Protective Effects of Exogenous Melatonin Administration on White Fat Metabolism Disruption Induced by Aging and a High-Fat Diet in Mice DOI Creative Commons

Dongying Lv,

Yujie Ren,

Jiayan Chen

и другие.

Antioxidants, Год журнала: 2024, Номер 13(12), С. 1500 - 1500

Опубликована: Дек. 9, 2024

Obesity has emerged as a major risk factor for human health, exacerbated by aging and changes in dietary habits. It represents significant health challenge, particularly older people. While numerous studies have examined the effects of obesity on fat metabolism independently, research their combined is limited. In present study, protective action against white accumulation after high-fat diet (HFD) exerted exogenous melatonin, circadian hormone endowed with antioxidant properties also involved metabolism, was investigated mouse model. For this purpose, battery tests applied before melatonin treatments animals, including epididymal adipose tissue (eWAT) histological evaluations, transcriptomic lipidomic analyses, real-time PCR tests, immunofluorescence staining, Western blot, appraisal serum levels, transmission electron microscopy. This study found that aged mice showed increased lipid deposition, inflammation, reduced glutathione (GSH) levels compared to younger mice. Lipidomic analyses revealed elevated triglycerides, diglycerides, ceramides, cholesterol, along decreased sphingomyelin fatty acids eWAT. The genes linked NF-κB signaling, autophagy, pathways, were significantly altered. HFD exhibited Melatonin supplementation GSH upregulated AANAT MTNR1A expression eWAT, suggesting alleviates eWAT damage via pathway. suppressed inflammatory markers (e.g., TNF-α, NLRP3, NF-κB, IL-1β, CEBPB) preserved mitochondrial function through enhanced mitophagy. highlights how affect gene expression, offering potential intervention strategies. These findings provide important insights into mechanisms deposition associated diet,

Язык: Английский

Phytochemicals Targeting Mitophagy to Treat Heart Diseases: Retrospective Insights and Prospective Directions DOI Open Access
Qin Dong, Yi Zhu,

Xinghai Zhang

и другие.

Phytotherapy Research, Год журнала: 2025, Номер unknown

Опубликована: Фев. 6, 2025

ABSTRACT Mitophagy is a process by which cells selectively eliminate damaged or dysfunctional mitochondria through the autophagy–lysosome pathway, thereby maintaining mitochondrial quality and cellular homeostasis. This closely linked to onset progression of various heart diseases. Modern pharmacological research has demonstrated that phytochemicals can regulate homeostasis in cardiomyocytes multiple mechanisms, influencing mitophagy protecting cardiomyocytes, turn exerts anti‐cardiovascular effects. However, underlying mechanisms these effects are not yet fully understood. study summarizes molecular diseases, aiming provide reference for treatment targeting against The results indicated (such as Berberine, Ginsenoside Rg1, Quercetin, Resveratrol, Baicalein, so on) exert preventive therapeutic on diseases cardiac toxicity damage, myocardial ischemia/reperfusion injury, failure, aging, hypertrophy, cardiomyopathy, on.) via regulating PINK1/Parkin FUNDC1‐dependent pathway. These compounds mainly their homeostasis, dynamics, oxidative stress, apoptosis, energy metabolism. provides have effect mitophagy. further in‐depth mechanistic clinical needed future.

Язык: Английский

Процитировано

0

pH-Induced Conformational Change of the Chromophore of the Large Stokes Shift Fluorescent Protein tKeima DOI Creative Commons
Yongbin Xu,

Yun Gyo Seo,

In Jung Kim

и другие.

Molecules, Год журнала: 2025, Номер 30(7), С. 1623 - 1623

Опубликована: Апрель 5, 2025

Fluorescent proteins (FPs) are widely used as optical probes in molecular and cell biology. tKeima is a tetrameric, large Stokes shift red fluorescent protein the ancestral of mt-Keima, which applied pH-sensitive probe. While pH sensitivity mt-Keima well characterized, pH-dependent properties have not been comprehensively elucidated. To obtain better understanding effects on tKeima, its emission intensity at various levels was measured, crystal structure 4.0 determined resolution 2.2 Å. The fluorescence decreased by approximately 65% compared with peak 10.0. revealed both cis trans conformations chromophore, contrast to previously structures 8.0, showed only conformation. This indicates that induces conformational change chromophore tKeima. Both were stabilized hydrogen bonds neighboring residues. A comparison basic pH, mKeima, highlights unique structural properties. These results provide deeper basis for pH-induced changes Keima family.

Язык: Английский

Процитировано

0

Exosomes-mediated delivery of miR-486-3p alleviates neuroinflammation via SIRT2-mediated inhibition of mitophagy after subarachnoid hemorrhage DOI Creative Commons
Bin Sheng, Sen Gao,

Xiangxin Chen

и другие.

Stroke and Vascular Neurology, Год журнала: 2024, Номер unknown, С. svn - 003509

Опубликована: Окт. 2, 2024

Background Neuroinflammation participates in the pathogenesis of subarachnoid haemorrhage (SAH); however, no effective treatments exist. MicroRNAs regulate several aspects neuronal dysfunction. In a previous study, we found that exosomal miR-486-3p is involved pathophysiology SAH. Targeted delivery without blood-brain barrier (BBB) restriction to alleviate SAH promising neuroinflammation approach. Methods this modified exosomes (Exo) form an RVG-miR-486-3p-Exo (Exo/miR) achieve targeted brain. Neurological scores, brain water content, BBB damage, flow cytometry and FJC staining were used determine effect on Western blot analysis, ELISA RT-qPCR measure relevant protein mRNA levels. Immunofluorescence laser confocal detection expression mitochondria, lysosomes autophagosomes, transmission electron microscopy was observe level mitophagy tissue mice after Results Tail vein injection Exo/miR improved targeting brains mice. The reduced levels neuroinflammation-related factors by changing phenotype switching microglia, inhibiting sirtuin 2 (SIRT2) enhancing mitophagy. treatment alleviated neurobehavioral disorders, oedema, damage neurodegeneration. Further research mechanism achieved regulating acetylation peroxisome proliferator-activated receptor γ coactivator l alpha (PGC-1α) SIRT2 enters nucleus. Conclusion attenuates stimulating mitophagy, suggesting potential clinical applications.

Язык: Английский

Процитировано

2

Acute hyperglycemia exacerbates neuroinflammation and cognitive impairment in sepsis-associated encephalopathy by mediating the ChREBP/HIF-1α pathway DOI Creative Commons
Peng Yao, Ling Wu, Hao Yao

и другие.

European journal of medical research, Год журнала: 2024, Номер 29(1)

Опубликована: Ноя. 14, 2024

Delirium is a prominent symptom of sepsis-associated encephalopathy (SAE) and highly prevalent in septic patients hospitalized the intensive care unit, being closely connected with raised mortality rates. Acute hyperglycemia (AH) has been recognized as separate risk factor for delirium worse prognosis critically sick patients. Nevertheless, exact contribution AH to advancement SAE still unknown. This research retrospectively evaluated connection between blood glucose levels (BGLs) incidence death rates ICU tertiary comprehensive hospital. In addition, rat model was induced through cecal ligation puncture (CLP), after which continuous infusion promptly initiated via central venous catheter post-surgery evaluate potential implications on SAE. Next, rats were assigned four groups based target BGLs: high group (HG, ≥ 300 mg/dL), moderate (MG, 200–300 normal (NG, < 200 insulin-treated (HI, mg/dL) receiving recombinant human insulin treatment (0.1 IU/kg/min). The sham (SG) received an equivalent volume saline denoted NG group. effects neuroinflammation cognitive function using behavioral tests, histopathological examination, TUNEL staining, ELISA, Western blot. microglial activation metabolism following lipopolysaccharide (LPS, 1 μg/mL) exposure assessed CCK8 assay, qRT-PCR, blot, ELISA. Our findings revealed that during sepsis assisted predicting occurrence. systemic inflammatory cytokines rats, promoting neuronal apoptosis, blood–brain barrier disruption, impairment. both vivo vitro, elevated challenge increased ChREBP, HIF-1α, glycolytic enzymes, expressions microglia CLP or LPS. These results collectively suggest can exacerbate by enhancing glycolysis under conditions, potentially mediated upregulation ChREBP/HIF-1α signaling pathway.

Язык: Английский

Процитировано

2

Macrophage polarization in sepsis: Emerging role and clinical application prospect DOI
Fei Hou, Jun Mi, Qiong Wang

и другие.

International Immunopharmacology, Год журнала: 2024, Номер 144, С. 113715 - 113715

Опубликована: Дек. 3, 2024

Язык: Английский

Процитировано

0

Protective Effects of Exogenous Melatonin Administration on White Fat Metabolism Disruption Induced by Aging and a High-Fat Diet in Mice DOI Creative Commons

Dongying Lv,

Yujie Ren,

Jiayan Chen

и другие.

Antioxidants, Год журнала: 2024, Номер 13(12), С. 1500 - 1500

Опубликована: Дек. 9, 2024

Obesity has emerged as a major risk factor for human health, exacerbated by aging and changes in dietary habits. It represents significant health challenge, particularly older people. While numerous studies have examined the effects of obesity on fat metabolism independently, research their combined is limited. In present study, protective action against white accumulation after high-fat diet (HFD) exerted exogenous melatonin, circadian hormone endowed with antioxidant properties also involved metabolism, was investigated mouse model. For this purpose, battery tests applied before melatonin treatments animals, including epididymal adipose tissue (eWAT) histological evaluations, transcriptomic lipidomic analyses, real-time PCR tests, immunofluorescence staining, Western blot, appraisal serum levels, transmission electron microscopy. This study found that aged mice showed increased lipid deposition, inflammation, reduced glutathione (GSH) levels compared to younger mice. Lipidomic analyses revealed elevated triglycerides, diglycerides, ceramides, cholesterol, along decreased sphingomyelin fatty acids eWAT. The genes linked NF-κB signaling, autophagy, pathways, were significantly altered. HFD exhibited Melatonin supplementation GSH upregulated AANAT MTNR1A expression eWAT, suggesting alleviates eWAT damage via pathway. suppressed inflammatory markers (e.g., TNF-α, NLRP3, NF-κB, IL-1β, CEBPB) preserved mitochondrial function through enhanced mitophagy. highlights how affect gene expression, offering potential intervention strategies. These findings provide important insights into mechanisms deposition associated diet,

Язык: Английский

Процитировано

0