Fig 1.
The effects of magnolol on blood pressure and insulin-induced vasodilatation in rats.
(A) The effect of magnolol of systolic blood pressure (SBP). (B) The effect of magnolol on diastolic pressure (DBP). Impairment of insulin-induced vasodilatation and the effect of magnolol on insulin-induced vasodilatation in aortic segments from SHRs (C). Either ACh (D) or SNAP (E) elicited a significant vasorelaxation effects in aortic vessels from both WKY rats and SHRs, and there was no difference in aortic vasorelaxation between the two strains in response to both vasodilators respectively. (F) Insulin-induced relaxation was abolished either by removal of the endothelium or by pretreatment with L-NAME of the vessels from SHRs by MAG treatment, and also was inhibited by PPARγ antagonist bisphenol A diglycidyl ether (BADGE) pretreatment in vivo. Mag, magnolol; L-NAME, Nω-nitro-L-argininemethyl ester; E−, endothelium denudation. n = 6, **P<0.01 vs. WKY; ##P<0.01 vs. SHR; $$P<0.01 vs. SHR+MAG.
Fig 2.
A and B, Representative blots and quantitative densitometry of PPARγ and TRB3 in the aortic segments from control or magnolol-treated WKY and SHRs.
C and D, Representative blots of total Akt and phosphorylated Akt and the ratio of phosphorylated Akt/total Akt, total eNOS and phosphorylated eNOS and the ratio of phosphorylated eNOS/total eNOS in the aortic segments with insulin treatment from control or magnolol-treated WKY and SHRs, and NO release (E) in the rat aortas. Data obtained from quantitative densitometry were presented as mean ± SEM of at least 5 independent experiments. M, magnolol. *P<0.05 vs. WKY, #P<0.05 vs. SHRs.
Fig 3.
Effects of magnolol incubation on PPARγ expression and insulin-stimulated Akt/endothelial NO synthase (eNOS)/NO signaling in human umbilical vein endothelial cells.
Representative western blots showing PPARγ (A), TRB3 (B), phosphorylated Akt / Akt (C), phosphorylated eNOS / eNOS (D), and NO release (E) in the conditioned medium. HG/HF, high glucose/high fat treatment. All values are presented as mean ± SEM. n = 5–6. *P<0.05 vs. Control, #P<0.05 vs. HG/HF.
Fig 4.
PPARγ antagonist blocked effects of MAG incubation on PPARγ expression and insulin-stimulated signaling pathway in human umbilical vein endothelial cells.
Representative western blots showing PPARγ (A), TRB3 (B), phosphorylated Akt / Akt (C), and phosphorylated eNOS / eNOS (D), and NO release (E) in the conditioned medium. HG/HF, high glucose/high fat treatment; Mag, magnolol; BADGE, PPARγ antagonist bisphenol A diglycidyl ether (BADGE). All values are presented as mean ± SEM. n = 5–6. *P<0.05 vs. Control, #P<0.05 vs. HG/HF, $P<0.05 vs. HG/HF+BADGE.
Fig 5.
PPARγ inhibition decreased effects of MAG incubation on PPARγ expression and insulin-stimulated signaling pathway in human umbilical vein endothelial cells.
Representative western blots showing PPARγ (A), TRB3 (B), phosphorylated Akt / Akt (C), and phosphorylated eNOS / eNOS (D), and NO release (E) in the conditioned medium. HG/HF, high glucose/high fat treatment; Mag, magnolol. All values are presented as mean ± SEM. n = 5–6. *P<0.05 vs. Control, #P<0.05 vs. HG/HF, $P<0.05 vs. HG/HF+Scrmbled siRNA.
Fig 6.
Improved insulin signaling of human umbilical vein endothelial cells by magnolol were abolished by upregulating TRB3 expression.
Representative western blots showing TRB3 (A), phosphorylated Akt / Akt (B), and phosphorylated eNOS / eNOS (C). Mag, magnolol, (D) NO release in the conditioned medium. (E) Proposed mechanisms of magnolol attenuates the vascular insulin resistance and reduces blood pressure. All values are presented as mean ± SEM. n = 5–6. *P<0.05 vs. Control, #P<0.05 vs. HG/HF, $P<0.05 vs. HG/HF+Chariot.