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1.
J Transl Med ; 21(1): 892, 2023 Dec 08.
Artículo en Inglés | MEDLINE | ID: mdl-38066566

RESUMEN

AMP-activated protein kinase (AMPK) is a ubiquitous sensor of energy and nutritional status in eukaryotic cells. It plays a key role in regulating cellular energy homeostasis and multiple aspects of cell metabolism. During macrophage polarisation, AMPK not only guides the metabolic programming of macrophages, but also counter-regulates the inflammatory function of macrophages and promotes their polarisation toward the anti-inflammatory phenotype. AMPK is located at the intersection of macrophage metabolism and inflammation. The metabolic characteristics of macrophages are closely related to immune-related diseases, infectious diseases, cancer progression and immunotherapy. This review discusses the structure of AMPK and its role in the metabolism, function and polarisation of macrophages. In addition, it summarises the important role of the AMPK pathway and AMPK activators in the development of macrophage-related diseases.


Asunto(s)
Proteínas Quinasas Activadas por AMP , Macrófagos , Humanos , Proteínas Quinasas Activadas por AMP/metabolismo , Macrófagos/metabolismo , Inflamación/metabolismo , Antiinflamatorios/uso terapéutico , Homeostasis , Metabolismo Energético
2.
Int Immunopharmacol ; 143(Pt 1): 113359, 2024 Dec 25.
Artículo en Inglés | MEDLINE | ID: mdl-39388895

RESUMEN

Inflammation and extracellular matrix (ECM) degradation are two major factors involved in the pathogenesis of osteoarthritis (OA). Wedelolactone, a natural compound classified as a coumestan, is isolated from the medicinal plants Eclipta alba and Wedelia calendulacea. In this study, we assessed the protective effects of Wedelolactone on chondrocytes in OA. Our findings show that pretreatment with Wedelolactone effectively inhibited the IL-1ß-induced upregulation of COX­2, iNOS, TNF-α, and IL6 in chondrocytes, contributing to inflammation suppression. Moreover, pretreatment with Wedelolactone followed by IL-1ß treatment significantly increased the expression of Collagen II and SOX9, while decreasing the expression of Adamts5, MMP1, MMP3, and MMP13, thereby promoting ECM protection. Through Network pharmacology Analysis, we identified 14 key targets that link Wedelolactone and OA. GO and KEGG pathway analysis suggested that Wedelolactone primarily impacted OA by targeting inflammatory responses, particularly the NF-κB signaling pathway. Further studies demonstrated Wedelolactone prevented IL-1ß-induced activation of NF-κB signaling pathway by inhibiting the translocation of p65 and the preventing the degradation of IκBα in human chondrocytes. Molecular docking studies also indicated that Wedelolactone can directly bind to the NF-κB complex, thereby inhibited the nuclear localization of p65. In vivo experiments demonstrated that Wedelolactone can alleviate cartilage damage in DMM mice model. In summary, Wedelolactone appears to mitigate inflammation and cartilage degeneration by suppressing the NF-κB signaling pathway, thereby alleviating OA progression. Our results suggested Wedelolactone may offer therapeutic advantages for OA treatment.


Asunto(s)
Condrocitos , Cumarinas , FN-kappa B , Osteoartritis , Transducción de Señal , Osteoartritis/tratamiento farmacológico , Osteoartritis/metabolismo , Osteoartritis/patología , FN-kappa B/metabolismo , Animales , Humanos , Condrocitos/efectos de los fármacos , Condrocitos/metabolismo , Transducción de Señal/efectos de los fármacos , Cumarinas/farmacología , Cumarinas/uso terapéutico , Ratones , Masculino , Interleucina-1beta/metabolismo , Ratones Endogámicos C57BL , Antiinflamatorios/farmacología , Antiinflamatorios/uso terapéutico , Células Cultivadas , Simulación del Acoplamiento Molecular , Inflamación/tratamiento farmacológico , Cartílago Articular/efectos de los fármacos , Cartílago Articular/patología , Cartílago Articular/metabolismo
3.
Front Neurol ; 14: 1108320, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-36873455

RESUMEN

Stroke and spinal cord injury are common neurological disorders that can cause various dysfunctions. Motor dysfunction is a common dysfunction that easily leads to complications such as joint stiffness and muscle contracture and markedly impairs the daily living activities and long-term prognosis of patients. Orthotic devices can prevent or compensate for motor dysfunctions. Using orthotic devices early can help prevent and correct deformities and treat muscle and joint problems. An orthotic device is also an effective rehabilitation tool for improving motor function and compensatory abilities. In this study, we reviewed the epidemiological characteristics of stroke and spinal cord injury, provided the therapeutic effect and recent advances in the application of conventional and new types of orthotic devices used in stroke and spinal cord injury in different joints of the upper and lower limbs, identified the shortcomings with these orthotics, and suggested directions for future research.

4.
Front Neurol ; 14: 1170420, 2023.
Artículo en Inglés | MEDLINE | ID: mdl-37273704

RESUMEN

Stroke is a group of cerebrovascular diseases with high prevalence and mortality rate. Stroke can induce many impairments, including motor and cognitive dysfunction, aphasia/dysarthria, dysphagia, and mood disorders, which may reduce the quality of life among the patients. Constraint-induced therapy has been proven to be an effective treatment method for stroke rehabilitation. It has been widely used in the recovery of limb motor dysfunction, aphasia, and other impairment like unilateral neglect after stroke. In recent years, constraint-induced therapy can also combine with telehealth and home rehabilitation. In addition, constraint-induced therapy produces significant neuroplastic changes in the central nervous system. Functional magnetic resonance imaging, diffusion tensor imaging, and other imaging/electrophysiology methods have been used to clarify the mechanism and neuroplasticity. However, constraint-induced therapy has some limitations. It can only be used under certain conditions, and the treatment time and effectiveness are controversial. Further research is needed to clarify the mechanism and effectiveness of CI therapy.

5.
Biofactors ; 49(1): 21-31, 2023 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-32997846

RESUMEN

Myostatin, a member of the transforming growth factor-ß (TGF-ß) superfamily, is a key autocrine/paracrine inhibitor of skeletal muscle growth. Recently, researchers have postulated that myostatin is a negative regulator of bone formation and metabolism. Reportedly, myostatin is highly expressed in the fracture area, affecting the endochondral ossification process during the early stages of fracture healing. Furthermore, myostatin is highly expressed in the synovium of patients with rheumatoid arthritis (RA) and is an effective therapeutic target for interfering with osteoclast formation and joint destruction in RA. Thus, myostatin is a potent anti-osteogenic factor and a direct modulator of osteoclast differentiation. Evaluation of the molecular pathway revealed that myostatin can activate SMAD and mitogen-activated protein kinase signaling pathways, inhibiting the Wnt/ß-catenin pathway to synergistically regulate muscle and bone growth and metabolism. In summary, inhibition of myostatin or the myostatin signaling pathway has therapeutic potential in the treatment of orthopedic diseases. This review focused on the effects of myostatin on bone formation and metabolism and discussed the potential therapeutic effects of inhibiting myostatin and its pathways in related orthopedic diseases.


Asunto(s)
Miostatina , Osteogénesis , Humanos , Miostatina/metabolismo , Factor de Crecimiento Transformador beta/metabolismo , Transducción de Señal , Sistema de Señalización de MAP Quinasas , Músculo Esquelético/metabolismo
6.
Heliyon ; 9(11): e21282, 2023 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-37964828

RESUMEN

Osteoarthritis (OA) is a prevalent chronic degenerative joint disease worldwide. Obesity has been linked to OA, and increased free fatty acid levels (e.g., palmitate) contribute to inflammatory responses and cartilage degradation. Xanthohumol (Xn), a bioactive prenylated chalcone, was shown to exhibit antioxidative, anti-inflammatory, and anti-obesity capacities in multiple diseases. However, a clear description of the preventive effects of Xn on obesity-associated OA is unavailable. This study aimed to assess the chondroprotective function of Xn on obesity-related OA. The in vitro levels of inflammatory and ECM matrix markers in human chondrocytes were assessed after the chondrocytes were treated with PA and Xn. Additionally, in vivo cartilage degeneration was assessed following oral administration of HFD and Xn. This study found that Xn treatment completely reduces the inflammation and extracellular matrix degradation caused by PA. The proposed mechanism involves AMPK signaling pathway activation by Xn, which increases mitochondrial biogenesis, attenuates mitochondrial dysfunction, and inhibits NLRP3 inflammasome and the NF-κB signaling pathway induced by PA. In summary, this study highlights that Xn could decrease inflammation reactions and the degradation of the cartilage matrix induced by PA by inhibiting the NLRP3 inflammasome and attenuating mitochondria dysfunction in human chondrocytes.

7.
Int J Mol Med ; 50(5)2022 11.
Artículo en Inglés | MEDLINE | ID: mdl-36102306

RESUMEN

Osteoarthritis (OA) is the most common degenerative disease affecting the joints, and inflammation appears to play a critical role in the initiation and progression of OA. Caffeic acid phenethyl ester (CAPE), a natural flavonoid compound, has anti­inflammatory and antioxidant functions. However, its anti­inflammatory effects on OA and the underlying mechanisms of action of CAPE in the treatment of OA remain elusive. Therefore, the present study investigated the anti­inflammatory effects of CAPE on IL­1ß­stimulated chondrocytes in vitro and surgically induced rat models of OA in vivo. In vitro, CAPE reduced the expression of inducible nitric oxide synthase and cyclooxygenase­2 in IL­1ß­stimulated chondrocytes, as well as the extracellular secretion of nitric oxide and prostaglandin E2 in the cell culture supernatants. In addition, CAPE attenuated the degradation of extracellular matrix by increasing the expression of aggrecan and collagen II, and decreasing the expression of MMP3, MMP13 and a disintegrin and metalloproteinase with thrombospondin motif­5. Furthermore, CAPE attenuated NF­κB signaling and activated the nuclear factor erythroid 2­related factor 2/heme oxygenase­1 signaling pathway in IL­1ß­stimulated chondrocytes. In vivo, CAPE protected cartilage from destruction and delayed the progression of OA in rats. Taken together, the findings of the present study indicated that CAPE may be a potential therapeutic agent for the prevention or treatment of OA.


Asunto(s)
Hemo Oxigenasa (Desciclizante)/metabolismo , FN-kappa B , Osteoartritis , Animales , Antiinflamatorios/farmacología , Ácidos Cafeicos , Factor 2 Relacionado con NF-E2/metabolismo , FN-kappa B/metabolismo , Osteoartritis/tratamiento farmacológico , Osteoartritis/metabolismo , Alcohol Feniletílico/análogos & derivados , Ratas , Transducción de Señal
8.
J Int Med Res ; 48(6): 300060520927881, 2020 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-32495667

RESUMEN

OBJECTIVE: To clarify the efficacy of functional magnetic stimulation (FMS) in improving hemiplegic upper extremity function in patients with sub-acute stroke. METHODS: In this randomized controlled trial, 40 sub-acute stroke patients with hemiplegia were recruited from inpatient wards in the Department of Rehabilitation and randomly assigned to two groups. In the FMS group, magnetic stimulation was applied to extensor muscle groups of the affected upper extremity. In the low-frequency repetitive transcranial magnetic stimulation (LF-rTMS) group, stimulation was applied to the contralesional primary motor cortex. All patients received occupational therapy. Hand and upper extremity motor function was evaluated using the Fugl-Meyer Assessment for upper extremity (FMA-UE), and the Barthel Index (BI) evaluated daily living abilities. RESULTS: The FMA-UE and BI scores were significantly increased in both groups following stimulation. Furthermore, a significant between-group difference was observed in both FMA-UE and BI scores after 2 weeks of therapy. In the FMS group, 6 of 19 patients regained wrist and finger extension abilities, but only 2 patients regained equivalent motor skills in the LF-rTMS group. CONCLUSIONS: FMS improves paretic upper extremity function and leads to better recovery of motor activity than LF-rTMS. FMS may be a novel modality to improve motor function.


Asunto(s)
Recuperación de la Función , Rehabilitación de Accidente Cerebrovascular/métodos , Accidente Cerebrovascular/complicaciones , Estimulación Magnética Transcraneal/métodos , Extremidad Superior/fisiopatología , Adolescente , Adulto , Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Corteza Motora/fisiopatología , Método Simple Ciego , Resultado del Tratamiento , Extremidad Superior/inervación , Adulto Joven
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