Neuroprotective effects and mechanisms of the YiQiWenYangSanHan formula on Parkinson's disease mice DOI Creative Commons
Jinling Liu, Dong Di,

Suping Sun

и другие.

IBRO Neuroscience Reports, Год журнала: 2025, Номер 18, С. 528 - 538

Опубликована: Апрель 5, 2025

Parkinson's disease (PD) is a complex neurodegenerative disease, which often treated with obvious side effects such as dopamine replacement therapy. Our team has validated the unique advantages of traditional Chinese medicine formula, YiQiWenYangSanHan formula (YQWYSHF), through in vitro experiments, confirming its therapeutic potential for PD. Nevertheless, further research and validation are required to fully understand protective underlying mechanisms against This study employed an vivo model investigate YQWYSHF on motor impairments, neuroinflammation, mitochondrial dysfunction C57BL/6 J mice caused by MPTP. Sixty were randomly divided into 5 groups, all groups except control group intraperitoneally administered MPTP 7 days (30 mg/kg). After 4 weeks drug intragastric treatment, we assessed dyskinesia different doses behavioral examination. Additionally, immunofluorescence was used examine expression ionized calcium binding adaptor protein 1 (IBA1) glial fibrillary acidic protein-positive (GFAP) cells. Western blotting assess level tyrosine hydroxylase (TH), pyrin domain-containing 3 (NLRP3), apoptosis-associated speck-like proteins (ASC), cysteine-containing aspartate protease-1 (Caspase-1), interleukin-1β (IL-1β), α-synuclein (α-syn), poly (ADP-ribose) polymerase (PARP1), ADP ribose (PAR). Furthermore, transmission electron microscopy revealed impairment neuronal cells substantia nigra (SN). treatment alleviated mouse Moreover, it increased TH expression, could reverse increase IBA1, GFAP, NLRP3, ASC, caspase-1,IL-1β, α-syn, PARP1 PAR induced protects dopaminergic neurons PD attenuating neuroinflammation dysfunction. provides new evidence clinical application

Язык: Английский

The roles of mitochondria in global and local intracellular calcium signalling DOI
Benjamín Cartes-Saavedra, Arijita Ghosh, György Hajnóczky

и другие.

Nature Reviews Molecular Cell Biology, Год журнала: 2025, Номер unknown

Опубликована: Янв. 27, 2025

Язык: Английский

Процитировано

3
CCAAT/Enhancer-Binding Protein Beta Nitration Participates in Hyperhomocysteinemia-Induced Cardiomyocyte Autophagic Flux Blockage by Inhibiting Transcription Factor EB Transcription DOI
Jiayin Chai, Jiahui Xu, Shangyue Zhang

и другие.

Antioxidants and Redox Signaling, Год журнала: 2025, Номер unknown

Опубликована: Янв. 9, 2025

Aims: Autophagy is a protective mechanism of cardiomyocytes. Hyperhomocysteinemia (HHcy) elevates oxidative and nitrosative stress levels, leading to an abnormal increase in nitration protein, possibly autophagy regulation However, the regulatory effect HHcy on at post-translational modification level still unclear. Here, we aimed explore transcription factor EB (TFEB) CCAAT/enhancer-binding protein beta (C/EBPβ), transcriptional repressor Tfeb,

Язык: Английский

Процитировано

0
Novel strategies targeting mitochondria-lysosome contact sites for the treatment of neurological diseases DOI Creative Commons
Yinyin Xie,

Wenlin Sun,

Aoya Han

и другие.

Frontiers in Molecular Neuroscience, Год журнала: 2025, Номер 17

Опубликована: Янв. 14, 2025

Mitochondria and lysosomes are critical for neuronal homeostasis, as highlighted by their dysfunction in various neurological diseases. Recent studies have identified dynamic membrane contact sites between mitochondria lysosomes, independent of mitophagy the lysosomal degradation mitochondrial-derived vesicles (MDVs), allowing bidirectional crosstalk these cell compartments, regulation organelle networks, substance exchanges. Emerging evidence suggests that abnormalities mitochondria-lysosome (MLCSs) contribute to diseases, including Parkinson’s disease, Charcot–Marie-Tooth (CMT) storage epilepsy. This article reviews recent research advances regarding tethering processes, regulation, function MLCSs role

Язык: Английский

Процитировано

0
Tracking spatiotemporal distribution of organelle contacts in vivo with SPLICS reporters DOI Creative Commons
Lucia Barazzuol,

Tetiana Tykhonenko,

T. Griffiths

и другие.

Cell Death and Disease, Год журнала: 2025, Номер 16(1)

Опубликована: Март 27, 2025

Abstract Organelle contact sites are crucial for cellular function, enabling the exchange of lipids, ions, and other molecules between different organelles. The ability to track these in vivo has been significantly advanced by development SPLICS (Split-GFP-based Contact Site Sensors) reporters, which have provided unprecedented insights into intricate network organelle communication. This innovative powerful tool allows real-time visualization interactions living cells thus unraveling complexity their dynamic context homeostasis. Recent studies highlighted nature either terms tethering/untethering movement itself time space: whether unique temporal behaviors site-specific dynamics exist is currently unknown. In this study, we investigated spatiotemporal distribution various using time-lapse vitro imaging discovered an evolutionarily conserved pattern among sites, influenced specific partner organelles involved. These findings highlight importance spatial regulation at may underlie diverse physiological functions. discovery opens new avenues understanding health disease, with potential implications developing targeted therapeutic strategies.

Язык: Английский

Процитировано

0
Neuroprotective effects and mechanisms of the YiQiWenYangSanHan formula on Parkinson's disease mice DOI Creative Commons
Jinling Liu, Dong Di,

Suping Sun

и другие.

IBRO Neuroscience Reports, Год журнала: 2025, Номер 18, С. 528 - 538

Опубликована: Апрель 5, 2025

Parkinson's disease (PD) is a complex neurodegenerative disease, which often treated with obvious side effects such as dopamine replacement therapy. Our team has validated the unique advantages of traditional Chinese medicine formula, YiQiWenYangSanHan formula (YQWYSHF), through in vitro experiments, confirming its therapeutic potential for PD. Nevertheless, further research and validation are required to fully understand protective underlying mechanisms against This study employed an vivo model investigate YQWYSHF on motor impairments, neuroinflammation, mitochondrial dysfunction C57BL/6 J mice caused by MPTP. Sixty were randomly divided into 5 groups, all groups except control group intraperitoneally administered MPTP 7 days (30 mg/kg). After 4 weeks drug intragastric treatment, we assessed dyskinesia different doses behavioral examination. Additionally, immunofluorescence was used examine expression ionized calcium binding adaptor protein 1 (IBA1) glial fibrillary acidic protein-positive (GFAP) cells. Western blotting assess level tyrosine hydroxylase (TH), pyrin domain-containing 3 (NLRP3), apoptosis-associated speck-like proteins (ASC), cysteine-containing aspartate protease-1 (Caspase-1), interleukin-1β (IL-1β), α-synuclein (α-syn), poly (ADP-ribose) polymerase (PARP1), ADP ribose (PAR). Furthermore, transmission electron microscopy revealed impairment neuronal cells substantia nigra (SN). treatment alleviated mouse Moreover, it increased TH expression, could reverse increase IBA1, GFAP, NLRP3, ASC, caspase-1,IL-1β, α-syn, PARP1 PAR induced protects dopaminergic neurons PD attenuating neuroinflammation dysfunction. provides new evidence clinical application

Язык: Английский

Процитировано

0