Curcumin analogue C66 attenuates obesity-induced myocardial injury by inhibiting JNK-mediated inflammation

Ye, Lin; Chen, Xiaojun; Jin, Leiming; Zhuang, Zaishou; Yang, Daona; Guan, Xiaofei; Самородов, Александр В.; Павлов, В. Н.; Chattipakorn, Nipon; Feng, Jiaxuan; Wang, Yi; Luo, Wei; Liang, Guang

doi:10.1016/j.biopha.2021.112121

Cited by 19 publications

(16 citation statements)

References 38 publications

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“…Diabetic cardiomyopathy is associated with a variety of signaling pathways, such as AMPK, Nrf2-ARE signaling pathway, Wnt/β-catenin signaling pathway, NF-κB signaling pathway, TGF-β1/Smads signaling pathway, PKC signaling pathway and PI3K/AKT signaling pathway [ 30 ]. It has been reported that curcumin derivative C66, an inhibitor of JNK phosphorylation, can reduce the high-glucose-activated JNK/NF-κB pathway in diabetic cardiomyopathy mice, thereby reducing the inflammatory response and apoptosis process and delaying the process of diabetic cardiomyopathy [ 31 ]. In the stage of diabetic cardiomyopathy, a variety of mechanisms and signaling pathways will promote pathological changes in cardiomyocytes, ultimately leading to arrhythmia and heart failure [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Novel dual glucagon-like peptide-1/ glucose-dependent insulinotropic polypeptide receptor agonist attenuates diabetes and myocardial injury through inhibiting hyperglycemia, inflammation and oxidative stress in rodent animals

Wang

Cai

et al. 2022

Bioengineered

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This study was aimed to evaluate the therapeutic effects and potent mechanisms of a novel GLP-1/GIP dual agonist on hyperglycemia and myocardial injury in diabetic mice. Novel dual-receptor agonists were designed and then evaluated via in vitro receptor activation assays. Acute hypoglycemic effects were assessed in diabetic mice induced by intraperitoneal injection of streptozotocin. Chronic effects of dual-receptor agonists on diabetes as well as diabetic cardiomyopathy were investigated in DCM model mice. Effects of the in vitro coculture of dual-receptor agonists with or without signaling pathway inhibitors on the cell viability and apoptosis of primary cardiomyocytes under a high-glucose state were assessed via MTT and western blotting methods to investigate the probable mechanism. AP5 exhibited balanced activities of dual-receptor activation in vitro and improved hypoglycemic ability in diabetic mice. Moreover, chronic treatment of AP5 achieved the prominently improved efficacy in reversing the deteriorative diabetic disorders and reducing the myocardial injury markers in DCM mice. Moreover, AP5 also inhibited the apoptosis and improved the survival rate of primary cardiomyocytes under a high-glucose state via increasing the expression levels of antiapoptotic proteins and inhibiting the release of apoptotic proteins, respectively, as well as activating the AMPK/PI3K/Akt signaling pathway. In conclusion, the dual GLP-1/GIP receptor agonist, AP5, can effectively improve diabetic symptoms and exert therapeutic effects on DCM via activating the AMPK/PI3K/Akt pathway, reducing the ROS production, oxidative stress and inflammatory markers in the rodent DCM model. Abbreviation: Diabetes mellitus, DM; diabetic cardiomyopathy, DCM; streptozotocin, STZ; glucagon-like peptide-1, GLP-1; malondialdehyde, MDA; glucose-dependent insulinotropic polypeptide, GIP; creatine kinase, CK; diabetic cardiomyopathy, DCM; serum superoxide dismutase; SOD; total superoxide disumutase, T-SOD; Methyl Thiazolyl Tetrazolium, MTT; lactate dehydrogenase; LDH; Adenosine Monophosphate-Activated Protein Kinase, AMPK; Dulbecco’s modified Eagle medium, DMEM; Fetal Bovine Serum, FBS; Reactive Oxygen Species, ROS; Glyceraldehyde-phosphate dehydrogenase, GAPDH; Surface Plasmon Resonance, SPR; Ethylene Diamine Tetraacetic Acid, EDTA; Interleukin-1β, IL-1β; Phosphoinositol 3-kinase, PI3K; Tumor necrosis factor, TNF-α; Renin-angiotensin-aldosterone system, RAAS; Glucose transporter, GLUT; Dipeptidyl peptidase-IV, DPP-IV; oxygen free radicals, OFR;

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Section: Discussionmentioning

confidence: 99%

Novel dual glucagon-like peptide-1/ glucose-dependent insulinotropic polypeptide receptor agonist attenuates diabetes and myocardial injury through inhibiting hyperglycemia, inflammation and oxidative stress in rodent animals

Wang

Cai

et al. 2022

Bioengineered

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“…MAPKs can be activated by pro‐inflammatory cytokines to regulate the inflammation response and mediate cardiac hypertrophy and fibrosis, which play a crucial function in driving the progression of HF (Imam et al, 2016; Korashy et al, 2015). MAPKs activation leads to inflammatory gene expression and subsequent cardiac fibrosis and hypertrophy (Liu et al, 2020; Ye et al, 2021). It is widely reported that the MAPK pathway could regulate multiple pathological processes, including inflammation, apoptosis, and proliferation (Palomer et al, 2020; Zhuang et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Sclareol attenuates angiotensin II‐induced cardiac remodeling and inflammation via inhibiting MAPK signaling

Yang

Zou

Luo

et al. 2022

Phytotherapy Research

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Chronic inflammation plays an important role in hypertensive heart failure. Suppressing angiotensin II (Ang II)‐induced cardiac inflammation may contribute to the treatment of hypertension‐associated heart failure. Sclareol, a natural product initially isolated from the leaves and flowers of Salvia sclarea, possesses antiinflammatory and immune‐regulation activity in various systems. However, its effect on Ang II‐induced cardiac remodeling remains unknown. In this study, we have explored the potential effects of sclareol on Ang II‐induced heart failure. In vivo experiments were conducted in mice with Ang II‐pump infusion for 28 days. Sclareol administration at 5 mg·kg−1·d−1 significantly reduced the expression of myocardial injury markers. Sclareol also exerts protective effects against Ang II‐induced cardiac dysfunction in mice which is associated with alleviated cardiac inflammation and fibrosis. Transcriptome analysis revealed that inhibition of the Ang II‐activated mitogen‐activated protein kinase (MAPK) pathway contributed to the protective effect of sclareol. Sclareol inhibits Ang II‐activated MAPKs pathway to reduce inflammatory response in mouse hearts and cultured cardiomyocytes. Blockage of MAPKs in cardiomyocytes abolished the antiinflammatory effects of sclareol. In conclusion, we show that sclareol protects hearts against Ang II‐induced injuries through inhibiting MAPK‐mediated inflammation, indicating the potential use of sclareol in the prevention of hypertensive heart failure.

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“…The curcumin analog C66 can reduce serum and heart hypertriglyceridemia, improve cardiac function, and interfere with cardiac inflammation and JNK signaling. C66 also inhibits high glucose‐induced generation of pro‐inflammatory cytokines by inactivating NF‐κB (Ye et al, 2021)and this was confirmed in a separate study in primary peritoneal macrophages (Camacho‐Barquero et al, 2007; Pan et al, 2012). Moreover, in a diabetic mouse model, curcumin derivative C66 counteracts high glucose‐induced cardiac lesions by interfering with JNK signaling.…”

Section: Curcumin Analogs and Their Effect On Diabetesmentioning

confidence: 80%

An update on molecular mechanisms of curcumin effect on diabetes

Shahidi

Khorsandi

et al. 2022

Journal of Food Biochemistry

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Owing to its prevalent nature, diabetes mellitus has become one of the most serious endocrine illnesses affecting a patient's quality of life due to the manifestation of side effects such as cardiovascular diseases, retinopathy, neuropathy, and nephropathy. Curcumin ((1E, 6E) 21, 7‐bis (4‐hydroxy‐3‐methoxyphenyl)‐1,6‐heptadiene‐3,5‐dione), a major compound of turmeric, has been used in conventional medicine because of its safe nature and cost‐effectiveness to meliorate diabetes and its comorbidities. These effects have also been observed in rodent models of diabetes resulting in a reduction of glycemia and blood lipids. Both the preventive and therapeutic activities of this compound are due to its antioxidant and anti‐inflammatory characteristics. Furthermore, preclinical outcomes and clinical investigation demonstrate that the use of curcumin neutralizes insulin resistance, obesity, and hyperglycemia. Despite the many benefits of curcumin, its two limiting factors, solubility and bioavailability, remain a challenge for researchers; therefore, several methods such as drug formulation, nano‐drug delivery, and the use of curcumin analogs have been developed to deliver curcumin and increase its bioavailability. Practical applications The rise of people with type 2 diabetes has become a major concern at the global healthcare level. The best diabetes treatments today are anti‐diabetic drug administration, lifestyle‐related interventions (such as healthy eating and daily physical activity), arterial pressure detection, and fat control. The polyphenol curcumin, found in turmeric, can promote health by acting on a variety of cellular signaling pathways. This review article discusses curcumin and its role in the treatment of diabetes.

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Curcumin analogue C66 attenuates obesity-induced myocardial injury by inhibiting JNK-mediated inflammation

Cited by 19 publications

References 38 publications

Novel dual glucagon-like peptide-1/ glucose-dependent insulinotropic polypeptide receptor agonist attenuates diabetes and myocardial injury through inhibiting hyperglycemia, inflammation and oxidative stress in rodent animals

Novel dual glucagon-like peptide-1/ glucose-dependent insulinotropic polypeptide receptor agonist attenuates diabetes and myocardial injury through inhibiting hyperglycemia, inflammation and oxidative stress in rodent animals

Sclareol attenuates angiotensin II‐induced cardiac remodeling and inflammation via inhibiting MAPK signaling

An update on molecular mechanisms of curcumin effect on diabetes

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