Larrea tridentata and its biological activities

2021 ◽  
Vol 21 ◽  
Author(s):  
Karen Y. Reyes-Melo ◽  
Adrián A. Galván-Rodrigo ◽  
Isaí E. Martínez-Olivo ◽  
Guillermo Núñez-Mojica ◽  
Francisco G. Ávalos-Alanís ◽  
...  
Keyword(s):  
Antioxidant Activities ◽  
Biological Activities ◽  
Nordihydroguaiaretic Acid ◽  
Antioxidant Response ◽  
Larrea Tridentata ◽  
Related Factor ◽  
Oxygen Species ◽  
Traditional Uses ◽  
Organic Extracts ◽  
Endogenous Antioxidant

Background: Larrea tridentata is a dominant shrub in the deserts of North America and is recognized for its various traditional uses. More than 50 traditional uses have been recorded. Regarding its chemical composition, the products of the mevalonate, shikimate, and malonate pathways are predominant. L. tridentata has nordihydroguaiaretic acid (NDGA), one of its most studied secondary metabolites that exhibited remarkable different biological activities: sequestration of reactive oxygen species, inhibition of lipoxygenases (LOX) and activation of the endogenous antioxidant response mediated by nuclear factor erythroid 2–related factor 2 (NRF2). Objective and Methods: This review seeks to draw attention to metabolites other than NDGA and which also contribute to the various biological activities of L. tridentata. Therefore, the present review includes those reports focused on the pharmacological properties of the organic extracts of L. tridentata and its natural products with promising values. Results and Conclusion: Among the most promising and widely reported metabolites from L. tridentata, are: 3’-demethoxy-6-O-demethylisoguaiacin, 3’-O-methylnordihydroguiaretic acid, meso-dihydroguaiaretic acid, and tetra-O-methylnorhydroguiaretic acid. These have been reported to exhibit antibacterial, antiprotozoal, anthelmintic, antifungal, antiviral, anticancer, and antioxidant activities.

scholarly journals The Keap1/Nrf2 Signaling Pathway in the Thyroid—2020 Update

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1082 ◽  
Author(s):  
Christina Thanas ◽  
Panos G. Ziros ◽  
Dionysios V. Chartoumpekis ◽  
Cédric O. Renaud ◽  
Gerasimos P. Sykiotis
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Antioxidant Systems ◽  
Related Factor ◽  
Oxygen Species ◽  
Nrf2 Signaling Pathway ◽  
The Face ◽  
Antioxidant Defense Systems ◽  
The One ◽  
Endogenous Antioxidant

The thyroid gland has a special relationship with oxidative stress. On the one hand, like all other tissues, it must defend itself against reactive oxygen species (ROS). On the other hand, unlike most other tissues, it must also produce reactive oxygen species in order to synthesize its hormones that contribute to the homeostasis of other tissues. The thyroid must therefore also rely on antioxidant defense systems to maintain its own homeostasis in the face of continuous self-exposure to ROS. One of the main endogenous antioxidant systems is the pathway centered on the transcription factor Nuclear factor erythroid 2-related factor 2 (Nrf2) and its cytoplasmic inhibitor Kelch-like ECH-associated protein 1 (Keap1). Over the last few years, multiple links have emerged between the Keap1/Nrf2 pathway and thyroid physiology, as well as various thyroid pathologies, including autoimmunity, goiter, hypothyroidism, hyperthyroidism, and cancer. In the present mini-review, we summarize recent studies shedding new light into the roles of Keap1/Nrf2 signaling in the thyroid.

scholarly journals NRF2 Regulation by Noncoding RNAs in Cancers: The Present Knowledge and the Way Forward

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3621
Author(s):  
Federico Pio Fabrizio ◽  
Angelo Sparaneo ◽  
Lucia Anna Muscarella
Keyword(s):  
Noncoding Rna ◽  
Gene Network ◽  
Noncoding Rnas ◽  
Antioxidant Response ◽  
Present Knowledge ◽  
Cellular Damage ◽  
Related Factor ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Cellular Mechanisms

Nuclear factor erythroid 2-related factor 2 (NRF2) is the key transcription factor triggered by oxidative stress that moves in cells of the antioxidant response element (ARE)-antioxidant gene network against reactive oxygen species (ROS) cellular damage. In tumors, the NRF2 pathway represents one of the most intriguing pathways that promotes chemo- and radioresistance of neoplastic cells and its activity is regulated by genetic and epigenetic mechanisms; some of these being poorly investigated in cancer. The noncoding RNA (ncRNA) network is governed by microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) and modulates a variety of cellular mechanisms linked to cancer onset and progression, both at transcriptional and post-transcriptional levels. In recent years, the scientific findings about the effects of ncRNA landscape variations on NRF2 machines are rapidly increasing and need to be continuously updated. Here, we review the latest knowledge about the link between NRF2 and ncRNA networks in cancer, thus focusing on their potential translational significance as key tumor biomarkers.

scholarly journals Effect of Hepatitis Viruses on the Nrf2/Keap1-Signaling Pathway and Its Impact on Viral Replication and Pathogenesis

2019 ◽  
Vol 20 (18) ◽  
pp. 4659 ◽  
Author(s):  
Bender ◽  
Hildt
Keyword(s):  
Chronic Infection ◽  
Inflammatory Diseases ◽  
Antioxidant Response ◽  
Target Sequence ◽  
Related Factor ◽  
Oxygen Species ◽  
Detoxifying Enzymes ◽  
Hepatitis Viruses ◽  
B Virus ◽  
The Impact

With respect to their genome and their structure, the human hepatitis B virus (HBV) and hepatitis C virus (HCV) are complete different viruses. However, both viruses can cause an acute and chronic infection of the liver that is associated with liver inflammation (hepatitis). For both viruses chronic infection can lead to fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Reactive oxygen species (ROS) play a central role in a variety of chronic inflammatory diseases. In light of this, this review summarizes the impact of both viruses on ROS-generating and ROS-inactivating mechanisms. The focus is on the effect of both viruses on the transcription factor Nrf2 (nuclear factor erythroid 2 (NF-E2)-related factor 2). By binding to its target sequence, the antioxidant response element (ARE), Nrf2 triggers the expression of a variety of cytoprotective genes including ROS-detoxifying enzymes. The review summarizes the literature about the pathways for the modulation of Nrf2 that are deregulated by HBV and HCV and describes the impact of Nrf2 deregulation on the viral life cycle of the respective viruses and the virus-associated pathogenesis.

Peptide and small molecule inhibitors of the Keap1–Nrf2 protein–protein interaction

2015 ◽  
Vol 43 (4) ◽  
pp. 674-679 ◽  
Author(s):  
Geoff Wells
Keyword(s):  
Small Molecule ◽  
Protein Interaction ◽  
Small Molecule Inhibitors ◽  
Biological Activities ◽  
Cancer Chemoprevention ◽  
Antioxidant Response ◽  
Related Factor ◽  
Promoter Regions ◽  
Protein Protein Interaction ◽  
Antioxidant Response Elements

The transcription factor nuclear factor erythroid-2-related factor 2 (Nrf2) up-regulates the expression of a range of cytoprotective enzymes with antioxidant response elements in their promoter regions and thus can protect cells against oxidative damage. Increasing Nrf2 activity has been proposed as a therapeutic intervention in a range of chronic neurodegenerative conditions and cancer chemoprevention. One of the main mechanisms by which Nrf2 is negatively regulated involves an interaction with the ubiquitination facilitator protein, Kelch-like ECH-associated protein 1 (Keap1) that facilitates degradation of Nrf2. Inhibition of this process underlies the mode of action of a broad group of compounds that increase Nrf2 activity. A number of natural products, including the isothiocyanate sulforaphane, up-regulate Nrf2 by interacting with Keap1 in a covalent manner to stall its activity. Recently, a number of peptide and small molecule inhibitors of the protein-protein interaction (PPI) between Keap1 and Nrf2 have been described. These classes of compound have contrasting modes of action at the molecular level and there is emerging evidence that their biological activities have similarities and differences. This review describes the various classes of PPI inhibitor that have been described in the literature and the biological evaluations that have been performed.

scholarly journals Protective Effects and Mechanisms of Procyanidins on Parkinson’s Disease In Vivo and In Vitro

Molecules ◽  
2021 ◽  
Vol 26 (18) ◽  
pp. 5558
Author(s):  
Juan Chen ◽  
Yixuan Chen ◽  
Yangfan Zheng ◽  
Jiawen Zhao ◽  
Huilin Yu ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Pc12 Cells ◽  
Antioxidant Activities ◽  
Antioxidant Response ◽  
Related Factor ◽  
Protective Effects ◽  
Neuroprotective Effects

This research assessed the molecular mechanism of procyanidins (PCs) against neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its metabolite 1-methyl-4-phenylpyridinium (MPP+) induced Parkinson’s disease (PD) models. In vitro, PC12 cells were incubated with PCs or deprenyl for 24 h, and then exposed to 1.5 mM MPP+ for 24 h. In vivo, zebrafish larvae (AB strain) 3 days post-fertilization (dpf) were incubated with deprenyl or PCs in 400 μM MPTP for 4 days. Compared with MPP+/MPTP alone, PCs significantly improved antioxidant activities (e.g., glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT)), and decreased levels of reactive oxygen species (ROS) and malondialdehyde (MDA). Furthermore, PCs significantly increased nuclear Nrf2 accumulation in PC12 cells and raised the expression of NQO1, HO-1, GCLM, and GCLC in both PC12 cells and zebrafish compared to MPP+/MPTP alone. The current study shows that PCs have neuroprotective effects, activate the nuclear factor-erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway and alleviate oxidative damage in MPP+/MPTP-induced PD models.

scholarly journals Antioxidant and Adaptative Response Mediated by Nrf2 during Physical Exercise

Antioxidants ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 196 ◽  
Author(s):  
Nancy Vargas-Mendoza ◽  
Ángel Morales-González ◽  
Eduardo Osiris Madrigal-Santillán ◽  
Eduardo Madrigal-Bujaidar ◽  
Isela Álvarez-González ◽  
...  
Keyword(s):  
Physical Exercise ◽  
High Performance ◽  
Metabolic Response ◽  
Antioxidant Response ◽  
Antioxidant Defenses ◽  
Related Factor ◽  
Oxygen Species ◽  
Regenerative Capacity ◽  
Exercise Preconditioning ◽  
Therapeutic Model

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a powerful nuclear transcription factor that coordinates an antioxidant cytoprotector system complex stimulated by the increase in inoxidative stress (OS). In the present manuscript, we conduct a review on the evidence that shows the effect different modalities of physical exercise exert on the antioxidant metabolic response directed by Nrf2. During physical exercise, the reactive oxygen species (ROS) are increased; therefore, if the endogenous and exogenous antioxidant defenses are unable to control the elevation of ROS, the resulting OS triggers the activation of the transcriptional factor Nrf2 to induce the antioxidant response. On a molecular basis related to physical exercise, hormesis maintenance (exercise preconditioning) and adaptative changes in training are supported by a growing body of evidence, which is important for detailing the health benefits that involve greater resistance to environmental aggressions, better tolerance to constant changes, and increasing the regenerative capacity of the cells in such a way that it may be used as a tool to support the prevention or treatment of diseases. This may have clinical implications for future investigations regarding physical exercise in terms of understanding adaptations in high-performance athletes but also as a therapeutic model in several diseases.

scholarly journals Nordihydroguaiaretic Acid Attenuates the Oxidative Stress-Induced Decrease of CD33 Expression in Human Monocytes

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Silvia Guzmán-Beltrán ◽  
José Pedraza-Chaverri ◽  
Susana Gonzalez-Reyes ◽  
Fernando Hernández-Sánchez ◽  
Ulises E. Juarez-Figueroa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Antioxidant Activity ◽  
Oxidant Stress ◽  
Nordihydroguaiaretic Acid ◽  
Larrea Tridentata ◽  
Ros Production ◽  
Oxygen Species ◽  
Human Monocytes

Nordihydroguaiaretic acid (NDGA) is a natural lignan with recognized antioxidant and beneficial properties that is isolated fromLarrea tridentata. In this study, we evaluated the effect of NDGA on the downregulation of oxidant stress-induced CD33 in human monocytes (MNs). Oxidative stress was induced by iodoacetate (IAA) or hydrogen peroxide (H2O2) and was evaluated using reactive oxygen species (ROS) production, and cell viability. NDGA attenuates toxicity, ROS production and the oxidative stress-induced decrease of CD33 expression secondary to IAA or H2O2in human MNs. It was also shown that NDGA (20 μM) attenuates cell death in the THP-1 cell line that is caused by treatment with either IAA or H2O2. These results suggest that NDGA has a protective effect on CD33 expression, which is associated with its antioxidant activity in human MNs.

scholarly journals Protective Effects of Evodiamine against LPS-Induced Acute Kidney Injury through Regulation of ROS-NF-κB-Mediated Inflammation

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Yan Shi ◽  
Qiuju Hua ◽  
Na Li ◽  
Min Zhao ◽  
Yan Cui
Keyword(s):  
Acute Kidney Injury ◽  
Cell Viability ◽  
Antioxidant Activities ◽  
Biological Activities ◽  
Kidney Injury ◽  
Potential Candidate ◽  
Ros Production ◽  
Oxygen Species ◽  
Protective Effects ◽  
New Strategies

Acute kidney injury (AKI) is a critical care syndrome, which is usually associated with sepsis-related endotoxemia. Evodiamine (EVO) is an active ingredient of many traditional medicinal formulations that possess a battery of biological activities. In the study, we aimed to evaluate the potential protective effect of EVO against lipopolysaccharide- (LPS-) induced AKI and cytotoxicity. LPS-resulted pathological injuries were significantly ameliorated by the administration of EVO. EVO reduced the levels of blood urea nitrogen (BUN) and creatinine in LPS-treated rats. EVO also inhibited LPS-induced reduction of cell viability in NRK-52E cells. LPS-resulting increase of TNFα and IL-1β in both serum and kidney of rats and NRK-52E cells was inhibited by EVO. LPS-induced increase of P65 NF-κB expression was markedly inhibited by EVO. EVO-induced reduction of TNFα and IL-1β expression in LPS-treated cells was blocked by overexpression of P65 NF-κB. Moreover, the increase of cell viability in LPS-treated cells induced by EVO was remarkably suppressed by overexpression of P65 NF-κB. LPS-resulting increase of reactive oxygen species (ROS) production was suppressed by EVO. H2O2 suppressed EVO-induced decrease of P65 NF-κB expression and increase of cell viability in LPS-treated NRK-52E cells. Moreover, the antioxidant NAC significantly promoted EVO-induced decrease of P65 NF-κB expression and increase of cell viability in LPS-treated NRK-52E cells. In conclusion, EVO had crucial protective effects against LPS-induced AKI and cytotoxicity through the antioxidant activities and thus the inhibition of inflammation. Our data highlight EVO as a potential candidate for the development of new strategies for the treatment of AKI.

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.

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