ABSTRACT
Previous studies have been reported on the properties of moxa and the effect it has on the self defense mechanism of the body. To study the characteristics of acupoints, the study this time is from the point of whether there are any differences in biological responses if the same stimuli (5mg/body and 15mg/body of moxa) are applied to different acupoints. The acupoints chosen were KIMON, which is the therapeutic acupoint of liver, and DAIO, which is the spleen meridian acupoint located on the same vertical line and which has no effect on the liver. Male ddy mice (6 weeks old) were used as experimental animals. A comparison of the clinical biochemical values of serum 1, 3, 6 and 24 hours after application was conducted. The amount of invasion on body function from each moxibustion stimulus through the strength and progress of biological response was studied. Increases in serum Amylase, LDH, CK, GOT, and GPT in the DAIO group were obtained as compared to that of the KIMON group. There was also a decrease in serum CHE in the DAIO group as compared to that of the KIMON group. It was suggested that there were difference in biological responses between different application points, even with the application of the same stimuli.
ABSTRACT
Morphological changes of sciatic and tivial nerves have been observed microscopically and cholinesterase activities of anterior tibial, gastrocnemius and soleus muscles have been examined by the biochemical determination and histochemical method. 25mg of moxa/body (3 times a week, x6) were treated on the acupuncture point, B-18, B-25 and G-34 in acrylamide neuropathy rats.<br>After 400p.p.m. acrylamide treatment, the degeneration of peripheral nerves with myelin ovoids and foldes, and shrunken myelinated axons were observed. These lesions were advanced in the tibial nerve than in the sciatic nerve. In B-25 and B-18 moxibustion rats, good results were obtained to decrease myelin degeneration in peripheral nerves, but the lesions were advanced in G-34 rats than in acrylamide ones.<br>In the acrylamide rats, no change of muscle cholinesterase activity was found except the increase in the enzyme activity in the homogenate of anterior tibial muscle. In the gastrocnemius muscle of moxibustion treated rats, the microsomal fraction which contained much more sarcoplasmic reticulum showed high cholinesterse activity. And the activity per muscle protein showed various changes.<br>It showed that the stimulation of moxibustion had a mild effect to recover the experimental peripheral neuropathy induced by 400p.p.m. acrylamide because of morphological changes of sciatic and tibial nerves and weight of skeletal muscles.
ABSTRACT
The establishment of experimental peripheral neuropathy and effect of moxibustion on it have been studied using male S. D. rats. To determine the condition of experimental peripheral neuropathy, rats were fed on the solution of acrylamide in the concentration of 100, 200, 300, 400 and 500p.p.m. The body weight decreased dependently on its concentration and the behavior in rats was also detriorated. Especially, ataxia, hindlimb weakness and muscle wasting in rats were remarkably observed.<br>The effect of moxibustion has been studied on the rats which fed on the 400p.p.m. acrylamide solution. The method of moxibustion is followes; 25mg of moxa was divided into 10 cones and they were treated by each 5 cones on right and left B-18, B-25 and G-34, respectively. The treatment of moxibustion was 6 times in 3 ones a week for 13 days.<br>As a results, after 12-13 days, moxibustion treated rats showed to improve the deterioration of behavior and muscle wasting induced by acrylamide. Especially, B-25 treated rats showed the improvement of weight in anterior tibial, gastrocnemius and soleus muscle. On the other hand, steadiness on slope was decreased by acrylamide feeding and decrease of the steadiness was not improved by the treatment of moxibustion.<br>It is suggested that the sutable stimulation of moxibustion improved the deterioration of behavior and muscle waste on the acrylamide induced peripheral neuropathy in rats.