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[Effects of Zhuang-medical thread moxibustion combined with needle-pricking on vascular oxidative stress injury in the rat].

OBJECTIVE
To observe the effect of Zhuang-medical thread moxibustion combined with needle-pricking on vascular oxidative stress injury in oxidative stress injury rats.


METHODS
Eighty Wistar rats were randomly allocated to normal control, sham operation (sham), model, and combined treatment groups (n=20 in each group). The oxidative stress injury model was established by ligation of the left sciatic nerve to induce chronic constriction injury (CCI) pain stress stimulation. Zhuang-medical thread moxibustion was applied to bilateral "Zusanli" (ST 36), once a day for 3 weeks. Needle-pricking was applied to left "Yanglingquan" (GB 34) and left "Huantiao" (GB 30), once a day for 3 weeks except Sundays. Plasma 6-keto-PGF 1α, thromboxane B 2 (TXB 2), NO and ET contents were assayed by radioimmunoassay. COX-2 immunoactivity of the femoral artery was determined by immunohistochemistry, and pathological changes of the femoral artery were detected by H. E. staining.


RESULTS
Compared with the control group, the levels of plasma 6-keto-PGF 1α and NO in the model group were significantly reduced (P<0.05), while those of plasma TXB 2 and ET and COX-2 expression in the femoral artery were obviously increased in the model group (P<0.01). After moxibustion plus needle-pricking treatment, CCI-induced decrease of plasma 6-keto-PGF 1α and NO contents, and increase of plasma TXB 2 and ET and COX-2 expression levels were obviously reversed (P<0.05, P<0.01). The tubal wall of the femoral artery in rats of the model group got thicker, while that of the combined treatment group was relatively thinner, suggesting an inhibition of vascular intimal hyperplasia after the treatment.


CONCLUSION
Zhuang-medical thread moxibustion combined with needle-pricking of ST 36, GB 34 and GB 30 can reduce the expression of femoral artery COX-2 and regulate the balance of both plasma PGI 2/TXA 2 and plasma NO/ET in CCI-induced oxidative stress rats, which may contribute to its effect in suppressing oxidative stress-induced vascular intimal hyperplasia.