| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5816846 | Phytomedicine | 2013 | 11 Pages |
Abstract
OMT prevents ventricular remodeling in SHR. The mechanisms may be related to inhibiting the gene overexpression of ACE and TGF-β1, suppressing the activation of signaling pathways of ERK 1/2, JNK and p38 MAPK.
Keywords
p38LVWHWIOxymatrineOMTSNSTBSTPKCChFRAASACETGF-β1BSAc-Jun N-terminal kinaseERK1/2JNK/SAPKbovine serum albuminangiotensin converting enzymeAngiotensin IIVentricular remodelingGene overexpressionTransforming growth factor-β1Tris-buffered salineELISAEnzyme-linked immunosorbent assayAng IIRenin-angiotensin-aldosterone systemsympathetic nervous systemextracellular signal regulated kinaseShrHeart rateSignaling pathwayWistar-Kyoto ratsWKY ratscongestive heart failureheart failuremapbody weightHeart weightProtein kinase C
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Authors
Xiao Yan Huang, Chang Xun Chen,