Umbelliferone alleviates hepatic injury in diabetic db/db mice via inhibiting inflammatory response and activating Nrf2-mediated antioxidant

Yin, Jiangning; Wang, Hanqing; Lu, Guoyuan

doi:10.1042/bsr20180444

Cited by 37 publications

(23 citation statements)

References 33 publications

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“…Another study by Yin et al reported that UMB inhibited inflammation in diabetic mice through suppressing NF-κB and TLR-4. In addition, UMB mitigated hepatic oxidative injury via activating the Nrf2mediated signal pathway [180]. Li et al reported that UMB significantly attenuated ROS accumulation and cytotoxicity induced by methylglyoxal (MG) through the activation of Nrf2/ARE signaling [181].…”

Section: Urolithin Amentioning

confidence: 99%

Coumarins as Modulators of the Keap1/Nrf2/ARE Signaling Pathway

Hassanein

Sayed

Hussein

et al. 2020

Oxidative Medicine and Cellular Longevity

164

106

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The Keap1/Nrf2/ARE system is a central defensive mechanism against oxidative stress which plays a key role in the pathogenesis and progression of many diseases. Nrf2 is a redox-sensitive transcription factor controlling a variety of downstream antioxidant and cytodefensive genes. Nrf2 has a powerful anti-inflammatory activity mediated via modulating NF-κB. Therefore, pharmacological activation of Nrf2 is a promising therapeutic strategy for the treatment/prevention of several diseases that are underlined by both oxidative stress and inflammation. Coumarins are natural products with promising pharmacological activities, including antioxidant, anticancer, antimicrobial, and anti-inflammatory efficacies. Coumarins are found in many plants, fungi, and bacteria and have been widely used as complementary and alternative medicines. Some coumarins have shown an ability to activate Nrf2 signaling in different cells and animal models. The present review compiles the research findings of seventeen coumarin derivatives of plant origin (imperatorin, visnagin, urolithin B, urolithin A, scopoletin, esculin, esculetin, umbelliferone, fraxetin, fraxin, daphnetin, anomalin, wedelolactone, glycycoumarin, osthole, hydrangenol, and isoimperatorin) as antioxidant and anti-inflammatory agents, emphasizing the role of Nrf2 activation in their pharmacological activities. Additionally, molecular docking simulations were utilized to investigate the potential binding mode of these coumarins with Keap1 as a strategy to disrupt Keap1/Nrf2 protein-protein interaction and activate Nrf2 signaling.

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Section: Urolithin Amentioning

confidence: 99%

Coumarins as Modulators of the Keap1/Nrf2/ARE Signaling Pathway

Hassanein

Sayed

Hussein

et al. 2020

Oxidative Medicine and Cellular Longevity

164

106

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“…In the present research, it has suggested that NF-κB and anti-oxidant enzymes system are necessary mediators of inflammation and oxidant stress injury [36,37]. In our study, we found that FGF21 improved the brains damage though decreasing the pro-inflammatory factors and increasing antioxidant enzymes which may connected with macrophage [38,39], but the detailed mechanism remains to be further studied.…”

Section: Discussionmentioning

confidence: 48%

FGF21 Attenuates Neurodegeneration though Modulating Neuroinflammation and Oxidant-stress

Kang

Wang

et al. 2020

Preprint

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Background It is reported that FGF21 can repair nerve injury, but the specific mechanism is less studied. The present study was designed to investigate the effects of FGF21 on neurodegeneration and possible mechanisms of the aging and diabetic mice, which were susceptible to Alzheimer's disease (AD). Methods The diabetic mice and aging mice were used to study the effects of FGF21 on neurodegeneration and possible mechanisms. These mice were administrated with PBS, FGF21 or metformin once daily for 4 or 6 months. Then the mechanism was verified in SH-SY5Y cells. The relative gene expressions for neurodegeneration were assessed by Quantitative Real Time-PCR, Western blot and others. Results FGF21 inhibited the loss of nerve cells and intracellular edema around hippocampus in diabetic mice and aging mice. In vivo results revealed that administration of FGF21 led to suppress the aggregation of Tau and β-Amyloid 1-42 , which resulted in apoptosis in nerve cells. Meanwhile, FGF21 significantly reduced the expression of NF-κB, IL6 and IL8 (p<0.05) and enhanced anti-oxidant enzymes (p<0.05) in diabetic mice. In addition, the phosphorylation of AKT and AMPKα was increased by FGF21 treated in diabetic mice, which were considered as anti-inflammation and anti-oxidant stress pathway. The relative gene expressions of neurodegeneration were also demonstrated in aging mice, which showed similar trends with diabetic mice. In vitro experiment showed that the aggregation of Tau and β-Amyloid 1-42 was increased by LPS in SH-SY5Y cells, and FGF21 inhibited the aggregation. Conclusion As shown above, FGF21 attenuated neurodegeneration by reducing neuroinflammation and oxidant stress though regulating the NF-κB pathway and AMPKα/AKT pathway, which enhanced the protective effect on mitochondria in nerve cells. Key words : FGF21, diabetes, neurodegeneration, inflammation, oxidant stress.

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“…Moreover, the renoprotection relys on the activation of Nrf2. Thus we speculate that other Nrf2 activating agents, such as paeonin (Xiao et al, 2018), polydatin (Zeng et al, 2018), salviae (Li et al, 2018b) and umbelliferone (Yin et al, 2018), may be available for renal oxidative damage. There is no doubt that natural product PRO provides a new approach for treatment of nephrotocicity and it is a novel and significant discovery in the process of probing new therapeutic agents to improve survival rate of patients with cisplatin chemotherapy.…”

Section: Discussionmentioning

confidence: 97%

Procyanidin protects HK-2 cells against cisplatin-induced injury through antioxidant action involving Nrf2/HO-1 signaling pathway

Chen

Feng

Jing

et al. 2019

Fundam. Toxicol. Sci.

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-Cisplatin (CP) is used as a chemotherapeutic drug for the treatment of various kinds of cancer. However, it is becoming increasingly difficult to ignore its side effects, especially nephrotoxicity which has to do with oxidative stress and inflammation. Procyanidin (PRO) has been proved to be a powerful antioxidant. Therefore, we investigated whether PRO could prevent Cisplatin-induced nephrotoxicity and explored the underlying mechanism. In cellular experiment, reactive oxygen species (ROS), the malondialdehyde (MDA) levels, the activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-PX) were measured for the assessment of cisplatin-induced oxidative cell damage. CCK-8 reagent and flow cytometry were used to detect the cell viability and apoptosis. Furthermore, the level of oxidative-related protein Nrf2 and HO-1 were carried out by western blot analysis. We found that cisplatin gave rise to the elevated levels of ROS and MDA and the decrease of the activities of T-SOD and GSH-PX with a related lower viability and higher apoptosis in HK-2 cells. Inversely, the pretreatment of PRO mitigated the oxidative damage, promoted the cell viability and lowered the apoptosis, activated nuclear related factor 2 (Nrf2) and elevated the expression of heme oxygenase-1 (HO-1), the above cytoprotection of PRO was blocked by siNrf2 or siHO-1. These results demonstrated that PRO has the potential to prevent cisplatin-induced nephrotoxicity through activation of Nrf2/HO-1 signaling pathway.

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Umbelliferone alleviates hepatic injury in diabetic db/db mice via inhibiting inflammatory response and activating Nrf2-mediated antioxidant

Cited by 37 publications

References 33 publications

Coumarins as Modulators of the Keap1/Nrf2/ARE Signaling Pathway

Coumarins as Modulators of the Keap1/Nrf2/ARE Signaling Pathway

FGF21 Attenuates Neurodegeneration though Modulating Neuroinflammation and Oxidant-stress

Procyanidin protects HK-2 cells against cisplatin-induced injury through antioxidant action involving Nrf2/HO-1 signaling pathway

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