Farnesylthiosalicylic Acid Through Inhibition of Galectin‐3 Improves Neuroinflammation in Alzheimer Disease via Multiple Pathways DOI Creative Commons

Qing Qiu,

Li Cui, Xiaoli Zhao

и другие.

CNS Neuroscience & Therapeutics, Год журнала: 2024, Номер 30(11)

Опубликована: Ноя. 1, 2024

Many factors affect the neuroinflammatory response in patients with Alzheimer disease (AD). Galectin-3 (Gal-3) is closely related to microglial activation nervous system and can promote aggregation of cancer cells tumors. This study aimed investigate mechanism by which farnesylthiosalicylic acid (FTS) affects neuroinflammation Aβ1-42 mice through Gal-3. We used Morris water maze, reverse transcription-polymerase chain reaction (RT-PCR), Western blotting, enzyme-linked immunosorbent assay (ELISA), immunofluorescence conduct our study. FTS reduced levels proinflammatory mice. inhibited total membrane expression Gal-3 mice, anti-inflammatory effect was reversed Gal-3-adeno-associated viral (AAV). toll-like receptors (TLRs), effects that were Gal-3-AAV. Moreover, ameliorated Aβ oligomerization accumulation also FTS, inhibition Gal-3-c-Jun N-terminal kinase (JNK) pathway, PS1 expression; addition, increased Aβ-degrading enzymes FTS-induced improvements cognition may inhibiting reduce TLR4 CD14 alleviate pathology, downregulating Aβ-stimulated TLR2, TLR4, expression, thus

Язык: Английский

Unravelling neuroregenerative and neuroprotective roles of Wnt/β-catenin pathway in ischemic stroke: Insights into molecular mechanisms DOI

Srikanth Yadava,

Dontiboina Harikrishna Reddy,

Venkata Prasuja Nakka

и другие.

Neuroscience, Год журнала: 2024, Номер unknown

Опубликована: Дек. 1, 2024

Язык: Английский

Процитировано

6
Decoding NLRP3 Inflammasome Activation in Alzheimer’s Disease: A Focus on Receptor Dynamics DOI

Ranika Maurya,

Abha Sharma,

Saba Naqvi

и другие.

Molecular Neurobiology, Год журнала: 2025, Номер unknown

Опубликована: Апрель 15, 2025

Язык: Английский

Процитировано

0
Farnesylthiosalicylic Acid Through Inhibition of Galectin‐3 Improves Neuroinflammation in Alzheimer Disease via Multiple Pathways DOI Creative Commons

Qing Qiu,

Li Cui, Xiaoli Zhao

и другие.

CNS Neuroscience & Therapeutics, Год журнала: 2024, Номер 30(11)

Опубликована: Ноя. 1, 2024

Many factors affect the neuroinflammatory response in patients with Alzheimer disease (AD). Galectin-3 (Gal-3) is closely related to microglial activation nervous system and can promote aggregation of cancer cells tumors. This study aimed investigate mechanism by which farnesylthiosalicylic acid (FTS) affects neuroinflammation Aβ1-42 mice through Gal-3. We used Morris water maze, reverse transcription-polymerase chain reaction (RT-PCR), Western blotting, enzyme-linked immunosorbent assay (ELISA), immunofluorescence conduct our study. FTS reduced levels proinflammatory mice. inhibited total membrane expression Gal-3 mice, anti-inflammatory effect was reversed Gal-3-adeno-associated viral (AAV). toll-like receptors (TLRs), effects that were Gal-3-AAV. Moreover, ameliorated Aβ oligomerization accumulation also FTS, inhibition Gal-3-c-Jun N-terminal kinase (JNK) pathway, PS1 expression; addition, increased Aβ-degrading enzymes FTS-induced improvements cognition may inhibiting reduce TLR4 CD14 alleviate pathology, downregulating Aβ-stimulated TLR2, TLR4, expression, thus

Язык: Английский

Процитировано

0