Electroacupuncture Attenuates Intestinal Barrier Disruption via the α7nAChR-Mediated HO-1/p38 MAPK/NF-κB Pathway in a Mouse Model of Metabolic Dysfunction-Associated Fatty Liver Disease: A Randomized, Single-Blind, Controlled Trial DOI Creative Commons
Xinghuan Wang,

Jiasen Sun,

Peng Wang

и другие.

Biomedicines, Год журнала: 2025, Номер 13(4), С. 802 - 802

Опубликована: Март 27, 2025

Background: Gut barrier integrity plays a crucial role in the pathogenesis of metabolic dysfunction-associated fatty liver disease (MAFLD). Electroacupuncture (EA) at ST-36 can ameliorate inflammatory responses via stimulating α7 nicotinic acetylcholine receptor (α7nAChR), but whether EA is effective preserving intestinal MAFLD has not been exactly illustrated. This investigation explored potential protection mechanisms targeting dismantled gut MAFLD. Methods: C57BL/6 mice were randomly allocated into several subgroups: control (CON), high-fat diet (HFD), HFD with EA, and α7nAChR inhibitor α-BGT, HO-1 knockout (KO). Body weight, visceral fat index, histopathological examination intestine determined. Serum biological indexes evaluated through corresponding kits. Furthermore, expressions HO-1, α7nAChR, barrier-associated proteins, molecular tissues assessed Western blot, RT-qPCR, immunohistology, or immunofluorescence examination. Results: treatment decreased body index gain mitigated function injury abnormal lipid indexes, exhibiting less severity hepatic steatosis, fibrosis, inflammation Lower permeability, epithelial disruption, upregulation tight junction proteins after suggested protective effects attenuating dysfunction. These abolished by α-BGT deletion. Mechanistically, markedly enriched expression phosphorylated p38 MAPK/NF-κB activation, which was lost KO treatment. Conclusions: The may be attributed to preserved barrier, thereby alleviating systemic preventing subsequent hits, where α7nAChR-mediated HO-1/p38 pathway maintain homeostasis.

Язык: Английский

Electroacupuncture Attenuates Intestinal Barrier Disruption via the α7nAChR-Mediated HO-1/p38 MAPK/NF-κB Pathway in a Mouse Model of Metabolic Dysfunction-Associated Fatty Liver Disease: A Randomized, Single-Blind, Controlled Trial DOI Creative Commons
Xinghuan Wang,

Jiasen Sun,

Peng Wang

и другие.

Biomedicines, Год журнала: 2025, Номер 13(4), С. 802 - 802

Опубликована: Март 27, 2025

Background: Gut barrier integrity plays a crucial role in the pathogenesis of metabolic dysfunction-associated fatty liver disease (MAFLD). Electroacupuncture (EA) at ST-36 can ameliorate inflammatory responses via stimulating α7 nicotinic acetylcholine receptor (α7nAChR), but whether EA is effective preserving intestinal MAFLD has not been exactly illustrated. This investigation explored potential protection mechanisms targeting dismantled gut MAFLD. Methods: C57BL/6 mice were randomly allocated into several subgroups: control (CON), high-fat diet (HFD), HFD with EA, and α7nAChR inhibitor α-BGT, HO-1 knockout (KO). Body weight, visceral fat index, histopathological examination intestine determined. Serum biological indexes evaluated through corresponding kits. Furthermore, expressions HO-1, α7nAChR, barrier-associated proteins, molecular tissues assessed Western blot, RT-qPCR, immunohistology, or immunofluorescence examination. Results: treatment decreased body index gain mitigated function injury abnormal lipid indexes, exhibiting less severity hepatic steatosis, fibrosis, inflammation Lower permeability, epithelial disruption, upregulation tight junction proteins after suggested protective effects attenuating dysfunction. These abolished by α-BGT deletion. Mechanistically, markedly enriched expression phosphorylated p38 MAPK/NF-κB activation, which was lost KO treatment. Conclusions: The may be attributed to preserved barrier, thereby alleviating systemic preventing subsequent hits, where α7nAChR-mediated HO-1/p38 pathway maintain homeostasis.

Язык: Английский

Процитировано

0