Effect of Modified Xiaoyaosan on ERK Signal Transduction Pathway of Dopamine Receptorin Model Rats with Hyperprolactinemia / 中国实验方剂学杂志
Chinese Journal of Experimental Traditional Medical Formulae
;
(24): 70-76, 2019.
Article
in Chinese
| WPRIM
| ID: wpr-802336
ABSTRACT
Objective:
To explore the mechanism of modified Xiaoyaosan on extracellular regulated protein kinase(ERK) signal transduction pathway of central dopamine receptor in hyperprolactinemia(HPRL)model rats by treating them with Shugan Jianpi as the core.Method:
The 96 SD female rats were randomly divided into normal group, model group, Bromocriptine group (0.001 g·kg-1), modified Xiaoyaosan high, medium and low dose group(60,30,15 g·kg-1), dopamine D1 receptor(D1R) antagonist group (SCH23390, SCH23390+ modified Xiaoyaosan group, SCH23390+bromocriptine group), dopamine D2 receptor(D2R) antagonist group (haloperidol group, haloperidol+modified Xiaoyaosan group,haloperidol+bromocriptine group).HPRL rat model was established by pituitary transplanta-tion. After 30 days of administration, renin-angiotensinsystem Ras and Raf protein expressions in thypothalamus of rats were detected by Western blot, and mitogen-activated protein kinase (MAPK) kinase 1/2(MEK1/2)mRNA and extracellular signaling regulates kinase 1/2(ERK1/2) mRNA expressions in the hypothalamus of rats were detected by Real-time PCR.The microstructures of mitochondria in ovarian granulosa cells were observed by electron microscopy.Result:
The Ras,Raf protein,MEK1/2 and ERK1/2 mRNA expression were significantly decreased in model group compared with normal group (PPPPConclusion:
Modified Xiaoyaosan stimulates D2R, inhibits D1R, regulates ERK/MAPK signaling pathway.It also effectively improve the mitochondrial function of ovarian granulosa cells and promote follicular development.It is suggested that the modified Xiaoyaosan with a multi-target mechanism in treating HPRL.
Full text:
Available
Index:
WPRIM (Western Pacific)
Language:
Chinese
Journal:
Chinese Journal of Experimental Traditional Medical Formulae
Year:
2019
Type:
Article
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