Oral administration of butylated hydroxytoluene induces neuroprotection in a streptozotocin-induced rat Alzheimer’s disease model via inhibition of neuronal ferroptosis DOI Creative Commons

Parisa Faraji,

Elham Parandavar,

Hartmut Kühn

и другие.

Molecular Medicine, Год журнала: 2024, Номер 30(1)

Опубликована: Ноя. 8, 2024

Alzheimer's disease (AD) is the most common human neurodegenerative disorder worldwide. Owing to its chronic nature, our limited understanding of pathophysiological mechanisms, and because lack effective anti-AD drugs, AD represents a significant socio-economic challenge for all industrialized countries. Neuronal cell death key factor in pathogenesis recent studies have suggested that neuronal ferroptosis may play major patho-physiological role. Since involves free radical-mediated lipid peroxidation, we hypothesized enteral administration radical scavenger butylated hydroxytoluene (BHT) might slow down or even prevent development AD-related symptoms an vivo animal model.

Язык: Английский

Swietenolide inhibits the TXNIP/NLRP3 pathways via Nrf2 activation to ameliorate cognitive dysfunction in diabetic mice DOI
Xinyue Song, Shunwu Fan,

Yuetong Gao

и другие.

Neuropharmacology, Год журнала: 2025, Номер unknown, С. 110312 - 110312

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0

Artemisinin antagonizes cognitive disorder in hyperuricemia through glutamate receptor-interacting protein 1-suppressed pyroptosis DOI
Yanfang Chen, Shuangxi Chen, Huiqing Wang

и другие.

Neuroreport, Год журнала: 2025, Номер unknown

Опубликована: Янв. 6, 2025

The prevalence of hyperuricemia (HUA) is climbing worldwide and persistent elevation serum uric acid impairs cognitive function. This study aimed to explore the mechanisms Artemisinin (Art) antagonizing disorder in HUA by suppressing pyroptosis. A mouse model was established intraperitoneal injection 300 mg/kg potassium oxonate (PO) C57BL/6 mice for 14 days. were simultaneously treated with Art, an agonist pyroptosis Polyphyllin VI (PPVI), or glutamate receptor-interacting protein 1 (GRIP1) knockdown lentiviral plasmid. After treatment, acid, IL-6, TNF-ɑ levels examined, as well hippocampal IL-1β IL-18 levels, function assessed Morris water maze test. Pathological changes CA1 hippocampus observed. Cleave-caspase-1, GSDMD-N, GRIP1 level quantified western blot. PO induction, escape latency time spent target quadrant increased mice, cell arrangement loose disorganized, obvious inflammatory infiltration serious damage being observed, had elevated cleaved-caspase-1, IL-1β, IL-18. Art treatment reduced improved mice. Administration PPVI aggravated Art-treated dysfunction inhibiting through upregulation GRIP1. blunts suffering from upregulating

Язык: Английский

Процитировано

0

Flotillin- 1 ameliorates experimental diabetic retinopathy by inhibiting ferroptosis in blood-retinal barrier DOI
Jie Zhang,

Ke Chang,

Yanyu Shangguan

и другие.

Journal of Molecular Medicine, Год журнала: 2025, Номер unknown

Опубликована: Апрель 8, 2025

Язык: Английский

Процитировано

0

Trelagliptin Ameliorates Memory Decline in Diabetic Rats through the AMPK/AKT/GSK-3β Pathway in the Cerebral Cortex DOI Creative Commons

Yue Yao,

Ting Shu,

Xiying Guo

и другие.

ACS Omega, Год журнала: 2025, Номер unknown

Опубликована: Апрель 11, 2025

Язык: Английский

Процитировано

0

Electroacupuncture Ameliorates Chronic Inflammatory Pain and Depression Comorbidity by Inhibiting Nrf2-Mediated Ferroptosis in Hippocampal Neurons DOI
Guanghua Liu, Di Liu, Dongliang Shi

и другие.

Neurochemical Research, Год журнала: 2025, Номер 50(3)

Опубликована: Апрель 21, 2025

Язык: Английский

Процитировано

0

Effective protective mechanisms of HO-1 in diabetic complications: a narrative review DOI Creative Commons
Jingjing Zhang, Ping Ni, Yi Song

и другие.

Cell Death Discovery, Год журнала: 2024, Номер 10(1)

Опубликована: Окт. 10, 2024

Diabetes mellitus is a metabolic disorder with persistent hyperglycemia caused by variety of underlying factors. Chronic can lead to diverse serious consequences and diversified complications, which pose threat patients. Among the major complications are cardiovascular disease, kidney diabetic foot ulcers, retinopathy, neurological disorders. Heme oxygenase 1 (HO-1) protective enzyme antioxidant, anti-inflammatory anti-apoptotic effects, has been intensively studied plays an important role in complications. By inducing expression activity HO-1, it enhance anti-inflammatory, capacity tissues, thus reduce degree damage The present study aims review relationship between HO-1 pathogenesis diabetes its involved regulation macrophage polarization promotes M1 state (pro-inflammatory) towards M2 (anti-inflammatory). Induction dendritic cells inhibits them maturation secretion pro-inflammatory cytokines regulatory T cell (T

Язык: Английский

Процитировано

2

Neuroprotective effects of traditional Chinese medicine Naofucong on diabetic cognitive impairment: Mechanisms involving insulin-degrading enzyme-mediated degradation of Amyloid-β and inhibition of ERK/JNK/p38 MAPK signaling pathway DOI Creative Commons

Yue Tian,

Guangchan Jing,

Ruiying Yin

и другие.

Brain Research, Год журнала: 2024, Номер unknown, С. 149365 - 149365

Опубликована: Ноя. 1, 2024

Язык: Английский

Процитировано

2

Different Types of Cell Death in Diabetic Neuropathy: A Focus on Mechanisms and Therapeutic Strategies DOI Open Access

Ye Shang,

Zilin Cheng,

Dongye Zhuo

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(15), С. 8126 - 8126

Опубликована: Июль 25, 2024

Diabetic neuropathy (DN) is a common complication of diabetes, affecting over 50% patients, leading to significant pain and burden. Currently, there are no effective treatments available. Cell death considered key factor in promoting the progression DN. This article reviews how cell initiated DN, emphasizing critical roles oxidative stress, mitochondrial dysfunction, inflammation, endoplasmic reticulum autophagy. Additionally, we thoroughly summarize mechanisms that may be involved pathogenesis including apoptosis, autophagy, pyroptosis, ferroptosis, among others, as well potential therapeutic targets offered by these mechanisms. provides pathways for prevention treatment diabetic future.

Язык: Английский

Процитировано

1

The Potential Role of Artemisinins Against Neurodegenerative Diseases DOI
Lei Xia,

Yiqiong Qiu,

Junjie Li

и другие.

The American Journal of Chinese Medicine, Год журнала: 2024, Номер unknown, С. 1 - 20

Опубликована: Сен. 30, 2024

Artemisinin (ART) and its derivatives, collectively referred to as artemisinins (ARTs), have been approved for the treatment of malaria decades. ARTs are converted into dihydroartemisinin (DHA), only active form, which is reductive in vivo. In this review, we provide a brief overview neuroprotective potential underlying mechanisms on several most common neurodegenerative diseases, particularly considering their application those associated with cognitive motor impairments including Alzheimer’s disease (AD), Parkinson’s (PD), Huntington’s (HD), amyotrophic lateral sclerosis (ALS). act autophagy balancers alleviate AD PD. They inhibit neuroinflammatory responses by regulating phosphorylation signal transduction proteins, such AKT, PI3K, ERK, NF-[Formula: see text]B, p38 MAPK, I[Formula: text]B[Formula: text]. addition, regulate GABAergic signaling dose-dependent manner. Although they competitively binding gephyrin receptors, low doses enhance signaling. can also ferroptosis, activate Akt/Bcl-2, AMPK, or ERK/CREB pathways reduce oxidative stress, maintain mitochondrial homeostasis, protecting neurons from stress injury. More importantly, structurally combine suppress [Formula: text]-Amyloid (A[Formula: text]-induced neurotoxicity, P-tau, O-GlcNAcylation/Phosphorylation balance, leading relieved pathological changes diseases. Collectively, these natural properties endow unique

Язык: Английский

Процитировано

1

Neuronal protective effect of Artemisinin in ischemic stroke: Achieved by blocking lysine demethylase 1A-mediated demethylation of sphingosine kinase 2 DOI
He Li, Ying Li,

Ying-Ju Wang

и другие.

Brain Research, Год журнала: 2024, Номер 1849, С. 149442 - 149442

Опубликована: Дек. 31, 2024

Язык: Английский

Процитировано

1