Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor

Xue, Yan; Li, Yanfei; Yu, Han; Wang, Wei; Wu, Chunyan; Yang, Yang; Hu, Yongjia; Shi, Xiujuan

doi:10.1038/s41598-017-08301-6

Cited by 23 publications

(11 citation statements)

References 40 publications

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“…www.nature.com/scientificreports www.nature.com/scientificreports/ The non-integrin cell surface receptor, 67-kDa laminin receptor (67LR) is highly expressed on the surfaces of various tumour cells and is widely recognized as a molecular marker of metastatic aggressiveness 20,21 . Moreover, 67LR is a membrane receptor of EGCG 22 , and the binding of EGCG to the 67LR protein reportedly mediates many of EGCG's beneficial activities, such as its anti-proliferative and apoptosis-inducing effects on multiple tumour cells 23 , antioxidant effects 24,25 , and anti-inflammatory activities 26,27 .…”

mentioning

confidence: 99%

(−)-Epigallocatechin-3-gallate (EGCG) attenuates salt-induced hypertension and renal injury in Dahl salt-sensitive rats

Luo

Chen

et al. 2020

Sci Rep

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Epigallocatechin-3-gallate (EGCG), a main active catechin in green tea, was reported to attenuate renal injury and hypertension. However, its effects on salt-induced hypertension and renal injury remain unclear. In the present study, we explored its effects on hypertension and renal damage in Dahl rats with salt-sensitive hypertension. We found that EGCG could lower blood pressure after 6 weeks of oral administration, reduce 24 h urine protein levels and decrease creatinine clearance, and attenuate renal fibrosis, indicating that it could attenuate hypertension by protecting against renal damage. Furthermore, we studied the renal protective mechanisms of EGCG, revealing that it could lower malondialdehyde levels, reduce the numbers of infiltrated macrophages and T cells, and induce the apoptosis of NRK-49F cells. Considering that the 67 kD laminin receptor (67LR) binds to EGCG, its role in EGCG-induced fibroblast apoptosis was also investigated. The results showed that an anti-67LR antibody partially abrogated the apoptosis-inducing effects of EGCG on NRK-49F cells. In summary, EGCG may attenuate renal damage and salt-sensitive hypertension via exerting anti-oxidant, antiinflammatory, and apoptosis-inducing effects on fibroblasts; the last effect is partially mediated by 67LR, suggesting that EGCG represents a potential strategy for treating salt-sensitive hypertension.Salt-sensitive hypertension is characterized by a significant increase in blood pressure after high salt intake. Patients with this condition are at high risk for cardiovascular and renal morbidity and mortality. Renal injury plays a key role in the pathogenesis of salt sensitive hypertension 1 . Recently, the roles of oxidative stress and inflammatory cell infiltration in the kidney in the pathogenesis of salt-sensitive hypertension were verified 2,3 . Renal fibrosis is a common pathway for a variety of chronic kidney diseases to progress to end-stage renal failure 4 and excessive proliferation of renal interstitial fibroblasts participates in the development of renal fibrosis 5,6 .(−)-Epigallocatechin-3-gallate (EGCG) is the most active and abundant polyphenol in green tea, accounting for approximately 50% of green tea polyphenols 7 . Recently, EGCG has attracted interest due to its wide range of biological activities, such as its antioxidant, NO-scavenging, anti-inflammatory, anti-arthritic and apoptosis-inducing effects in multiple types of tumour cells 8,9 . EGCG benefits a broad spectrum of hypertension disorders, including renovascular hypertension 10 and spontaneous hypertension 11 . The renoprotective effect of EGCG has been reported in several renal disease models 12 , such as acute kidney injury 13 , cisplatin-induced nephrotoxicity 14 , obstructive nephropathy 15 , glomerulonephritis 16 , lupus nephritis 17 , diabetic nephropathy 18 , and high-fat diet-induced kidney injury 19 . However, the effects of EGCG on salt-induced hypertension and renal injury remain unclear.

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confidence: 99%

(−)-Epigallocatechin-3-gallate (EGCG) attenuates salt-induced hypertension and renal injury in Dahl salt-sensitive rats

Luo

Chen

et al. 2020

Sci Rep

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“…5 e and f). EGCG has previously been reported to have a modulatory effect on the expression of apoptosis-related genes; mouse vascular smooth muscle cells cultured in a conditioned environment with H 2 O 2 showed significantly reduced expression of the pro-apoptotic genes caspase-3,8,9 and BAX and a significant increase in the expression of the anti-apoptotic gene BCL-2 after pre-treatment with EGCG [46] . Our results confirmed that the EGCG coating on the surface of PCL film was biologically active and influenced anti-oxidative signaling processes within hADSCs cultured on EGCG-coated film.…”

Section: Anti-apoptotic and Anti-oxidative Activities Of Egcg-coated Pcl Film Against H 2 Omentioning

confidence: 94%

Evaluation of the anti-oxidative and ROS scavenging properties of biomaterials coated with epigallocatechin gallate for tissue engineering

Lee

Byun

et al. 2021

Acta Biomaterialia

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In tissue engineering, excessively generated reactive oxygen species (ROS) during biomaterial implantation or cell transplantation is a one of major causes of diminishing therapeutic effects. In this study, we prepared biomaterial surfaces coated with antioxidant epigallocatechin gallate (EGCG) and metal ions, and evaluated their anti-oxidative and ROS scavenging properties. We revealed that EGCG-coating on polycaprolactone (PCL) film surface increased hydrophilicity and anti-oxidative properties as a function of total phenol content (TPC) potentially due to the increase in phenolic -OH and π -electrons from structural maintenance and directly removed the hydrogen peroxide (H 2 O 2 ) by resonance-stabilization. Furthermore, EGCG-coated PCL film increased attachment, spreading area, and viability of human adipose-derived stem cells (hADSCs) against H 2 O 2 treatment while stimulated the cellular signaling to reduce apoptotic gene and enhance anti-oxidative enzyme expression. Further, we applied EGCG coating on the surface of poly-L-lactic acid (PLLA) fibers. Spheroids incorporating EGCG-coated PLLA fibers were able to maintain their shape and showed improved viability and anti-oxidative activities in response to H 2 O 2 -induced oxidative stress than control spheroids. Therefore, metal-phenolic network (MPN) coating of EGCG is a suitable method to impart the anti-oxidative properties to biomaterials by evaluating the structural properties and biological effects. Statement of SignificanceThis manuscript describes an antioxidant coating for biomaterials to control reactive oxygen species (ROS). Antioxidant epigallocatechin gallate (EGCG) was coated on the PCL film surface via metal-phenolic network (MPN). We revealed that the phenolic functional groups of EGCG are structurally maintained as confirmed by quantitative reducing power, radical scavenging assays. EGCG coating not only removed ROS directly, but also is involved in cell signaling to enhance the anti-apoptotic gene, anti-oxidative enzyme expression. Furthermore, human adipose-derived stem cells (hADSCs) spheroid produced by self-assembly with EGCG-coated poly-L-lactic aicd (PLLA) fibers showed anti-oxidative properties from inside of spheroids. Thus, our evaluation of the anti-oxidative properties of EGCG coating can be applied to various tissue engineering applications.

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“…Increasing evidence had suggested the contribution of the vascular smooth muscle cells (VSMCs) apoptosis to the pathogenesis of cardiovascular diseases, including hypertension, atherosclerosis, and even myocardial infarction (Kumar et al, 2014;Mill et al, 2014). Therefore, inhibiting VSMCs apoptosis could be a potential preventive strategy in slowing down the development of cardiovascular disease, especially for atherosclerosis (Yan et al, 2017). As oxidative stress is considered one of the most important pro-apoptotic stimuli leading to VSMCs apoptosis in atherosclerotic plaques (Korshunov and Berk, 2008), an effective antioxidant is imperatively needed to attenuate the oxidative stress-induced VSMCs apoptosis.…”

Section: Introductionmentioning

confidence: 99%

6-Shogaol Inhibits Oxidative Stress-Induced Rat Vascular Smooth Muscle Cell Apoptosis by Regulating OXR1-p53 Axis

Liu

et al. 2022

Front. Mol. Biosci.

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Apoptosis of vascular smooth muscle cells (VSMCs) is closely related to the pathogenesis of cardiovascular diseases, and oxidative stress is an important cause of VSMCs’ death. Inhibiting VSMCs apoptosis is an effective preventive strategy in slowing down the development of cardiovascular disease, especially for atherosclerosis. In this study, we found that oxidation resistance protein 1 (OXR1), a crucial participator for responding to oxidative stress, could modulate the expression of p53, the key regulator of cell apoptosis. Our results revealed that oxidative stress promoted VSMCs apoptosis by overexpression of the OXR1-p53 axis, and 6-shogaol (6S), a major biologically active compound in ginger, could effectively attenuate cell death by preventing the upregulated expression of the OXR1-p53 axis. Quantitative proteomics analysis revealed that the degradation of p53 mediated by OXR1 might be related to the enhanced assembly of SCF ubiquitin ligase complexes, which is reported to closely relate to the modification of ubiquitination or neddylation and subsequent degradation of p53.

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Epigallocatechin-3-gallate inhibits H2O2-induced apoptosis in Mouse Vascular Smooth Muscle Cells via 67kD Laminin Receptor

Cited by 23 publications

References 40 publications

(−)-Epigallocatechin-3-gallate (EGCG) attenuates salt-induced hypertension and renal injury in Dahl salt-sensitive rats

(−)-Epigallocatechin-3-gallate (EGCG) attenuates salt-induced hypertension and renal injury in Dahl salt-sensitive rats

Evaluation of the anti-oxidative and ROS scavenging properties of biomaterials coated with epigallocatechin gallate for tissue engineering

6-Shogaol Inhibits Oxidative Stress-Induced Rat Vascular Smooth Muscle Cell Apoptosis by Regulating OXR1-p53 Axis

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