BuyangHuanwu Decoction alleviates Endothelial Cell Apoptosis and Coronary Microvascular Dysfunction via Regulation of the MAPKK4/p38 Signaling Axis DOI Creative Commons

Xing Chang,

Dan Wu, Xin Gao

и другие.

International Journal of Medical Sciences, Год журнала: 2024, Номер 21(13), С. 2464 - 2479

Опубликована: Янв. 1, 2024

MAPKK4 has been implicated in the pathological mechanisms underlying myocardial and vascular injury, specifically influencing endothelial cell damage programmed death via subcellular pathways. Nevertheless, regulatory role of coronary microvascular injury following infarction remains unconfirmed, exploration targeted mitochondrial protective therapeutic agents unaddressed. In light this gap, we established a gene-modified mouse model ischemia-reperfusion employed Buyang Huanwu decoction (BYHW), traditional cardiovascular formula, to assess its efficacy treating post-ischemia-reperfusion. The study aimed elucidate mechanism by which BYHW mitigates induced through attenuation apoptosis. Experimental outcomes revealed that high-dose significantly ameliorated post-ischemia-reperfusion, restoring structural integrity microvasculature reducing inflammation oxidative stress. Contrarily, transgenic mice overexpressing MAPKK4, intervention failed attenuate To further investigate, simulated hypoxia/reoxygenation cells using MAPKK4-related cellular gene modification model. results indicated attenuates inflammatory enhances viability hypoxic stress, inhibiting apoptosis pathway. However, overexpression MAPKK4/p38 negated effects BYHW, showing no impact on stress under conditions. Molecular interaction studies confirmed active components Astragaloside IV Ligustrazine, interact with MAPKK4/P38 axis.

Язык: Английский

Advancing Diabetic Wound Care: The Role of Copper-containing Hydrogels DOI Creative Commons

Mohammad Ebrahim Astaneh,

Narges Fereydouni

Heliyon, Год журнала: 2024, Номер 10(20), С. e38481 - e38481

Опубликована: Сен. 26, 2024

Язык: Английский

Процитировано

6
In Vitro models of leukemia development: the role of very small leukemic stem-like cells in the cellular transformation cascade DOI Creative Commons
Jan Jakub Lica, Joanna Jakóbkiewicz‐Banecka,

Andrzej Hellmann

и другие.

Frontiers in Cell and Developmental Biology, Год журнала: 2025, Номер 12

Опубликована: Янв. 3, 2025

Recent experimental findings indicate that cancer stem cells originate from transformed very small embryonic-like cells. This finding represents an essential advancement in uncovering the processes drive onset and progression of cancer. In continuously growing cell lines, for first time, our team's follow-up research on leukemia, lung cancer, healthy embryonic kidney revealed stages resembles precursor review explores origin leukemic stem-like establish We explore theoretical model acute myeloid leukemia initiation progresses through various stages, as well basing HL60 line, present its hierarchical stage development vitro, highlighting role these primitive stages. also discuss potential implications further into unique cellular advancing treatment prevention.

Язык: Английский

Процитировано

0
Hybrid hydrogel based on porcine-derived matrix with gallic acid and cerium-doped mesoporous bioactive glass for diabetic wound healing DOI Creative Commons

Haozeng,

Qinghong Lai,

Wanyou Liao

и другие.

Materials & Design, Год журнала: 2025, Номер unknown, С. 113714 - 113714

Опубликована: Фев. 1, 2025

Язык: Английский

Процитировано

0
BuyangHuanwu Decoction alleviates Endothelial Cell Apoptosis and Coronary Microvascular Dysfunction via Regulation of the MAPKK4/p38 Signaling Axis DOI Creative Commons

Xing Chang,

Dan Wu, Xin Gao

и другие.

International Journal of Medical Sciences, Год журнала: 2024, Номер 21(13), С. 2464 - 2479

Опубликована: Янв. 1, 2024

MAPKK4 has been implicated in the pathological mechanisms underlying myocardial and vascular injury, specifically influencing endothelial cell damage programmed death via subcellular pathways. Nevertheless, regulatory role of coronary microvascular injury following infarction remains unconfirmed, exploration targeted mitochondrial protective therapeutic agents unaddressed. In light this gap, we established a gene-modified mouse model ischemia-reperfusion employed Buyang Huanwu decoction (BYHW), traditional cardiovascular formula, to assess its efficacy treating post-ischemia-reperfusion. The study aimed elucidate mechanism by which BYHW mitigates induced through attenuation apoptosis. Experimental outcomes revealed that high-dose significantly ameliorated post-ischemia-reperfusion, restoring structural integrity microvasculature reducing inflammation oxidative stress. Contrarily, transgenic mice overexpressing MAPKK4, intervention failed attenuate To further investigate, simulated hypoxia/reoxygenation cells using MAPKK4-related cellular gene modification model. results indicated attenuates inflammatory enhances viability hypoxic stress, inhibiting apoptosis pathway. However, overexpression MAPKK4/p38 negated effects BYHW, showing no impact on stress under conditions. Molecular interaction studies confirmed active components Astragaloside IV Ligustrazine, interact with MAPKK4/P38 axis.

Язык: Английский

Процитировано

1