Role of acetylcholine in gelsenicine-induced death in mice.
- Author:
Zhou-Yi LAI
1
;
Hai-Bo WANG
2
;
Rui-Ling LV
1
;
Qiu-Chan TAN
1
;
Zhi-Qin DENG
1
;
Yuan WANG
1
;
Xiao-Xue SUN
1
;
Jia-Bao WU
2
;
Lin-Yan ZHU
2
;
Lei WANG
3
;
Li-Xin CHEN
2
;
Wen-Cai YE
3
;
Li-Wei WANG
4
Author Information
1. Department of Physiology, Medical College, Jinan University, Guangzhou 510632, China.
2. Department of Pharmacology, Medical College, Jinan University, Guangzhou 510632, China.
3. College of Pharmacy, Jinan University, Guangzhou 510632, China.
4. Department of Physiology, Medical College, Jinan University, Guangzhou 510632, China. twangliwei@jnu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Acetylcholine;
Animals;
Death;
Indole Alkaloids;
Mice
- From:
Acta Physiologica Sinica
2016;68(3):249-254
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to investigate the relationship between the acetylcholine concentration in the blood and gelsenicine-induced death in mice. Kunming mice were given intraperitoneal injections of normal saline, gelsenicine or different doses of acetylcholine chloride. Atropine was given to the mice which received gelsenicine or medium dose acetylcholine chloride injection. The blood was sampled immediately when the mice died or survived for 20 min after injection. The acetylcholine concentration and acetylcholinesterase activity in the blood were measured by the testing kits, and the mortality was calculated and analyzed. The results showed that half lethal dose of gelsenicine (0.15 mg/kg) reduced the acetylcholinesterase activity and increased the blood acetylcholine concentration. The blood acetylcholine concentration of the dead mice in the gelsenicine group was increased to 43.0 μg/mL (from 31.1 μg/mL in the control), which was lower than that (53.9 μg/mL) of the dead mice in the medium dose acetylcholine chloride group, but almost equal to that (42.7 μg/mL) of the survival mice in the medium dose acetylcholine chloride group. Atropine could successfully rescue the mice from acetylcholine poisoning, but its efficiency of rescuing the mice from gelsenicine intoxication was weak. These results suggest that gelsenicine can inhibit acetylcholinesterase activity and increase blood acetylcholine concentration, but the accumulation of acetylcholine may not be the only or main cause of the death induced by gelsenicine in mice.
