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纸质出版日期:2015
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曾宪彪, 李嘉, 韦桂宁, 等. 玉叶金花皂苷U对M胆碱能神经支配器官的影响[J]. 中国实验方剂学杂志, 2015,21(20):159-162.
ZENG Xian-biao, LI Jia, WEI Gui-ning, et al. Effect of Mussaendoside U on M Cholinergic Innervation Organs[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(20): 159-162.
曾宪彪, 李嘉, 韦桂宁, 等. 玉叶金花皂苷U对M胆碱能神经支配器官的影响[J]. 中国实验方剂学杂志, 2015,21(20):159-162. DOI: 10.13422/j.cnki.syfjx.2015200159.
ZENG Xian-biao, LI Jia, WEI Gui-ning, et al. Effect of Mussaendoside U on M Cholinergic Innervation Organs[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(20): 159-162. DOI: 10.13422/j.cnki.syfjx.2015200159.
目的:研究玉叶金花皂苷U对M胆碱能神经支配器官(回肠平滑肌、瞳孔、唾液腺)的影响。方法:①用离体肌收缩力测量装置获取肌收缩力信息。分别往装置浴槽加入阿托品
使其终质量浓度为10 mg·L-1或玉叶金花皂苷U
使其终质量浓度分别为100
50
25 mg·L-1
10 min后开始累积加入溴化乙酰胆碱
观察药物对不同终浓度溴化乙酰胆碱引起肌收缩力的影响
重复试验10次。②小鼠分为正常组和5个造模型组
每组10只
模型组ip毛果芸香碱20 mg·kg-11次
造成M胆碱能神经兴奋模型
15 min后
给成模小鼠尾静脉注射阿托品2.5 mg·kg-1或玉叶金花皂苷U 10
5
2.5 mg·kg-1
并ig碳末悬液
测量ig碳末30 min后小肠碳末推进率。③小鼠分组、造模和给药方法同2
分别于给药后15
60
240 min
测量瞳孔直径和唾液腺分泌量。结果:玉叶金花皂苷U降低肠平滑肌收缩力
使溴化乙酰胆碱终质量浓度与肌收缩力之间的量-效反应曲线右移;玉叶金花皂苷U(5 mg·kg-1)组
小肠碳末推进为(64.20±10.14)%
较模型组降低;给药后15
60
240 min
瞳孔直径分别为(2.5±0.19)
(2.2±0.18)
(2.1±0.40) mm
较模型组扩大
唾液腺分泌量分别为(102.3±13.57)
(90.2±20.51)
(68.0±21.52) mg
较模型组减少(P<0.05)。结论:玉叶金花皂苷U能抑制M胆碱能神经兴奋。
Objective: To study the effect of mussaendoside U on M cholinergic innervation organs (ileum smooth muscle
pupil and salivary gland). Method: ①Muscle contraction force information was obtained using muscle force measuring device in vitro. Atropine was added to bath to achieve a final concentration of 10 mg·L-1
or mussaendoside U was added in bath to achieve a final concentration of 100
50
25 mg·L-1 respectively. After 10 min
acetylcholine bromide was cumulatively added to observed the effect of drug on contraction force of muscle induced by different final concentration of acetylcholine bromide. The experiment was repeated for 10 times. ②Mice were divided into normal group and 5 model groups
with 10 mice in each group. Model group received intraperitoneal injection of pilocarpine once at a dose of 20 mg·kg-1to make M cholinergic nerve excitement model. After 15 min
modeled mice received intravenous injection of atropine at a dose of 2.5 mg·kg-1
or mussaendoside U at a dose of 10
5
2.5 mg·kg-1
and received telecarbon suspension ig at the same time. Telecarbon propulsion rate at intestine was measured after 30 min. ③Methods of mice grouping
modeling and treatment were identical with those in above.Pupil diameter and salivary gland secretion were measured respectively 15
60
240 min after administration. Result: Mussaendoside U reduced contraction force of intestine smooth muscle;dose-effect curve between acetylcholine bromide and muscle contraction force was shifted to right;telecarbon propulsion rate at intestine in mussaendoside U (5 mg·kg-1) group was (64.20±10.14)%
lower than that in model group;pupil diameters were (2.5±0.19)
(2.2±0.18)
(2.1±0.40) mm respectively 15
60
240 min after administration
bigger than those in model group;salivary gland secretion was (102.3±13.6)
(90.2±20.5)
(68.0±21.5) mg
lower than those in model group (P<0.05). Conclusion: Mussaendoside U may inhibit M cholinergic nerve excitement as a kind of anticholinergic drug.
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