Piceatannol alleviates inflammation and oxidative stress via modulation of the Nrf2/HO-1 and NF-κB pathways in diabetic cardiomyopathy

Li, Hao; Shi, Youyang; Wang, Xuliang; Li, Ping; Zhang, Songyue; Wu, Tingting; Yan, Yizhen; Zhan, Yi; Ren, Yue; Rong, Xing; Xia, Tianhe; Chu, Maoping; Wu, Rongzhou

doi:10.1016/j.cbi.2019.108754

Cited by 75 publications

(66 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the present study, significant upregulation of WBC counts implicated the immunopotentiation of C. nasus in response to salinity stress. Research studies of Nrf2 on mice and human beings indicated that Nrf2 also played a vital role in protection against inflammation [49][50][51]. Likewise, in this study, the C. nasus Nrf2-mediated antioxidant pathway was activated and further stimulated the upregulation of immune enzymes and molecules, indicating the regulatory role that Nrf2 plays in immunopotentiation in response to salinity stress (Figure 7).…”

Section: Antioxidant Regulation and Immunopotentiation Of C Nasus Nrsupporting

confidence: 60%

Nrf2 is involved in osmoregulation, antioxidation and immunopotentiation inCoilia nasusunder salinity stress

Wang

Zhu

2019

Biotechnology & Biotechnological Equipment

View full text Add to dashboard Cite

Coilia nasus is a rare anadromous fish species found in China's Yangtze River and is a precious commercial commodity. The anti-stress mechanism of C. nasus has become the focus of research due to the animal's strong stress responses. Salinity has been reported to weaken the C. nasus stress response. Nrf2 is an important anti-stress transcription factor that plays key regulatory roles in mediating salinity stress. In the present study, we cloned the full-length sequence of C. nasus Nrf2 for the first time and evaluated its differential expression in tissues. We also investigated the regulatory role of Nrf2 in osmoregulation, antioxidation and immunopotentiation in C. nasus under salinity stress. The results indicate that the C. nasus Nrf2 sequence is highly conserved. C. nasus Nrf2 is activated and plays a coordinated osmoregulatory role together with AQP1 under salinity stress and stimulates the activity of downstream antioxidant enzymes, including superoxide dismutase, glutathione peroxidase and so on. Nrf2 also triggers immunopotentiation via stimulation of lysozyme activity and an elevation of white blood cell counts. All of these C. nasus constructed adaptive Nrf2 regulatory networks act in response to salinity stress. This study lays a theoretical foundation for further research on the anti-stress mechanisms of C. nasus and will provide a reference for the further optimization of the C. nasus breeding mode.

show abstract

Section: Antioxidant Regulation and Immunopotentiation Of C Nasus Nrsupporting

confidence: 60%

Nrf2 is involved in osmoregulation, antioxidation and immunopotentiation inCoilia nasusunder salinity stress

Wang

Zhu

2019

Biotechnology & Biotechnological Equipment

View full text Add to dashboard Cite

show abstract

“…Importantly, in diabetic cardiomyopathy, piceatannol alleviates inflammation and oxidative stress by regulating the Nrf2/HO-1 and NF-kB pathways. Knockdown of Nrf2 suppressed PIC-induced enhancement of HO-1 expression and abolished the anti-inflammatory effects of PIC [ 15 ]. Moreover, piceatannol attenuates homocysteine-induced apoptosis, oxidative stress, and endoplasmic reticulum stress via Nrf2-dependent HO-1 expression in endothelial cells [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Piceatannol inhibits pyroptosis and suppresses oxLDL-induced lipid storage in macrophages by regulating miR-200a/Nrf2/GSDMD axis

Zhang

Peng

2020

Bioscience Reports

View full text Add to dashboard Cite

As a major bioactive compound from grapes, piceatannol has been reported to exert anti-atherosclerotic activity in various studies. Nevertheless, the mechanism underlying the effect of piceatannol against atherosclerosis is elusive. Our study identified miR-200a/Nrf2/GSDMD signaling pathway as critical mediators in the effect of piceatannol on macrophages. In this study, we confirmed that treatment of piceatannol repressed the oxLDL-induced lipid storage in macrophages. Compared to control group, piceatannol inhibited TG storage and the activity of caspase1. It is noting that in response to oxLDL challenge, piceatannol abated the pyroptosis in RAW264.7 cells, with a decreased expression of caspase1, GSDMD, IL-18, IL-1b and NLRP3. Moreover, we investigated the role of miR-200a/Nrf2 signaling pathway in the effect of piceatannol. The results declared that after transfection of si-miR-200a or si-Nrf2 plasmids, the effects of piceatannol on macrophages were converted, including lipid storage and pyroptosis. Importantly, si-miR-200a plasmid reduced the expression of Nrf2, indicating that miR-200a acted as an enhancer of Nrf2 in macrophages. Collectively, our findings demonstrate that piceatannol exerts anti-atherosclerotic activity on RAW264.7 cells by regulating miR-200a/Nrf2/GSDMD signaling. This study is the first time to identify miR-200a as a candidate target in atherosclerosis and declared an association between miR-200a and pyroptosis, which provides a novel therapy for the treatment of atherosclerosis.

show abstract

“…Nrf-2 has been considered as an effective regulator of antioxidative genes expression, for example, HO-1 and NQO-1, and in modulating ROS-eliminating enzymes 34 . Many natural compounds with antioxidative properties, such as honokiol 35 , notoginsenoside 36 , and piceatannol 37 , could facilitate the treatment of diabetic complications by activating Nrf-2-mediated signaling pathway. Recently, Yerra et al 16 demonstrated that promoting Nrf-2mediated antioxidative response could mediate the protective effects of ISL on diabetic neuropathy.…”

Section: Discussionmentioning

confidence: 99%

Isoliquiritigenin prevents hyperglycemia-induced renal injuries by inhibiting inflammation and oxidative stress via SIRT1-dependent mechanism

Huang

Shi²,

Chen

et al. 2020

Cell Death Dis

View full text Add to dashboard Cite

Diabetic nephropathy (DN) as a global health concern is closely related to inflammation and oxidation. Isoliquiritigenin (ISL), a natural flavonoid compound, has been demonstrated to inhibit inflammation in macrophages. Herein, we investigated the effect of ISL in protecting against the injury in STZ-induced type 1 DN and in high glucose-induced NRK-52E cells. In this study, it was revealed that the administration of ISL not only ameliorated renal fibrosis and apoptosis, but also induced the deterioration of renal function in diabetic mice. Mediated by MAPKs and Nrf-2 signaling pathways, respectively, upstream inflammatory response and oxidative stress were neutralized by ISL in vitro and in vivo. Moreover, as further revealed by the results of molecular docking, sirtuin 1 (SIRT1) binds to ISL directly, and the involvement of SIRT1 in ISL-mediated renoprotective effects was confirmed by studies using in vitro models of SIRT1 overexpression and knockdown. In summary, by reducing inflammation and oxidative stress, ISL has a significant pharmacological effect on the deterioration of DN. The benefits of ISL are associated with the direct binding to SIRT1, the inhibition of MAPK activation, and the induction of Nrf-2 signaling, suggesting the potential of ISL for DN treatment.

show abstract

Piceatannol alleviates inflammation and oxidative stress via modulation of the Nrf2/HO-1 and NF-κB pathways in diabetic cardiomyopathy

Cited by 75 publications

References 34 publications

Nrf2 is involved in osmoregulation, antioxidation and immunopotentiation inCoilia nasusunder salinity stress

Nrf2 is involved in osmoregulation, antioxidation and immunopotentiation inCoilia nasusunder salinity stress

Piceatannol inhibits pyroptosis and suppresses oxLDL-induced lipid storage in macrophages by regulating miR-200a/Nrf2/GSDMD axis

Isoliquiritigenin prevents hyperglycemia-induced renal injuries by inhibiting inflammation and oxidative stress via SIRT1-dependent mechanism

Contact Info

Product

Resources

About