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Métodos Terapéuticos y Terapias MTCI
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1.
Artículo en Chino | WPRIM | ID: wpr-777321

RESUMEN

OBJECTIVE@#To explore the impact of electroacupuncture (EA) on the AMPKα-HDAC5-HIF-1α signaling in the heart of the rats with myocardial ischemia (MI) via detecting the expressions of AMP-activated protein kinase α (AMPKα), histone deacetylase 5 (HDAC5), hypoxia inducible factor (HIF-1α) and vascular endothelial growth factor (VEGF).@*METHODS@#Thirty-six healthy male SD rats were randomized into a sham operation group (6 rats), a sham + EA group (6 rats), a model group (12 rats) and an EA group (12 rats). We ligated the left anterior descending artery (LAD) for MI model, and exposed the heart of rats after opening the chest without ligation for the rats in the sham operation gorup and the sham + EA group. On the 2nd day after LAD ligation, EA was applied at "Neiguan" (PC 6) with 2 Hz/15 Hz and 1.5-2 mA for 30 min in the EA group and sham+EA group, once a day for 4 days. The same fixation was used in the sham operation group and the model group, without EA. Myocardial infarction area was observed by TTC staining and serum cardiac troponin T (cTnT) was detected by radioimmunoassay. The expression of VEGF mRNA was detected by real time PCR. The protein expressions of AMPKα, HDAC5, HIF-1α and VEGF were detected by western blot.@*RESULTS@#Compared with the sham operation group, 4 days after LAD ligation, the myocardial infarction was obvious and the expression of serum cTnT increased in the model group (0.05). After EA for 4 days, the myocardial infarction area and cTnT expression decreased in the EA group (both <0.01); the VEGF mRNA and protein expressions and AMPKα, HDAC5, HIF-1α protein expressions increased (<0.05, <0.01).@*CONCLUSION@#EA could regulate the AMPKα-HDAC5-HIF-1α signaling in myocardial tissue, which may activate VEGF expression for angiogenesis signaling, reduce myocardial infarction area so as to achieve cardioprotective effect.


Asunto(s)
Animales , Masculino , Ratas , Proteínas Quinasas Activadas por AMP , Electroacupuntura , Histona Desacetilasas , Subunidad alfa del Factor 1 Inducible por Hipoxia , Isquemia Miocárdica , Ratas Sprague-Dawley , Transducción de Señal , Factor A de Crecimiento Endotelial Vascular
2.
Artículo en Chino | WPRIM | ID: wpr-711344

RESUMEN

Objective To investigate how electroacupuncture activates the AMPKαpathway in the treatment of functional dyspepsia ( FD) . Methods Tail clipping stimulation was combined with an irregular diet to induce FD in 20 Sprague-Dawley rats. They were randomly divided into a model group and an electroacupuncture group, each of 10. Ten others had no FD induced and formed a normal group. The rats in the electroacupuncture group were given 10 days of electroacupuncture treatment, while those in the normal and model groups were restrained and fixed like those in the electroacupuncture group, but not given electroacupuncture. The expression of phosphorylated adenosine mono-phosphate-activated protein kinase alpha (p-AMPKα), phosphorylated tuberin (p-TSC2) and Rheb protein in the stomachs and small intestines of each group were detected using the western blotting. Levels of mTOR mRNA were quantified using the reverse-transcription polymerase chain reaction ( RT-PCR) . Results The western blotting re-sults showed that compared with the normal group, the expression levels of p-AMPKα and p-TSC2 in the stomachs and small intestines of the model group decreased significantly, while that of Rheb protein increased significantly. Compared with the model group, the expression of p-AMPKαand p-TSC2 increased significantly after the electroacu-puncture treatment, while that of Rheb protein decreased significantly. According to the RT-PCR results, the expres-sion of mTOR mRNA in the stomachs and small intestines of the model group was up-regulated significantly compared with the normal group. Compared with the model group, expression of mTOR mRNA in the electroacupuncture group was significantly down-regulated. Conclusion Electroacupuncture can activate the AMPKα pathway, up-regulate the expression of the related protein p-TSC2, and decrease the expression of Rheb protein, thereby down-regulating the transcription of the mTOR gene. That would serve to treat FD.

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