Methylglyoxal-derived hydroimidazolone-1 evokes inflammatory reactions in endothelial cells via an interaction with receptor for advanced glycation end products

Ishibashi, Yuji; Matsui, Takanori; Nakamura, Nobutaka; Sotokawauchi, Ami; Higashimoto, Yuichiro; Yamagishi, Sho‐ichi

doi:10.1177/1479164117715855

Cited by 24 publications

(19 citation statements)

References 15 publications

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“…This injury was attenuated by pretreatment with 25 μM NGR1, as indicated by a decrease in LDH release. The mechanism that causes cardiac injury by AGEs is reported to be associated with detrimental endoplasmic reticulum stress, inflammation, oxidative stress and mitochondrial damage ( Yang et al, 2015 ; Zhao et al, 2016 ; Ishibashi et al, 2017 ). Consistent with previous literature, in our study, AGEs were found to strongly inhibit H9c2 cell viability accompanied by aggressive ROS and massive apoptosis both in vitro (Figures 2 , 3 ), and in vivo (Figure 7 ).…”

Section: Discussionmentioning

confidence: 99%

Notoginsenoside R1 Protects Against Diabetic Cardiomyopathy Through Activating Estrogen Receptor α and Its Downstream Signaling

Zhang

et al. 2018

Front. Pharmacol.

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Diabetic cardiomyopathy (DCM) leads to heart failure and death in diabetic patients, no effective treatment is available. Notoginsenoside R1 (NGR1) is a novel saponin that is derived from Panax notoginseng and our previous studies have showed cardioprotective and neuroprotective effects of NGR1. However, its role in protecting against DCM remains unexplored. Herein, we examine potential effects of NGR1 on cardiac function of diabetic db/db mice and H9c2 cardiomyocytes treated by advanced glycation end products (AGEs). In vitro experiments revealed that pretreatment with NGR1 significantly decreased AGEs-induced mitochondria injury, limited an increase in ROS, and reduced apoptosis in H9c2 cells. NGR1 eliminated ROS by promoting estrogen receptor α expression, which subsequently activated Akt and Nrf2-mediated anti-oxidant enzymes. In vivo investigation demonstrated that NGR1 significantly reduced serum lipid levels, insulin resistance, the expression of enzymes related to cardiomyopathy, and the expression of apoptotic proteins. Finally, NGR1 improved cardiac dysfunction and attenuated histological abnormalities, as evidenced by elevating ejection fraction and fractional shortening, and reducing cardiac fibrosis. Mechanistically, NGR1 promoted ERα expression, which led to the activation of Akt-Nrf2 signaling and the inhibition of the TGFβ pathway. Collectively, these results strongly indicate that NGR1 exerts cardioprotective effects against DCM through its inhibition of oxidative stress and apoptosis, and eventually suppresses cardiac fibrosis and hypertrophy, which suggests that NGR1 is a potential therapeutic medicine for the treatment of DCM.

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Section: Discussionmentioning

confidence: 99%

Notoginsenoside R1 Protects Against Diabetic Cardiomyopathy Through Activating Estrogen Receptor α and Its Downstream Signaling

Zhang

et al. 2018

Front. Pharmacol.

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“…Numerous studies revealed that the plasma MGO level is significantly increased in diabetic patients and is involved in diabetes-related vascular disorders such as hypertension, nephropathy, and retinopathy [ 28 – 31 ]. Recently, it indicated that MGO-derived hydroimidazolone-1 evokes inflammatory reactions in human umbilical vein endothelial cells via RAGE [ 32 ]. In our study, we showed an increased MGO level in RA patients and these levels were markedly increased in patients with high activity disease.…”

Section: Discussionmentioning

confidence: 99%

Methylglyoxal: A Relevant Marker of Disease Activity in Patients with Rheumatoid Arthritis

Knani

Bouzidi²,

Zrour

et al. 2018

Disease Markers

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Background The contribution of methylglyoxal (MGO) and soluble receptor for advanced glycation end products (sRAGE) in the presence of rheumatoid arthritis (RA) is still unknown. We investigated whether serum MGO and sRAGE were related to the presence of disease activity in RA. Methods 80 patients with RA and 30 control subjects were included in a cross-sectional study. The severity of RA was assessed using the disease activity score for 28 joints (DAS28). Serum MGO and sRAGE were measured by ELISA. Results Serum MGO levels were significantly higher in patients with RA versus control subjects (P < 0.001) and were increased in RA patients with higher disease activity versus RA patients with moderate disease activity (P = 0.019). Serum sRAGE concentrations were significantly decreased in RA patients with higher disease activity versus RA patients with moderate disease activity and versus control subjects (P = 0.004; P = 0.002, resp.). A multiple logistic regression analysis demonstrated that MGO was independently associated with the presence of activity disease in RA (OR = 1.17, 95% CI: 1.02–1.31, P = 0.01). Conclusion Serum MGO and sRAGE levels are inversely related to the activity of RA, and MGO is independently associated with a higher disease activity of RA.

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“…This condition frequently leads to increased intracellular levels of MG-derived AGEs, a state known as “glycative stress” [ 1 ]. In turn, glycative stress can lead to increased formation of reactive oxygen species (ROS) [ 2 ], activation of inflammatory pathways through the receptor for AGEs (RAGE) [ 3 ], activation of the mitochondrial pathway of apoptosis [ 4 , 5 ], and induction of epithelial-to mesenchymal transition [ 6 ]. Given that all these biological responses underpin the genesis of several human diseases, MG and MG-derived MG-H1, as well as Glo1, have been proved to play a crucial role in the etiogenesis of many diseases, including cancer [ 7 , 8 , 9 ], infertility [ 5 , 10 ], osteoporosis [ 2 , 11 ], obesity and diabetes [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Methylglyoxal-Dependent Glycative Stress Is Prevented by the Natural Antioxidant Oleuropein in Human Dental Pulp Stem Cells through Nrf2/Glo1 Pathway

et al. 2021

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Methylglyoxal (MG) is a potent precursor of glycative stress (abnormal accumulation of advanced glycation end products, AGEs), a relevant condition underpinning the etiology of several diseases, including those of the oral cave. At present, synthetic agents able to trap MG are known; however, they have never been approved for clinical use because of their severe side effects. Hence, the search of bioactive natural scavengers remains a sector of strong research interest. Here, we investigated whether and how oleuropein (OP), the major bioactive component of olive leaf, was able to prevent MG-dependent glycative stress in human dental pulp stem cells (DPSCs). The cells were exposed to OP at 50 µM for 24 h prior to the administration of MG at 300 µM for additional 24 h. We found that OP prevented MG-induced glycative stress and DPSCs impairment by restoring the activity of Glyoxalase 1 (Glo1), the major detoxifying enzyme of MG, in a mechanism involving the redox-sensitive transcription factor Nrf2. Our results suggest that OP holds great promise for the development of preventive strategies for MG-derived AGEs-associated oral diseases and open new paths in research concerning additional studies on the protective potential of this secoiridoid.

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Methylglyoxal-derived hydroimidazolone-1 evokes inflammatory reactions in endothelial cells via an interaction with receptor for advanced glycation end products

Cited by 24 publications

References 15 publications

Notoginsenoside R1 Protects Against Diabetic Cardiomyopathy Through Activating Estrogen Receptor α and Its Downstream Signaling

Notoginsenoside R1 Protects Against Diabetic Cardiomyopathy Through Activating Estrogen Receptor α and Its Downstream Signaling

Methylglyoxal: A Relevant Marker of Disease Activity in Patients with Rheumatoid Arthritis

Methylglyoxal-Dependent Glycative Stress Is Prevented by the Natural Antioxidant Oleuropein in Human Dental Pulp Stem Cells through Nrf2/Glo1 Pathway

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