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Suppression of TGF-β1/Smad signaling pathway by sesamin contributes to the attenuation of myocardial fibrosis in spontaneously hypertensive rats.

Zhao M, Zheng S, Yang J, Wu Y, Ren Y, Kong X, Li W, Xuan J - PLoS ONE (2015)

Bottom Line: Though sesamin had no significant influence on Ang II levels, and the hypotensive effect was also significantly inferior to that of captopril (P <0.05 or P <0.01), however, the improvement of LVH and collagen deposition was similar to that in captopril group.Sesamin markedly reduced transforming growth factor-β1 (TGF-β1) content in cardiac tissues, with Smad3 phosphorylation decreased and Smad7 protein expression increased notably (P <0.05 or P <0.01).In addition, sesamin significantly increased total antioxidant capacity and superoxide dismutase protein in cardiac tissues (P <0.05 or P <0.01), while the expression of NADPH oxidase subunit p47phox and malondialdehyde content were reduced markedly (P <0.05 or P <0.01).

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Wannan Medical College, Wuhu, 241002, China.

ABSTRACT
This study investigated the effect of sesamin on myocardial fibrosis in spontaneously hypertensive rats (SHRs) and the possible mechanisms involved. Twenty-eight male SHRs were randomly allocated to SHR group, Ses160 group (sesamin 160 mg/kg), Ses80 group (sesamin 80 mg/kg) and Cap30 group (captopril 30 mg/kg). Seven male WKY rats were used as control. Sesamin and captopril were administered intragastrically for 12 weeks. Captopril significantly reduced systolic blood pressure and angiotensin II (Ang II) levels in SHRs, accompanied by a marked attenuation of left ventricular hypertrophy (LVH) and collagen deposition (P <0.05 or P <0.01). Though sesamin had no significant influence on Ang II levels, and the hypotensive effect was also significantly inferior to that of captopril (P <0.05 or P <0.01), however, the improvement of LVH and collagen deposition was similar to that in captopril group. Sesamin markedly reduced transforming growth factor-β1 (TGF-β1) content in cardiac tissues, with Smad3 phosphorylation decreased and Smad7 protein expression increased notably (P <0.05 or P <0.01). Protein expression of type I collagen and type III collagen, target genes of Smad3, was down-regulated markedly by sesamin (P <0.05 or P <0.01). In addition, sesamin significantly increased total antioxidant capacity and superoxide dismutase protein in cardiac tissues (P <0.05 or P <0.01), while the expression of NADPH oxidase subunit p47phox and malondialdehyde content were reduced markedly (P <0.05 or P <0.01). In vitro studies also demonstrated that sesamin was able to suppress Ang II induced phosphorylation of Smad3 and secretion of TGF-β1 and type I and type III collagen in cultured rat cardiac fibroblasts. These data suggest that sesamin is capable of attenuating hypertensive myocardial fibrosis through, at least partly, suppression of TGF-β1/Smad signaling pathway.

No MeSH data available.


Related in: MedlinePlus

Effect of sesamin on left ventricular mass index (LVMI) in rats.After 12 weeks of supplementation with sesamin or captopril, rats were anaesthetized with pentobarbital sodium and sacrificed, followed by dissection of left ventricles. LVMI is calculated as the ratio of left ventricular weight to body weight (mg/g). Data were presented as mean±SD (n = 7). b P <0.01 vs. WKY group; c P <0.05, d P <0.01 vs. SHR group.
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pone.0121312.g002: Effect of sesamin on left ventricular mass index (LVMI) in rats.After 12 weeks of supplementation with sesamin or captopril, rats were anaesthetized with pentobarbital sodium and sacrificed, followed by dissection of left ventricles. LVMI is calculated as the ratio of left ventricular weight to body weight (mg/g). Data were presented as mean±SD (n = 7). b P <0.01 vs. WKY group; c P <0.05, d P <0.01 vs. SHR group.

Mentions: As shown in Fig. 2, LVMI (mg/g) of SHR group was notably higher than that of WKY group (3.28 ± 0.17 vs 1.90 ± 0.12, P <0.01), indicating that SHRs developed significant left ventricular hypertrophy. Supplementation with sesamin resulted in a marked reduction in LVMI (3.08 ± 0.14 and 2.90 ± 0.10, P <0.05 or P <0.01), suggesting that sesamin can effectively ameliorate left ventricular hypertrophy in hypertensive rats. Treatment with captopril also led to a significant alleviation of left ventricular hypertrophy (2.78 ± 0.14, P <0.01). Both captopril and sesamin can induce only partial reduction of LVMI in SHRs as compared to WKY group (P <0.01).


Suppression of TGF-β1/Smad signaling pathway by sesamin contributes to the attenuation of myocardial fibrosis in spontaneously hypertensive rats.

Zhao M, Zheng S, Yang J, Wu Y, Ren Y, Kong X, Li W, Xuan J - PLoS ONE (2015)

Effect of sesamin on left ventricular mass index (LVMI) in rats.After 12 weeks of supplementation with sesamin or captopril, rats were anaesthetized with pentobarbital sodium and sacrificed, followed by dissection of left ventricles. LVMI is calculated as the ratio of left ventricular weight to body weight (mg/g). Data were presented as mean±SD (n = 7). b P <0.01 vs. WKY group; c P <0.05, d P <0.01 vs. SHR group.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4368740&req=5

pone.0121312.g002: Effect of sesamin on left ventricular mass index (LVMI) in rats.After 12 weeks of supplementation with sesamin or captopril, rats were anaesthetized with pentobarbital sodium and sacrificed, followed by dissection of left ventricles. LVMI is calculated as the ratio of left ventricular weight to body weight (mg/g). Data were presented as mean±SD (n = 7). b P <0.01 vs. WKY group; c P <0.05, d P <0.01 vs. SHR group.
Mentions: As shown in Fig. 2, LVMI (mg/g) of SHR group was notably higher than that of WKY group (3.28 ± 0.17 vs 1.90 ± 0.12, P <0.01), indicating that SHRs developed significant left ventricular hypertrophy. Supplementation with sesamin resulted in a marked reduction in LVMI (3.08 ± 0.14 and 2.90 ± 0.10, P <0.05 or P <0.01), suggesting that sesamin can effectively ameliorate left ventricular hypertrophy in hypertensive rats. Treatment with captopril also led to a significant alleviation of left ventricular hypertrophy (2.78 ± 0.14, P <0.01). Both captopril and sesamin can induce only partial reduction of LVMI in SHRs as compared to WKY group (P <0.01).

Bottom Line: Though sesamin had no significant influence on Ang II levels, and the hypotensive effect was also significantly inferior to that of captopril (P <0.05 or P <0.01), however, the improvement of LVH and collagen deposition was similar to that in captopril group.Sesamin markedly reduced transforming growth factor-β1 (TGF-β1) content in cardiac tissues, with Smad3 phosphorylation decreased and Smad7 protein expression increased notably (P <0.05 or P <0.01).In addition, sesamin significantly increased total antioxidant capacity and superoxide dismutase protein in cardiac tissues (P <0.05 or P <0.01), while the expression of NADPH oxidase subunit p47phox and malondialdehyde content were reduced markedly (P <0.05 or P <0.01).

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Wannan Medical College, Wuhu, 241002, China.

ABSTRACT
This study investigated the effect of sesamin on myocardial fibrosis in spontaneously hypertensive rats (SHRs) and the possible mechanisms involved. Twenty-eight male SHRs were randomly allocated to SHR group, Ses160 group (sesamin 160 mg/kg), Ses80 group (sesamin 80 mg/kg) and Cap30 group (captopril 30 mg/kg). Seven male WKY rats were used as control. Sesamin and captopril were administered intragastrically for 12 weeks. Captopril significantly reduced systolic blood pressure and angiotensin II (Ang II) levels in SHRs, accompanied by a marked attenuation of left ventricular hypertrophy (LVH) and collagen deposition (P <0.05 or P <0.01). Though sesamin had no significant influence on Ang II levels, and the hypotensive effect was also significantly inferior to that of captopril (P <0.05 or P <0.01), however, the improvement of LVH and collagen deposition was similar to that in captopril group. Sesamin markedly reduced transforming growth factor-β1 (TGF-β1) content in cardiac tissues, with Smad3 phosphorylation decreased and Smad7 protein expression increased notably (P <0.05 or P <0.01). Protein expression of type I collagen and type III collagen, target genes of Smad3, was down-regulated markedly by sesamin (P <0.05 or P <0.01). In addition, sesamin significantly increased total antioxidant capacity and superoxide dismutase protein in cardiac tissues (P <0.05 or P <0.01), while the expression of NADPH oxidase subunit p47phox and malondialdehyde content were reduced markedly (P <0.05 or P <0.01). In vitro studies also demonstrated that sesamin was able to suppress Ang II induced phosphorylation of Smad3 and secretion of TGF-β1 and type I and type III collagen in cultured rat cardiac fibroblasts. These data suggest that sesamin is capable of attenuating hypertensive myocardial fibrosis through, at least partly, suppression of TGF-β1/Smad signaling pathway.

No MeSH data available.


Related in: MedlinePlus