The Effect of Chemical Sympathectomy on Moxibustion-Induced Immunomodulation in the Rat Spleen
Immune Network
;
: 109-114, 2002.
Article
in Korean
| WPRIM
| ID: wpr-37605
ABSTRACT
BACKGROUND:
To investigate the role of sympathetic nervous system (SNS) in moxibustion-induced immunomodulation, the effects of chemical sympathectomy on moxibustion-induced changes in splenic NK cell cytotoxicity, T and B cell proliferation were studied in Sprague-Dawley male rats.METHODS:
Chemical sympathectomy was achieved with intraperitoneal injection of 6-hydroxydopamine 50 mg/kg/day for 3 successive days. Direct moxibustion (6-minute interval, 9 moxa ball, each of which weighing 0.007 g and burning for 40 seconds) was applied on unilateral anterior tibial muscle region where Zusanli (ST36) acupoint is located, once a day for 7 successive days. NK cell cytotoxicity was measured by 4hr-51Cr release assay. Mitogen-induced lymphocyte proliferation was analyzed by [3H]-thymidine incorporation assay.RESULTS:
NK cell cytotoxicity was suppressed by moxibustion, more in sympathectomized rats than in vehicle-treated rats. T cell proliferation induced by concanavalin A was not affected by moxibustion. B cell proliferation induced by lipopolysaccharide showed no significant change in vehicle- treated rats, but an increase in sympathectomized rats by moxibustion. Sympathectomy alone induced augmentation of NK cell cytotoxicity and suppression of T cell proliferation.CONCLUSION:
These results suggest that SNS has no direct relation with moxibution-induced immunomodulation but has an important role in the mechanism to keep the homeostasis of immune system by tonically inhibiting excessive changes of various immune components.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Spleen
/
Sympathectomy
/
Sympathectomy, Chemical
/
Sympathetic Nervous System
/
Burns
/
B-Lymphocytes
/
Killer Cells, Natural
/
Lymphocytes
/
T-Lymphocytes
/
Acupuncture Points
Limits:
Animals
/
Humans
/
Male
Language:
Korean
Journal:
Immune Network
Year:
2002
Type:
Article
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