Key result
QGQS granule demonstrated an antihypertensive effect in spontaneously hypertensive rats by regulating lipid metabolism and inhibiting profilin-1 protein overexpression.
Why the study?
Does QGQS granule reduce blood pressure and alter metabonomics pathways in spontaneously hypertensive rats?
Does QGQS granule reduce blood pressure and alter metabonomics pathways in spontaneously hypertensive rats?
Answers are grounded in this paper and cite their sources.
QGQS granule lowers blood pressure in hypertensive rats, likely through RAAS modulation and inhibition of profilin-1.
QGQS granule is effective for the therapeutic of hypertension in clinic. The aim of this research is to observe the antihypertension effect of QGQS granule on SHR and explain the mechanism of its lowering blood pressure. 30 SHR were selected as model group, captopril group, and QGQS group, 10 WKYr were used as control group, and RBP were measured on tail artery consciously. And all the serum sample analysis was carried out on UPLC-TOF-MS system to determine endogenous metabolites and to find the metabonomics pathways. Meanwhile, ELISA kits for the determination pharmacological indexes of PRA, AngI, AngII, and ALD were used for pathway confirmatory; WB for determination of profilin-1 protein expression was conducted for Ang II pathway analysis as well. It is demonstrated that QGQS granule has an excellent therapeutic effect on antihypertension, which exerts effect mainly on metabonomics pathway by regulating glycerophospholipid, sphingolipid, and arachidonic acid metabolism, and it could inhibit the overexpression of the profilin-1 protein. We can come to a conclusion that RAAS should be responsible mainly for the metabonomics pathway of QGQS granule on antihypertension, and it plays a very important role in protein of profilin-1 inhibition.
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Li et al. (2017) studied Hypertension (n=40). QGQS granule vs. Model group, captopril group, and WKYr control group was evaluated on Blood pressure and metabonomics pathways. QGQS granule demonstrated an antihypertensive effect in spontaneously hypertensive rats by regulating lipid metabolism and inhibiting profilin-1 protein overexpression.
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