scholarly journals Epigallocatechin Gallate for Management of Heavy Metal-Induced Oxidative Stress: Mechanisms of Action, Efficacy, and Concerns

2021 ◽  
Vol 22 (8) ◽  
pp. 4027
Author(s):  
Iwona Zwolak
Keyword(s):  
Epigallocatechin Gallate ◽  
Neural Cells ◽  
Related Factor ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Tea Polyphenol ◽  
Protective Mechanisms ◽  
Mitochondrial Functions ◽  
Green Tea Polyphenol

In this review, we highlight the effects of epigallocatechin gallate (EGCG) against toxicities induced by heavy metals (HMs). This most active green tea polyphenol was demonstrated to reduce HM toxicity in such cells and tissues as testis, liver, kidney, and neural cells. Several protective mechanisms that seem to play a pivotal role in EGCG-induced effects, including reactive oxygen species scavenging, HM chelation, activation of nuclear factor erythroid 2-related factor 2 (Nrf2), anti-inflammatory effects, and protection of mitochondria, are described. However, some studies, especially in vitro experiments, reported potentiation of harmful HM actions in the presence of EGCG. The adverse impact of EGCG on HM toxicity may be explained by such events as autooxidation of EGCG, EGCG-mediated iron (Fe3+) reduction, depletion of intracellular glutathione (GSH) levels, and disruption of mitochondrial functions. Furthermore, challenges hampering the potential EGCG application related to its low bioavailability and proper dosing are also discussed. Overall, in this review, we point out insights into mechanisms that might account for both the beneficial and adverse effects of EGCG in HM poisoning, which may have a bearing on the design of new therapeutics for HM intoxication therapy.

scholarly journals Epigallocatechin Gallate (EGCG), a Green Tea Polyphenol, Reduces Coronavirus Replication in a Mouse Model

Viruses ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2533
Author(s):  
Rackhyun Park ◽  
Minsu Jang ◽  
Yea-In Park ◽  
Yeonjeong Park ◽  
Woochul Jung ◽  
...  
Keyword(s):  
Mouse Model ◽  
Green Tea ◽  
Particle Production ◽  
Epigallocatechin Gallate ◽  
Tea Polyphenols ◽  
Green Tea Polyphenols ◽  
Tea Polyphenol ◽  
Green Tea Polyphenol

The COVID-19 pandemic has resulted in a huge number of deaths from 2020 to 2021; however, effective antiviral drugs against SARS-CoV-2 are currently under development. Recent studies have demonstrated that green tea polyphenols, particularly EGCG, inhibit coronavirus enzymes as well as coronavirus replication in vitro. Herein, we examined the inhibitory effect of green tea polyphenols on coronavirus replication in a mouse model. We used epigallocatechin gallate (EGCG) and green tea polyphenols containing more than 60% catechin (GTP60) and human coronavirus OC43 (HCoV-OC43) as a surrogate for SARS-CoV-2. Scanning electron microscopy analysis results showed that HCoV-OC43 infection resulted in virion particle production in infected cells. EGCG and GTP60 treatment reduced coronavirus protein and virus production in the cells. Finally, EGCG- and GTP60-fed mice exhibited reduced levels of coronavirus RNA in mouse lungs. These results demonstrate that green tea polyphenol treatment is effective in decreasing the level of coronavirus in vivo.

scholarly journals Azilsartan Suppresses Osteoclastogenesis and Ameliorates Ovariectomy-Induced Osteoporosis by Inhibiting Reactive Oxygen Species Production and Activating Nrf2 Signaling

2021 ◽  
Vol 12 ◽  
Author(s):  
Bin Pan ◽  
Lin Zheng ◽  
Jiawei Fang ◽  
Ye Lin ◽  
Hehuan Lai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Signaling Pathways ◽  
Bone Microarchitecture ◽  
Reactive Oxygen ◽  
Related Factor ◽  
Nuclear Factor ◽  
Oxygen Species

Osteoporosis is characterized by a decrease in bone mass and destruction of the bone microarchitecture, and it commonly occurs in postmenopausal women and the elderly. Overactivation of osteoclasts caused by the inflammatory response or oxidative stress leads to osteoporosis. An increasing number of studies have suggested that intracellular reactive oxygen species (ROS) are strongly associated with osteoclastogenesis. As a novel angiotensin (Ang) II receptor blocker (ARB), azilsartan was reported to be associated with the inhibition of intracellular oxidative stress processes. However, the relationship between azilsartan and osteoclastogenesis is still unknown. In this study, we explored the effect of azilsartan on ovariectomy-induced osteoporosis in mice. Azilsartan significantly inhibited the receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclastogenesis and downregulated the expression of osteoclast-associated markers (Nfatc1, c-Fos, and Ctsk) in vitro. Furthermore, azilsartan reduced RANKL-induced ROS production by increasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2). Mechanistically, azilsartan inhibited the activation of MAPK/NF-κB signaling pathways, while Nrf2 silencing reversed the inhibitory effect of azilsartan on MAPK/NF-κB signaling pathways. Consistent with the in vitro data, azilsartan administration ameliorated ovariectomy (OVX)-induced osteoporosis, and decreased ROS levels in vivo. In conclusion, azilsartan inhibited oxidative stress and may be a novel treatment strategy for osteoporosis caused by osteoclast overactivation.

scholarly journals Effects of Pterostilbene on the Activation of Nuclear Factor Erythroid 2-Related Factor 2 Pathway During in vitro Maturation of Mouse Oocytes

2018 ◽  
Vol 10 (7) ◽  
pp. 35
Author(s):  
Obaid Ullah ◽  
Li Zhongshu ◽  
Ihsan Ali ◽  
Lijie Xu ◽  
Haixing Liu ◽  
...  
Keyword(s):  
Protein Expression ◽  
In Vitro Maturation ◽  
Biological Activities ◽  
Related Factor ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Bcl2 Family ◽  
Mouse Oocytes ◽  
Anticancer Effects

Pterostilbene (PTS) is a natural polyphonic compound known to have biological activities, such as antioxidant and anticancer effects. This study was designed to regulate the effect of pterostilbene on the in vitro maturation (IVM) of mouse oocytes denuded of the cumulus (DOs). Different concentration of PTS was added to IVM media with immature DOs. After maturation, meiosis II (MII) stage rates oocytes, Measurement of reactive oxygen species (ROS) and glutathione (GSH) levels, activation of the Nuclear Factor Erythroid 2 like 2 (NFE2L2) pathway and apoptotic expression of BCL2 family in MII oocytes were determined. Our results showed that: PTS significantly increased the MII rate of DOs (P < 0.05). Moreover, PTS decreased the ROS levels in DOs (P < 0.05) and increased the GSH levels (P < 0.05). Furthermore, PTS addition in DOs significantly increased the protein expression of NFE2L2 in the nucleus and decreased Kelch-like ECH-associated protein1 (KEAP1). PTS significantly increased the antioxidant enzyme expression of catalase (CAT), heme oxygenase1 (HMOX1), and superoxide dismutase (SOD). In addition, PTS lowered the protein expression of apoptotic Bcl-2-associated X protein (BAX) and increased the protein expression of anti-apoptotic B-cell lymphoma2 (BCL2) as well as PTS treatment significantly increased the gene expression of BCL2 and reduced the expression of apoptotic BAX in matured DOs. These results indicated that pterostilbene significantly improved the IVM quality matured of DOs and activate NFE2L2-Keap1 pathway during maturation of oocytes.

scholarly journals Nuclear factor erythroid 2-related factor 2 activation mediates hyperhomocysteinemia-associated lipolysis suppression in adipocytes

2018 ◽  
Vol 243 (11) ◽  
pp. 926-933 ◽  
Author(s):  
Xin Li ◽  
Yuhong Cheng ◽  
Xiuli Zhong ◽  
Bing Zhang ◽  
Zhiwei Bao ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Epigallocatechin Gallate ◽  
Underlying Mechanism ◽  
Control Group ◽  
Related Factor ◽  
Nuclear Factor ◽  
Glycerol Release ◽  
Nrf2 Activation

Hyperhomocysteinemia (HHcy) is associated with suppressed lipolytic response in adipocytes/adipose tissue, however, the underlying mechanism remains to be extensively studied. Nuclear factor erythroid 2-related factor 2 (Nrf2), a master transcriptional factor regulating antioxidant generation, has been recently reported to mediate lipid metabolism. Employing both fully differentiated 3T3-L1 adipocytes and male C57BL/6 mice, in the present study, we investigated the potential involvement of Nrf2 activation in HHcy-mediated lipolytic suppression. Our results showed that homocysteine (Hcy) treatment resulted in suppressed lipolysis, evidenced by increased intracellular triglyceride (TG) accumulation, decreased glycerol and free fatty acid (FFA) in fully differentiated 3T3-L1 adipocytes. Interestingly, Hcy exposure was associated with Nrf2 activation in adipocytes. Further studies showed that Nrf2 knockdown via siRNA transfection ameliorated Hcy-induced glycerol release in adipocytes. On the contrary, Nrf2 activators, epigallocatechin gallate (EGCG) and tert-butylhydroquinone (t-BHQ), increased intracellular TG content and decreased glycerol release in adipocytes. Importantly, our in vitro observations were corroborated by our in vivo findings, in which Hcy feeding (0.1% wt/vol) for four weeks induced Nrf2 expression in adipose tissue and lowered circulating FFA and glycerol levels in mice. Furthermore, EGCG injection (5 mg/kg/d) decreased circulating glycerol levels in comparison to the control group in mice. In conclusion, these results indicated that Nrf2 activation in response to HHcy plays an important role in mediating Hcy-suppressed lipolysis in adipocytes.

scholarly journals Iron Regulates the Warburg Effect and Ferroptosis in Colorectal Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Yin Yuan ◽  
Shuo Ni ◽  
Aoxiang Zhuge ◽  
Bo Li ◽  
Lanjuan Li
Keyword(s):  
Colorectal Cancer ◽  
Warburg Effect ◽  
Related Factor ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Therapeutic Approaches ◽  
Enhanced Resistance ◽  
The Warburg Effect

Iron promotes the proliferation of cancer cells, but it also contributes to cell death. Here we explored whether iron could promote the Warburg effect of colorectal cancer (CRC) cells and suppress sensitivity to ferroptosis by inducing reactive oxygen species (ROS) and regulating nuclear factor erythroid 2-related factor 2 (NRF2). In this study, cell proliferation abilities were measured by CCK-8, EdU incorporation, and colony formation assays. Seahorse XF96 respirometry assays were used to detect the Warburg effect and the level of ROS was assess by DCFH-DA fluorescent probes. Results showed that iron exposure promoted the Warburg effect of CRC cells by inducing ROS and activating NRF2 both in vivo and in vitro. In addition, iron exposure also induced ferroptosis in CRC cells, but at the same time its inhibitory proteins SLC7A11 and GPX4 were also upregulated, indicating an enhanced resistance to ferroptosis. Our results revealed that iron can effectively promote tumorigenesis. Meanwhile, iron elimination or a low-iron diet might be valid therapeutic approaches for CRC.

Trilobatin Protects Cardiomyocytes from Hypoxia/ Reperfusion Injury by Regulating the Nuclear Factor Erythroid 2-Related Factor 2/Heme Oxygenase-1 Pathway

2020 ◽  
Vol 19 (2) ◽  
pp. 133-138
Author(s):  
Wenyu Chen ◽  
Hui He
Keyword(s):  
Heme Oxygenase ◽  
Molecular Mechanisms ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Cellular Injury ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
H9c2 Cells ◽  
Natural Plant ◽  
Induced Changes

Trilobatin is a natural plant-derived glycosylated flavonoid that has been shown to exhibit multiple beneficial pharmacologic activities including protection of heart against H/R-induced cardiomyocyte injury. However, the molecular mechanisms underlying protection from H/R-induced cardiomyocyte injury remain unknown. Using H9C2 cells as a model, we examined the effect of trilobatin on H/R-induced cellular injury, apoptosis, and generation of reactive oxygen species. The results showed that trilobatin protected H9C2 cells not only from cell death and apoptosis, but also counteracted H/R-induced changes in malondialdehyde, superoxide dismutase, glutathione, and glutathione peroxidase. The evaluation of the mechanism underlying the effect of trilobatin on protection from H/R-induced cellular injury suggested changes in the regulation of nuclear factor erythroid 2-related factor 2/heme oxygenase-1 pathway.

Maltol inhibits the progression of osteoarthritis via the nuclear factor-erythroid 2-related factor-2/heme oxygenase-1 signal pathway in vitro and in vivo

2021 ◽  
Author(s):  
Ding-Chao Zhu ◽  
Yi-Han Wang ◽  
Jia-Hao Lin ◽  
Zhi-Min Miao ◽  
Jia-Jing Xu ◽  
...  
Keyword(s):  
Cartilage Degeneration ◽  
Degenerative Joint Disease ◽  
Signal Pathway ◽  
Joint Disease ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Articular Cartilage Degeneration

Osteoarthritis (OA) is a common degenerative joint disease characterized by articular cartilage degeneration and inflammation. Currently, there is hardly any effective treatment for OA due to its complicated pathology and...

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