Effects of electroacupuncture at neiguan (PC6) on c-Jun NH2-teminal kinase signaling pathways in hypertrophic myocardial cells.
- Author:
Hua WANG
1
;
Jia LI
;
Ya-qun HONG
Author Information
- Publication Type:Journal Article
- MeSH: Acupuncture Points; Animals; Cardiomegaly; metabolism; therapy; Electroacupuncture; Female; JNK Mitogen-Activated Protein Kinases; metabolism; Myocytes, Cardiac; metabolism; Rats; Rats, Sprague-Dawley; Signal Transduction
- From: Chinese Journal of Integrated Traditional and Western Medicine 2012;32(8):1099-1102
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects of electroacupuncture (EA) at Neiguan (PC6) on c-Jun NH2-terminal kinases (JNK) signaling pathways in hypertrophic myocardial cells.
METHODSThirty female SD rats were randomly divided into three groups, i.e., the normal group, the model group, and the EA group, 10 in each group. Isoprenaline hydrochloride (ISO) injection at the daily dose of 3 mg/kg was subcutaneously injected for 14 days to establish the cardiac hypertrophy (CH) model. Rats in normal group were subcutaneously injected with an equal volume of normal saline. EA at Neiguan (PC6) was applied for rats in the EA group while modeling, once daily, for 14 successive days. The left ventricular weight index (LVWI) and heart weight index (HWI) were calculated in all rats. The content of angiotensin II (Ang II) in the cardiac muscular tissue was tested using radioimmunoassay. The protein expressions of JNK and phosphorated JNK (p-JNK) in cardiocytes were detected using Western blot.
RESULTSCompared with the normal group, LVWI and HWI, the Ang II content, and the expressions of JNK and p-JNK were significantly higher in the model group, showing statistical difference (P < 0.01). The aforesaid indices were obviously lower in the EA group than in the model group with statistical difference (P < 0.05).
CONCLUSIONSEA at PC6 could prevent and treat CH possibly correlated with regulation of JNK signaling pathways. EA might play a role possibly through regulating its upstream neuroendocrine factors.