…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA ameliorates diabetic cardiomyopathy by inhibiting Grp78 and CHOP expression in STZ‑induced diabetes rats

et al. 2019

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Diabetic cardiomyopathy (DCM), one of the common diabetic complications, causes a high rate of mortality in patients with diabetes. Tanshinone IIA (TSIIA), one of the components of Salvia miltiorrhiza (Danshen), has anti-oxidative stress activity and is widely used to treat diabetes-associated diseases. However, its efficacy on DCM remains unclear. The present study aimed to investigate the potential therapeutic function of TSIIA on DCM in an experimental diabetic rat model. Streptozotocin (STZ)-induced diabetic rats were intraperitoneally injected with TSIIA for 6 weeks. The present results indicated that blood glucose concentration was slightly reduced in the low-dose TSIIA treatment group. TSIIA injection was also noted to improve cardiac function, and restore loss of mitochondrial cristae, swollen mitochondrial matrix and disorganized myofibrils in myocardial cells, which are thought to be characteristics of apoptosis. Furthermore, TSIIA injection could increase the activity of superoxide dismutase in STZ-induced diabetic rats, and suppress the endoplasmic reticulum (ER) stress signaling pathway via reducing the expression of glucose-regulated protein 78 and C/EBP homologous protein. These results provide evidence that TSIIA may ameliorate DCM in diabetic rats, possibly via suppressing oxidative stress and ER stress activation.

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“…Perilla fruit is rich in alpha-linolenic acid which exerts an endothelial protective effect against high glucose injury via PI3K/Akt pathway [ 13 ]. Previous pharmacological experiments showed that oleanolic acid, an important ingredient in glossy privet fruit, has hypoglycemic effects [ 14 , 15 ]. In clinical practices, Modified Sanzi Yangqin Decoction worked quite well for treating diabetic patients (Supplementary Table 1 ).…”

Section: Introductionmentioning

confidence: 99%

Effects of Modified Sanzi Yangqin Decoction on Tyrosine Phosphorylation of IRS-1 in Skeletal Muscle of Type 2 Diabetic Rats

Wang

Tian

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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This study aimed to investigate the effect of Modified Sanzi Yangqin Decoction on tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) in skeletal muscle of type 2 diabetic rats. The rat model of type 2 diabetes was induced by high-fat diet and multiple low-dose streptozotocin injections. Diabetic model rats were randomly divided into 5 groups: the model control group, the metformin group, and Modified Sanzi Yangqin Decoction groups of low, medium, and high doses. OGTT was conducted every two weeks during treatment period. At the end of the treatment, the fasting blood glucose (FBG) level and the fasting C-peptide level were measured to calculate insulin resistance index. The levels of IRS-1, p-IRS-1(Tyr895), and protein tyrosine phosphates 1B (PTP1B) in skeletal muscle were also measured. Modified Sanzi Yangqin Decoction significantly reduced the FBG level, increased the fasting C-peptide level, and lowered the insulin resistance index in type 2 diabetic rats. It also significantly increased the protein level of p-IRS-1(Tyr895) and reduced the PTP1B protein level in skeletal muscle of type 2 diabetic rats. Modified Sanzi Yangqin Decoction increases tyrosine phosphorylation of IRS-1 in skeletal muscle of type 2 diabetic rats, which results from the increase of p-IRS-1(Tyr895) protein and is related to the suppression of PTP1B protein.

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Oleanolic acid protects against diabetic cardiomyopathy via modulation of the nuclear factor erythroid 2 and insulin signaling pathways

Cited by 13 publications

References 25 publications

Oleanolic acid reprograms the liver to protect against hepatotoxicants, but is hepatotoxic at high doses

Oleanolic acid reprograms the liver to protect against hepatotoxicants, but is hepatotoxic at high doses

Tanshinone IIA ameliorates diabetic cardiomyopathy by inhibiting Grp78 and CHOP expression in STZ‑induced diabetes rats

Effects of Modified Sanzi Yangqin Decoction on Tyrosine Phosphorylation of IRS-1 in Skeletal Muscle of Type 2 Diabetic Rats

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