Multifactor Analyses of Frontal Cortex Lipids in the APP/PS1 Model of Familial Alzheimer’s Disease Reveal Anomalies in Responses to Dietary n-3 PUFA and Estrogenic Treatments DOI Open Access
Mario Dı́az

Genes, Год журнала: 2024, Номер 15(6), С. 810 - 810

Опубликована: Июнь 19, 2024

Brain lipid homeostasis is an absolute requirement for proper functionality of nerve cells and neurological performance. Current evidence demonstrates that alterations are linked to neurodegenerative diseases, especially Alzheimer's disease (AD). The complexity the brain lipidome its metabolic regulation has hampered identification critical processes associated with onset progression AD. While most experimental studies have focused on effects known factors development pathological hallmarks in AD, e.g., amyloid deposition, tau protein neurofibrillary tangles, neuroinflammation, etc., addressing causative remain largely unexplored. In present study, we used a multifactor approach combining diets containing different amounts polyunsaturated fatty acids (PUFAs), estrogen availabilities, genetic backgrounds, i.e., wild type (WT) APP/PS1 (FAD), analyze phenotype frontal cortex middle-aged female mice. First, observed severe n-3 PUFA deficiency impacts long-chain (LCPUFA) composition, yet it was notably mitigated by hepatic de novo synthesis. n-6 LCPUFAs, ether-linked acids, saturates were also changed dietary condition, but extent changes dependent background hormonal condition. Likewise, phospholipids mostly modified genotype (FAD>WT) nuanced from treatment. Cholesterol (but not sterol esters) (WT>FAD) condition (higher DHA-free conditions, WT mice). However, treatment relation phospholipid remodeling genotype-dependent manner. Analyses lipid-derived variables indicate cell membrane biophysics significantly affected three factors, lower microviscosity fluidity) values obtained FAD animals. conclusion, our analyses revealed genotype, diet, status modulate cortex, both as independent through their interactions. Altogether, outcomes point potential strategies based interventions aimed at stabilizing composition neuropathology.

Язык: Английский

Ferroptosis in Cancer Therapy: Mechanisms, Small Molecule Inducers, and Novel Approaches DOI Creative Commons

YiLin Luo,

Xin Yue Bai,

L.J. Zhang

и другие.

Drug Design Development and Therapy, Год журнала: 2024, Номер Volume 18, С. 2485 - 2529

Опубликована: Июнь 1, 2024

Abstract: Ferroptosis, a unique form of programmed cell death, is initiated by an excess iron accumulation and lipid peroxidation-induced damage. There growing body evidence indicating that ferroptosis plays critical role in the advancement tumors. The increased metabolic activity higher levels tumor cells make them particularly vulnerable to ferroptosis. As result, targeted induction becoming increasingly promising approach for cancer treatment. This review offers overview regulatory mechanisms ferroptosis, delves into mechanism action traditional small molecule inducers their effects on various In addition, latest progress inducing using new means such as proteolysis-targeting chimeras (PROTACs), photodynamic therapy (PDT), sonodynamic (SDT) nanomaterials summarized. Finally, this discusses challenges opportunities development ferroptosis-inducing agents, focusing discovering targets, improving selectivity, reducing toxic side effects. Keywords: inducers, molecules, PROTACs, PDT, SDT,

Язык: Английский

Процитировано

8
Bioactive Compounds Protect Mammalian Reproductive Cells from Xenobiotics and Heat Stress-Induced Oxidative Distress via Nrf2 Signaling Activation: A Narrative Review DOI Creative Commons
Muhammad Zahoor Khan, Adnan Khan,

Bingjian Huang

и другие.

Antioxidants, Год журнала: 2024, Номер 13(5), С. 597 - 597

Опубликована: Май 13, 2024

Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and body’s antioxidant defenses. It poses a significant threat to physiological function reproductive cells. Factors such as xenobiotics heat can worsen this stress, leading cellular damage apoptosis, ultimately decreasing efficiency. The nuclear factor erythroid 2–related 2 (Nrf2) signaling pathway plays crucial role in defending against oxidative protecting cells via enhancing responses. Dysregulation Nrf2 has been associated with infertility suboptimal performance mammals. Recent advancements therapeutic interventions have underscored critical mitigating restoring functional integrity In narrative review, we delineate harmful effects xenobiotic-induced on explain how provides protection these challenges. studies shown that activating using various bioactive compounds ameliorate distress apoptosis mammalian By comprehensively analyzing existing literature, propose key target for caused by exposure xenobiotic stress. Additionally, based synthesis findings, discuss potential therapies focused improve

Язык: Английский

Процитировано

6
Molecular Mechanisms of Neuroprotection: The Interplay of Klotho, SIRT-1, Nrf2, and HO-1 in Neurological Health DOI

R.S. Rana,

R Mukherjee,

Sidharth Mehan

и другие.

Behavioural Brain Research, Год журнала: 2025, Номер unknown, С. 115545 - 115545

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0
Green algal polysaccharides and derivatives as potential therapeutics for metabolic diseases DOI
Yufan Qiu, Zhengxin Chen, Yong‐Guan Zhu

и другие.

Food Bioscience, Год журнала: 2024, Номер 62, С. 105310 - 105310

Опубликована: Окт. 18, 2024

Язык: Английский

Процитировано

3
Multifactor Analyses of Frontal Cortex Lipids in the APP/PS1 Model of Familial Alzheimer’s Disease Reveal Anomalies in Responses to Dietary n-3 PUFA and Estrogenic Treatments DOI Open Access
Mario Dı́az

Genes, Год журнала: 2024, Номер 15(6), С. 810 - 810

Опубликована: Июнь 19, 2024

Brain lipid homeostasis is an absolute requirement for proper functionality of nerve cells and neurological performance. Current evidence demonstrates that alterations are linked to neurodegenerative diseases, especially Alzheimer's disease (AD). The complexity the brain lipidome its metabolic regulation has hampered identification critical processes associated with onset progression AD. While most experimental studies have focused on effects known factors development pathological hallmarks in AD, e.g., amyloid deposition, tau protein neurofibrillary tangles, neuroinflammation, etc., addressing causative remain largely unexplored. In present study, we used a multifactor approach combining diets containing different amounts polyunsaturated fatty acids (PUFAs), estrogen availabilities, genetic backgrounds, i.e., wild type (WT) APP/PS1 (FAD), analyze phenotype frontal cortex middle-aged female mice. First, observed severe n-3 PUFA deficiency impacts long-chain (LCPUFA) composition, yet it was notably mitigated by hepatic de novo synthesis. n-6 LCPUFAs, ether-linked acids, saturates were also changed dietary condition, but extent changes dependent background hormonal condition. Likewise, phospholipids mostly modified genotype (FAD>WT) nuanced from treatment. Cholesterol (but not sterol esters) (WT>FAD) condition (higher DHA-free conditions, WT mice). However, treatment relation phospholipid remodeling genotype-dependent manner. Analyses lipid-derived variables indicate cell membrane biophysics significantly affected three factors, lower microviscosity fluidity) values obtained FAD animals. conclusion, our analyses revealed genotype, diet, status modulate cortex, both as independent through their interactions. Altogether, outcomes point potential strategies based interventions aimed at stabilizing composition neuropathology.

Язык: Английский

Процитировано

1