[Effect of Moxibustion Stimulation of "Feishu" (BL 13) and "Xinshu" (BL 15) on Expression of Myocardial MyD 88 Protein and Caspase 3 mRNA in Chronic Heart Failure Rats].

Objective: To observe the effect of moxibustion stimulation of "Feishu" (BL 13) and "Xinshu" (BL 15) on pathological changes of myocardium and the expression of myocardial myeloid differentiation factor 88 (MyD 88) protein and Caspase 3 mRNA in chronic heart failure (CHF) rats, so as to explore its mechanism underlying improvement of CHF.

Methods: SD male rats were randomly divided into normal (=9), model (=8), moxibustion (=8), medication (=8) and moxibustion + medication (=8) groups. In addition, the other 6 rats (3/normal and 3/model groups) were used for measuring cardiac ventricle weight and H.E. stain. The CHF model was made by intraperitoneal injection of Adriamycin (ADR, from 1 to 4 mg/kg, once every other day for 15 days). Mild moxibustion was applied to bilateral BL13 and BL15 for 15 min, once daily for 3 weeks. Rats of the medication group were treated by Captopril (gavage) for 3 weeks. The expression of myocardial Caspase 3 mRNA and MyD 88 protein of the left ventricle was determined by quantitative real time-PCR and Western blot, respectively.

Results: In comparison with the normal group, the myocardial damage (cell swelling, cytoplasma vaculation, and disordered arrangement, rupture and lysis of some cardiac muscle fibers), and the expression levels of myocardial MyD 88 protein and Caspase 3 mRNA were obviously increased in the model group(<0.01). After the interventions, the myocardial damage was relatively milder, and the expression of myocardial MyD 88 protein and Caspase 3 mRNA were significantly down-regulated in the moxibustion, me-dication and moxibustion+medication groups in comparison with the model group(<0.05). No significant differences were found among the 3 treatment groups in the expression levels of MyD 88 protein and Caspase 3 mRNA(>0.05).

Conclusions: Moxibustion intervention can suppress CHF induced up-regulation of expression of myocardial MyD 88 protein and Caspase 3 mRNA in rats, which may contribute to its effect in relieving myocardial injury.