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 Improves Learning and Memory Impairment in Rats with Cerebral Ischemia/Reperfusion Injury by Promoting Microglia/Macrophage M2 Polarization Through Nrf2/HO-1 Pathway DOI Creative Commons

Yuqian Xiao,

Yan-Jie Bai,

Kexin Sun

и другие.

Journal of Inflammation Research, Год журнала: 2025, Номер Volume 18, С. 2925 - 2941

Опубликована: Фев. 1, 2025

While electroacupuncture (EA) has shown effectiveness in treating learning and memory deficits associated with ischemic stroke (IS), the specific mechanisms involved remain unclear. The goal of this study was to investigate whether EA improves MCAO rats by regulating microglia/macrophage polarization through nuclear factor red lineage 2-related 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. Sprague-Dawley were subjected modeling treated 24 hours post-MCAO for a period two weeks. To involvement Nrf2/HO-1 effects EA, tin protoporphyrin (SnPPIX), an inhibitor HO-1, injected into left ventricle before initiating treatment. Neurological function evaluated using neurological deficit score. on assessed Morris water maze (MWM) open field test (OFT). Hematoxylin-Eosin (HE) staining used observe hippocampal structural morphology, 2,3,5-Triphenyltetrazolium Chloride (TTC) assess infarct volume. Protein expression levels pathway microglial/macrophage determined ELISA, immunofluorescence double-labeling, Western blotting (WB), real-time quantitative polymerase chain reaction PCR (qRT-PCR). significantly enhanced upregulating NRF2/HO-1 promoting M2 microglia/macrophages. However, administration SnPPIX, HO-1 inhibitor, counteracted beneficial improvement rats, while also worsening cerebral volume inflammatory response. effectively improved impairments activating pathway, leading promotion

Язык: Английский

Процитировано

0
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