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1. 复旦大学医学院神经生物教研室,上海,200032
2. 医学神经生物学国家重点实验室
纸质出版日期:2001
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肇晖, 吴根诚, 曹小定. 电针对创伤大鼠脑内孤啡肽及白介素-1β基因表达的调节作用[J]. 针刺研究, 2001,(3):218-219.
Modulation of Electroacupuncture on Brain OFQ and IL-1β Expression of Traumatic Rats[J]. Acupuncture research, 2001, (3): 218-219.
Electroacupuncture (EA) has been used to alleviate the immuno suppression o n account of its modulating function. Many investigations showed that EA could m odulate immune function through the actions of sympathetic nervous system and hy pothalamic pituitary adrenal axis. It was also indicated that EA stimulation o f "Z usanli" (ST 36) point could improve the immuno suppression induced by trauma. T he present experiment was to elucidate the central mechanism of EA on immune modul ation. Using immunohistochemistry and in situ hybridization techniques
it was o bserved that the endogenous orphanin FQ (OFQ) and its receptor opioid receptor l ike receptor (OP 4) transcripts were widely distributed in the central nervous sy stem (CNS) of normal rats
but the OFQ immuno reactive cells in hippocampus
ce r ebral cortex and hypothalamus in traumatic group were significantly decreased to 25.2±5.07
31.1±10.50
24.5±5.44
compared with control group (72.4±7.99
1 15.7±19.47
64.1±8.90) (P<0.05). After EA stimulation of "Zusanli" point the expression of OFQ was markedly increased
the OFQ immuno reactive cel ls were recovered to 60.0±5.48 in hippocampus
111.0±11.64 in cerebral cortex
and 64.0±10.01 in hypothalamus (P<0.05). The similar changes were al so observed in OP 4 mRNA transcripts in the CNS. However
different changes occu rred in IL 1β transcripts in the CNS. The IL 1β mRNA immuno reactive cells were 15.9±3.93
7.9± 3.07
8.6±2.41 in control group; 38.1±6.33
78.9±5. 13
49.1±9.84 in traumatic group; 22.7± 3.30
30.8±8.74
11.6±2.80 in trauma+ EA g roup
respectively. It indicated that the IL 1β mRNA transcripts were augm ente d by trauma and inhibited by EA. The above results suggested that OFQ had a clos e correlation with IL 1β in the CNS. The neuroimmune modulation of EA may be d ependent on the sustaining precise interactions between OFQ and IL 1β.
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