Asset Details
Do you wish to reserve the book?
The protective roles of eugenol on type 1 diabetes mellitus through NRF2-mediated oxidative stress pathway
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
The protective roles of eugenol on type 1 diabetes mellitus through NRF2-mediated oxidative stress pathway
Do you wish to request the book?
The protective roles of eugenol on type 1 diabetes mellitus through NRF2-mediated oxidative stress pathway
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
The protective roles of eugenol on type 1 diabetes mellitus through NRF2-mediated oxidative stress pathway
2025
Overview
Type 1 diabetes mellitus (T1DM), known as insulin-dependent diabetes mellitus, is characterized by persistent hyperglycemia resulting from damage to the pancreatic β cells and an absolute deficiency of insulin, leading to multi-organ involvement and a poor prognosis. The progression of T1DM is significantly influenced by oxidative stress and apoptosis. The natural compound eugenol (EUG) possesses anti-inflammatory, anti-oxidant, and anti-apoptotic properties. However, the potential effects of EUG on T1DM had not been investigated. In this study, we established the streptozotocin (STZ)-induced T1DM mouse model in vivo and STZ-induced pancreatic β cell MIN6 cell model in vitro to investigate the protective effects of EUG on T1DM, and tried to elucidate its potential mechanism. Our findings demonstrated that the intervention of EUG could effectively induce the activation of nuclear factor E2-related factor 2 (NRF2), leading to an up-regulation in the expressions of downstream proteins NQO1 and HMOX1, which are regulated by NRF2. Moreover, this intervention exhibited a significant amelioration in pancreatic β cell damage associated with T1DM, accompanied by an elevation in insulin secretion and a reduction in the expression levels of apoptosis and oxidative stress-related markers. Furthermore, ML385, an NRF2 inhibitor, reversed these effects of EUG. The present study suggested that EUG exerted protective effects on pancreatic β cells in T1DM by attenuating apoptosis and oxidative stress through the activation of the NRF2 signaling pathway. Consequently, EUG holds great promise as a potential therapeutic candidate for T1DM.
Publisher
eLife Sciences Publications Ltd
Subject
/ Diabetes
/ Diabetes mellitus (insulin dependent)
/ Diabetes Mellitus, Experimental - drug therapy
/ Diabetes Mellitus, Experimental - metabolism
/ Diabetes Mellitus, Type 1 - drug therapy
/ Diabetes Mellitus, Type 1 - metabolism
/ eugenol
/ Glucose
/ Heme Oxygenase-1 - metabolism
/ Insulin
/ Insulin-Secreting Cells - drug effects
/ Insulin-Secreting Cells - metabolism
/ Male
/ Mice
/ NAD(P)H Dehydrogenase (Quinone) - genetics
/ NAD(P)H Dehydrogenase (Quinone) - metabolism
/ NF-E2-Related Factor 2 - genetics
/ NF-E2-Related Factor 2 - metabolism
/ Oxidative Stress - drug effects
/ Polyuria
/ Proteins
/ Signal Transduction - drug effects
/ Urine
