[This corrects the article DOI: 10.1371/journal.pone.0023703.].
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5874069 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0195246 | PLOS |
Publication Analysis
Top Keywords
Similar Publications
[Curcumin prevents the arsenic-induced neuroimmune injury through JAK2/STAT3 pathway].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
December 2024
Department of Toxicology, School of Public Health, Shenyang Medical College, Shenyang 110034, China. *Corresponding author, E-mail:
Objective To investigate the protective effect of curcumin (Cur) against arsenic-induced neuroimmune toxicity and the underlying molecular mechanisms in vivo. Methods Eighty SPF female C57BL/6 mice were randomly assigned to four groups: a control group, an arsenic-treated group, a Cur-treated group and an arsenic+Cur group, with 20 mice in each group. The control group received distilled water; the arsenic-treated group was given 50 mg/L NaAsO in the drinking water; the Cur-treated group was gavaged with 200 mg/kg of curcumin for 45 days; and the arsenic+Cur group received distilled water and was gavaged with 200 mg/kg of curcumin.
View Article and Find Full Text PDFThe Neuroprotective Effects of Caffeine in a Neonatal Hypoxia-Ischemia Model are Regulated through the AMPK/mTOR Pathway.
Int J Biol Sci
January 2025
Department of Neonatology and Pediatric Intensive Care, Children's Hospital University of Bonn, Bonn, Germany.
Article Synopsis
- Neonatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of death and disability in newborns, and caffeine has shown promise in mitigating its effects.
- In a neonatal rat model, caffeine administration post-injury reduced brain damage and inflammation compared to controls, highlighting its potential benefits.
- The study found that caffeine influences the AMPK/mTOR pathway, suggesting that targeting this pathway could enhance neuroprotection and improve outcomes for HIE, especially in regions lacking sufficient resources for treatment.
Author Correction: π-HuB: the proteomic navigator of the human body.
Nature
December 2024
State Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, China.
Crosstalk between mitochondrial homeostasis and AMPK pathway mediate the receptor-mediated cardioprotective effects of estradiol in ovariectomized female rats.
PLoS One
December 2024
Department of Biochemistry, Medical Research Institute, Alexandria University, Alexandria, Egypt.
Estrogen (E2) deficiency is a risk factor for cardiovascular disease (CVD), however, the exact mechanism for the E2 protective effect on CVD remains unclear. This study aimed to investigate the estrogen receptor (ER) and non-receptor mediated effects of E2 treatment on the cardiac expression of adenosine monophosphate-dependent protein kinase (AMPK), autophagic, mitophagy and mitochondrial homeostasis-regulating genes in ovariectomized (OVX) rats. Female rats were divided into two main groups; sham and bilaterally OVX rats, then each group was subdivided into four subgroups according to treatment; untreated, subcutaneously treated with E2 (30 μg/kg), or Fulvestrant (F) (5 mg/Kg), or a combination of both drugs for 28 days.
View Article and Find Full Text PDFChaperone Activators.
Subcell Biochem
December 2024
Department of Biotechnology Engineering, ORT Braude College, Karmiel, Israel.
Ageing is a complex yet universal and inevitable degenerative process that results in a decline in the cellular capacity for repair and adaptation to external stresses. Therefore, maintaining the appropriate balance of the cellular proteome is crucial. In addition to the ubiquitin-proteasome and autophagy-lysosomal systems, molecular chaperones play a vital role in a sophisticated protein quality control system.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!