Effects of trigonelline inhibition of the Nrf2 transcription factor &amp;lt;italic&amp;gt;in vitro&amp;lt;/italic&amp;gt; on &amp;lt;italic&amp;gt;Echinococcus granulosus&amp;lt;/italic&amp;gt;

Qin, Wenjuan; Guan, Dongfang; Ma, Rongji; Yang, Rentan; Xing, Guoqiang; Shi, Hongjuan; Tang, Guangyao; Li, Jiajie; Lv, Hailong; Jiang, Yufeng

doi:10.1093/abbs/gmx067

Cited by 16 publications

(6 citation statements)

References 66 publications

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“…To date, a parasiticidal ideal agent that is both effective and riskless has not been identified. Our previous experiments confirmed that the use of MAPK or Nrf2 signaling pathway inhibitors can affect PSCs viability by denaturing and structurally disrupting the E. granulosus PSCs [ 24 , 25 ]. The purpose of this study was to elucidate the association between MAPK and Nrf2 signaling pathways in vitro in E. granulosus , which may be useful in providing areas for more drug research in the treatment of CE.…”

Section: Discussionsupporting

confidence: 71%

“…Gu et al [23] found that propofol-induced protection of human neuroblastoma cells (SH-SY5Y) against H 2 O 2 is associated with HO-1 via the ERK Pathway. Our previous study has confirmed that MAPK and Nrf2 are both expressed in E. granulosus PSCs and play an important role in the growth and development of E. granulosus [24,25]. Under the stimulation of other injurious effects of oxidative stress, the interaction between MAPK and Nrf2/HO-1 signaling pathways in E. granulosus has not been established experimentally.…”

Section: Introductionmentioning

confidence: 93%

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Propofol Induces the Expression of Nrf2 and HO-1 in Echinococcus granulosus via the JNK and p38 Pathway In Vitro

Luo

Ma²,

Jiang

et al. 2023

TropicalMed

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The purpose of this study was to establish the relationship between mitogen-activated protein kinase (MAPK) and Nrf2 signaling pathways in Echinococcus granulosus (E. granulosus). E. granulosus protoscoleces (PSCs) cultured in vitro were divided into different groups: a control group, PSCs were pretreated with various concentrations of propofol followed by exposure to hydrogen peroxide (H2O2), and PSCs were pretreated with MAPK inhibitors, then co-treated with propofol and incubated in the presence of H2O2. PSCs activity was observed under an inverted microscope and survival rate was calculated. Reactive oxygen species (ROS) was detected by fluorescence microscopy, western blotting was used to detect the expression of Nrf2, Bcl-2, and heme oxygenase 1 (HO-1) in the PSCs among different groups. Pretreatment of PSCs with 0–1 mM propofol for 8 h prevented PSCs death after exposure to 0.5 mM H2O2. PSCs were pretreated with PD98059, SB202190, or SP600125 for 2 h, co-treated with propofol for an additional 8 h, and then exposed to 0.5 mM H2O2 for 6 h. On day 6, the PSCs viability was 42% and 39% in the p38 and JNK inhibitor groups, respectively. Additionally, pretreatment with propofol significantly attenuated the generation of ROS following H2O2 treatment. Propofol increased the expression of Nrf2, HO-1, and BCL2 compared with that of the control group. Pretreatment PSCs with SP600125 or SB202190, co-incubation with propofol and H2O2, can reduce the expression of Nrf2, HO-1, and BCL2 (p < 0.05). These results suggest that propofol induces an upregulated expression of HO-1 and Nrf2 by activation of the JNK and p38 MAPK signaling pathways. This study highlights the cross role of metabolic regulation of ROS signaling and targeting signalling pathways that may provide a promising strategy for the treatment of E. granulosus disease.

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 93%

Propofol Induces the Expression of Nrf2 and HO-1 in Echinococcus granulosus via the JNK and p38 Pathway In Vitro

Luo

Ma²,

Jiang

et al. 2023

TropicalMed

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“…As a prelude to examining whether SFX-01 also achieves its effects on osteoclasts via the modulation of NFR2, our studies were initially focused on whether pharmacological NRF2 modulators, namely Trig and RA839, exerted direct effects on osteoclast formation and function. The alkaloid, Trig, has been used in many studies as an inhibitor of NRF2 in other cell types [41][42][43]. On the other hand, RA839 has only recently been characterised as a non-covalent KEAP1 binding partner and selective activator of NRF2 [44]; neither have been used in assays of osteoclastogenesis previously.…”

Section: Discussionmentioning

confidence: 99%

Stable Sulforaphane Targets the Early Stages of Osteoclast Formation to Engender a Lasting Functional Blockade of Osteoclastogenesis

Louka,

Orriss,

Pitsillides

2024

Cells

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Sulforaphane, the native but unstable form of SFX-01, is an antioxidant that activates the NRF2 and inhibits the NF-KB pathways to achieve its actions. Resolving the mechanism(s) by which SFX-01 serves to control the various osteoclastogenic stages may expose pathways that could be explored for therapeutic use. Here we seek to identify the stage of osteoclastogenesis targeted by SFX-01 and explore whether, like SFN, it exerts its actions via the NRF2 and NF-KB pathways. Osteoclasts generated from the bone marrow (BM) of mice were cultured with SFX-01 at different timepoints to examine each phase of osteoclastogenesis separately. This showed that SFX-01 exerted actions throughout the process of osteoclastogenesis, but had its largest effects in the early osteoclast precursor differentiation stage. Thus, treatment with SFX-01 for the duration of culture, for the initial 3 days differentiation or for as little as the first 24 h was sufficient for effective inhibition. This aligned with data suggesting that SFX-01 reduced DC-STAMP levels, osteoclast nuclear number and modified cytoskeletal architecture. Pharmacological regulation of the NRF2 pathways, via selective inhibitors/activators, supported the anti-osteoclastogenic roles of an SFX-01-mediated by NRF2 activation, as well as the need for tight NF-KB pathway regulation in osteoclast formation/function.

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“…TRG showed an impact on parasites such as Echinococcus granulosus which caused cystic echinococcosis or hydatid disease in various organs in humans. TRG could induce damage to Echinococcus granulosus protoscoleces, including hook deformation, lesions, and digitiform protuberances, by decreasing Nrf2, NQO-1, and HO-1 expression and increasing caspase-3 activity [ 103 ].…”

Section: Antiviral Antimicrobial and Antifungal Effects Of Trgmentioning

confidence: 99%

Pharmacological Activities, Therapeutic Effects, and Mechanistic Actions of Trigonelline

Nguyen,

Taine,

Meng

et al. 2024

IJMS

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Trigonelline (TRG) is a natural polar hydrophilic alkaloid that is found in many plants such as green coffee beans and fenugreek seeds. TRG potentially acts on multiple molecular targets, including nuclear factor erythroid 2-related factor 2 (Nrf2), peroxisome proliferator-activated receptor γ, glycogen synthase kinase, tyrosinase, nerve growth factor, estrogen receptor, amyloid-β peptide, and several neurotransmitter receptors. In this review, we systematically summarize the pharmacological activities, medicinal properties, and mechanistic actions of TRG as a potential therapeutic agent. Mechanistically, TRG can facilitate the maintenance and restoration of the metabolic homeostasis of glucose and lipids. It can counteract inflammatory constituents at multiple levels by hampering pro-inflammatory factor release, alleviating inflammatory propagation, and attenuating tissue injury. It concurrently modulates oxidative stress by the blockage of the detrimental Nrf2 pathway when autophagy is impaired. Therefore, it exerts diverse therapeutic effects on a variety of pathological conditions associated with chronic metabolic diseases and age-related disorders. It shows multidimensional effects, including neuroprotection from neurodegenerative disorders and diabetic peripheral neuropathy, neuromodulation, mitigation of cardiovascular disorders, skin diseases, diabetic mellitus, liver and kidney injuries, and anti-pathogen and anti-tumor activities. Further validations are required to define its specific targeting molecules, dissect the underlying mechanistic networks, and corroborate its efficacy in clinical trials.

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Effects of trigonelline inhibition of the Nrf2 transcription factor <italic>in vitro</italic> on <italic>Echinococcus granulosus</italic>

Cited by 16 publications

References 66 publications

Propofol Induces the Expression of Nrf2 and HO-1 in Echinococcus granulosus via the JNK and p38 Pathway In Vitro

Propofol Induces the Expression of Nrf2 and HO-1 in Echinococcus granulosus via the JNK and p38 Pathway In Vitro

Stable Sulforaphane Targets the Early Stages of Osteoclast Formation to Engender a Lasting Functional Blockade of Osteoclastogenesis

Pharmacological Activities, Therapeutic Effects, and Mechanistic Actions of Trigonelline

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