[Effects of Gadol and Ganoderma spores on the adiponectin signal pathway in hypertrophic myocardium of spontaneous hypertensive rats].
OBJECTIVE
To investigate the alteration of the adiponectin signal pathway in hypertrophic myocardium of spontaneous hypertensive rats (SHR) and to observe the effects of Gadol (GD) and Ganoderma spores (GS) on the hemodynamic parameters and the adiponectin signal pathway of SHR.


METHODS
SHRs, 8 weeks old, were randomly divided into four groups: the untreated group, and the three treated groups treated with GD, GS, and GD + GS respectively by gastrogavage for 4 weeks. Controlled with 8-week-old WKY rats, the hemodynamic parameters in all rats were recorded through the carotid artery intubation; the serum level of adiponectin was determined with ELISA; the mRNA expressions of adiponectin receptors (AdipoRs) and carnitine palmitoyl transferase (CPT-1) were determined by RT-PCR; and the protein expression of adenosine monophosphate activated protein kinase (AMPK), both phosphorylated and un-phosphorylated, was detected by Western blot.


RESULTS
Compared with the WKY rats, the systolic blood pressure (SBP), diastolic blood pressure (DBP) and myocardial hypertrophy index (MHI) in SHR were significantly higher; the serum levels of adiponectin and phosphorylated AMPK, mRNA expressions of AdipoR1 and CPT-1 in SHR heart tissue were lower (P < 0.05). Compared with the SHR, medication of GD and GS, either alone or in combination, could reduce SBP, DBP and MHI significantly (P < 0.01, P < 0.05), and elevate the mRNA expression of CPT-1 (P < 0.05) in heart, but levels of adiponectin, AdipoR1 and phosphorylated AMPK could only be raised by combined use of the two (P < 0.05).


CONCLUSIONS
Adiponectin signal transduction pathway alteration presents in the myocardium of SHR, which might be one of the molecular mechanisms that cause hypertrophic metabolic abnormality. GD and GS could improve the hemodynamic index in SHR, and enhance the level of adiponectin and the expression of its related signal transduction molecules.
Zhang
Zhi-guo
ZG
Department of Physiology and Pathophysiology, Health Science Center of Peking University, Beijing.
Wang
Cheng
C
Li
Li
L
D052242:Adiponectin / Q000378:metabolism* / Q000502:physiology; D000818:Animals; D002312:Cardiomyopathy, Hypertrophic / Q000209:etiology / Q000378:metabolism*; D004365:Drugs, Chinese Herbal / Q000494:pharmacology; D032902:Ganoderma / Q000737:chemistry*; D006439:Hemodynamics / Q000187:drug effects; D006973:Hypertension / Q000150:complications*; D008297:Male; D011897:Random Allocation; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D029771:Rhodiola / Q000737:chemistry*; D015398:Signal Transduction / Q000187:drug effects; D013170:Spores
D052242:Adiponectin; D004365:Drugs, Chinese Herbal